Zaburzenia rytmu serca
Patofizjologia i mechanizm

Zaburzenia rytmu serca (arytmie) wynikają z dwóch głównych mechanizmów: nieprawidłowego powstawania impulsów (zwiększona lub nieprawidłowa automatyczność oraz aktywność wyzwalana) oraz zaburzeń przewodzenia (pobudzenie nawrotne, reentry). Automatyczność obejmuje zmiany w funkcji węzła zatokowego i ektopowych rozruszników, z udziałem mutacji genetycznych, np. kanału HCN4, prowadzących do bradykardii lub tachykardii. Aktywność wyzwalana dzieli się na późne (DAD) i wczesne następcze depolaryzacje (EAD), które są związane z zaburzeniami elektrolitowymi, uszkodzeniem mięśnia sercowego i działaniem katecholamin, np. w katecholaminergicznym polimorficznym częstoskurczu komorowym (CPVT). Reentry, odpowiedzialne za 80-90% klinicznych arytmii, wymaga substratu tkankowego, jednokierunkowego bloku przewodzenia i wolnego przewodzenia alternatywnego, i może mieć charakter anatomiczny (np. nawrotny częstoskurcz przedsionkowo-komorowy) lub funkcjonalny (np. migotanie przedsionków). Zaburzenia jonowe, w tym mutacje kanałów jonowych (np. Kir2.1, NaV1.5), oraz elektrolitowe (hipokaliemia, hipermagnezemia, hiperkalcemia) znacząco wpływają na patogenezę arytmii.

Patogeneza zaburzeń rytmu serca

Zaburzenia rytmu serca (arytmie) to odchylenia od prawidłowej częstości i/lub rytmu serca, które nie są fizjologicznie uzasadnione. W ostatnich latach dokonano znacznego postępu w zrozumieniu mechanizmów elektrofizjologicznych leżących u podstaw rozwoju różnych zaburzeń rytmu serca. Mechanizmy odpowiedzialne za arytmie dzieli się zasadniczo na dwie główne kategorie: (1) wzmożone lub nieprawidłowe powstawanie impulsów (tj. aktywność ogniskowa) oraz (2) zaburzenia przewodzenia (tj. pobudzenie nawrotne).1 Aby w pełni zrozumieć mechanizmy leżące u podstaw arytmii, należy przeanalizować podstawowe zjawiska elektrofizjologiczne zachodzące na poziomie komórkowym, tkankowym i narządowym, które prowadzą do rozwoju tych zaburzeń.23

Zaburzenia powstawania impulsów

Powstawanie nieprawidłowych impulsów w sercu może prowadzić do arytmii poprzez dwa główne mechanizmy: zwiększoną lub nieprawidłową automatyczność oraz aktywność wyzwalaną.4

Nieprawidłowa automatyczność

Automatyczność to właściwość komórek serca do samoistnego generowania potencjałów czynnościowych bez uprzedniej stymulacji zewnętrznej.5 Obejmuje ona zarówno zmniejszoną automatyczność, która powoduje bradykardię, jak i zwiększoną automatyczność, która powoduje tachykardię. Arytmie spowodowane nieprawidłową automatycznością mogą wynikać z różnych mechanizmów. Zmiany częstości rytmu zatokowego mogą być związane z przesunięciem dominującego rozrusznika w obrębie węzła zatokowego lub do pomocniczych miejsc rozrusznikowych gdzie indziej w przedsionkach. Przewodzenie impulsów z węzła zatokowo-przedsionkowego (SA) może być upośledzone lub zablokowane w wyniku choroby lub zwiększonej aktywności nerwu błędnego, co prowadzi do rozwoju bradykardii.6

Bradykardia może wystąpić w strukturalnie prawidłowym sercu z powodu mutacji genetycznych, które powodują nieprawidłowości w mechanizmach automatyczności związanych z kanałami błonowymi lub wapniowymi. Jednym z przykładów jest mutacja kanału HCN4 (hyperpolarization-activated nucleotide-gated channel), który jest częścią kanałów przenoszących prąd If. Mutacje HCN4 mogą powodować rodzinną bradykardię. Powszechne choroby, takie jak niewydolność serca i migotanie przedsionków, mogą być związane ze znaczną dysfunkcją węzła zatokowego.7

Nieprawidłowa automatyczność występuje, gdy ektopowy rozrusznik wyzwala impulsy z nieprawidłową częstotliwością, przejmując kontrolę nad rytmem serca od prawidłowego węzła zatokowego.8 Ważnym wyróżnikiem normalnej automatyczności jest zjawisko tłumienia przez przyspieszenie (overdrive suppression). Wymuszenie na rozruszniku pomocniczym częstości wyższej niż jego własna częstość wewnętrzna zmniejsza nachylenie fazy 4, co jest głównie związane ze zwiększoną aktywnością pompy Na/K.9

Zasadnicza różnica między zwiększoną normalną a nieprawidłową automatycznością polega na tym, że ta druga jest mniej wrażliwa na tłumienie przez przyspieszenie, chociaż istnieją sytuacje, w których można to zaobserwować.10 Nieprawidłowa automatyczność może wystąpić w przypadkach podwyższonego poziomu potasu pozakomórkowego, niskiego wewnątrzkomórkowego pH i nadmiaru katecholamin.11

Aktywność wyzwalana

Aktywność wyzwalana (ang. triggered activity) definiuje się jako inicjację impulsów spowodowaną następczymi depolaryzacjami (oscylacjami potencjału błonowego, które występują podczas lub bezpośrednio po poprzedzającym potencjale czynnościowym).1213 Wyróżnia się dwa główne typy aktywności wyzwalanej:

Późne następcze depolaryzacje (DAD – Delayed Afterdepolarization) są oscylacjami potencjału błonowego, które występują po zakończeniu repolaryzacji potencjału czynnościowego (podczas fazy 4).14 DAD są zazwyczaj obserwowane w tkankach sercowych narażonych na uszkodzenie, zaburzenia elektrolitowe, hipoksję, kwasicę, katecholaminy i środki farmakologiczne, w tym leki przeciwarytmiczne.15

Przykładem arytmii wywołanej przez DAD jest polimorficzny częstoskurcz komorowy zależny od katecholamin (CPVT), który może być spowodowany mutacją receptora rianodynowego typu 2 (RyR2) lub kalsekwestryny (CSQ2). Głównym mechanizmem leżącym u podstaw tych arytmii jest „przeciekający” receptor rianodynowy, co nasila się podczas stymulacji katecholaminami. Typowym klinicznym fenotypem CPVT jest dwukierunkowy częstoskurcz komorowy, który występuje również w przypadku zatrucia naparstnicą.16

Wczesne następcze depolaryzacje (EAD – Early Afterdepolarization) są oscylacjami potencjału, które występują podczas plateau potencjału czynnościowego (faza 2 EAD) lub podczas późnej repolaryzacji (faza 3 EAD).17 EAD są typowo obserwowane w tkankach sercowych narażonych na uszkodzenie, zaburzenia elektrolitowe, hipoksję, kwasicę, katecholaminy i środki farmakologiczne, w tym leki przeciwarytmiczne. Przerost komór i niewydolność serca również predysponują do rozwoju EAD.18

Chociaż konkretne mechanizmy indukcji EAD mogą się różnić, krytyczne wydłużenie repolaryzacji towarzyszy większości, ale nie wszystkim EAD. Leki hamujące prądy potasowe lub zwiększające prądy dokomórkowe predysponują do rozwoju EAD.19

W 2003 roku Burashnikov i Antzelevitch opisali nowy mechanizm dający początek aktywności wyzwalanej, nazywany późną fazą 3 EAD, który łączy właściwości zarówno EAD, jak i DAD, ale ma swój własny unikalny charakter. Późne fazy 3 EAD to mechanizm arytmogenezy, w którym skrócona repolaryzacja pozwala na normalne uwalnianie wapnia przez siateczkę sarkoplazmatyczną, co wywołuje wyzwalaną odpowiedź za pośrednictwem EAD, szczególnie w warunkach umożliwiających wewnątrzkomórkowe gromadzenie wapnia.20

Mechanizm nawrotnego pobudzenia (reentry)

Reentry (pobudzenie nawrotne) zasadniczo różni się od automatyczności lub aktywności wyzwalanej pod względem mechanizmu, w jakim inicjuje i podtrzymuje arytmie serca. Reentry krążące występuje, gdy front aktywacji rozchodzi się wokół anatomicznej lub funkcjonalnej przeszkody czy rdzenia, a następnie ponownie pobudza miejsce pochodzenia. W tym typie reentry wszystkie komórki kolejno powracają ze stanu pobudzenia, aby były gotowe do ponownego pobudzenia, gdy nadejdzie następna fala pobudzenia.21

Reentry jest prawdopodobnie najczęstszym mechanizmem odpowiedzialnym za tachyarytmie, zarówno nadkomorowe, jak i komorowe. Szacuje się, że 80-90% klinicznych arytmii występuje z powodu zjawiska reentry.22

Reentry zostało podzielone na dwie główne grupy: anatomiczne lub klasyczne reentry, gdzie obwód jest określony przez struktury anatomiczne, oraz reentry funkcjonalne, które z kolei obejmuje różne mechanizmy.2324

Warunki konieczne do powstania reentry obejmują:2526

  • Substrat: obecność połączonej tkanki mięśnia sercowego o różnych właściwościach elektrofizjologicznych, przewodzeniu i refrakcyjności
  • Jednokierunkowy blok przewodzenia w jednej z dróg
  • Wolne przewodzenie w alternatywnej drodze, umożliwiające ustąpienie refrakcji w miejscu bloku jednokierunkowego

Klasyczny mechanizm reentry oparty jest na niepobudliwej przeszkodzie anatomicznej otoczonej okrężną drogą, w której front fali może ponownie wejść, tworząc stałe i stabilne obwody reentry.2728 Kliniczne przykłady obejmują: nawrotny częstoskurcz przedsionkowo-komorowy związany z dodatkową drogą przewodzenia, nawrotny częstoskurcz węzłowy, trzepotanie przedsionków, nawrotny częstoskurcz komorowy po zawale mięśnia sercowego i częstoskurcz z gałęzi pęczka Hisa.29

W reentry funkcjonalnym obwód nie jest określony przez przeszkody anatomiczne; jest definiowany przez dynamiczną heterogenność we właściwościach elektrofizjologicznych zaangażowanej tkanki.30 Trzy warunki sprzyjające reentry to: skrócenie refrakcyjności tkanki (np. poprzez stymulację współczulną), wydłużenie drogi przewodzenia (np. z powodu przerostu lub nieprawidłowych dróg przewodzenia) oraz zwolnienie przewodzenia impulsów (np. z powodu niedokrwienia).31

Rola zaburzeń jonowych i kanałów jonowych w patogenezie arytmii

Zaburzenia jonowe i nieprawidłowości w funkcjonowaniu kanałów jonowych są kluczowymi czynnikami w patogenezie wielu typów zaburzeń rytmu serca.32 Prawidłowe funkcjonowanie elektrofizjologiczne serca opiera się na złożonej interakcji różnych prądów jonowych, które regulują depolaryzację i repolaryzację komórek mięśnia sercowego.

Zaburzenia równowagi elektrolitowej

Zaburzenia elektrolitowe mogą znacząco wpływać na ryzyko wystąpienia arytmii. Wapń i magnez mogą wpływać na ryzyko migotania przedsionków, które jest główną przyczyną śmierci sercowej, niewydolności serca i udaru niedokrwiennego.33 Podwyższone stężenie wapnia w surowicy wiąże się z wyższą śmiertelnością wewnątrzszpitalną, zwiększonym całkowitym kosztem hospitalizacji i zwiększoną długością pobytu w szpitalu w porównaniu z pacjentami bez hiperkalcemii z migotaniem przedsionków.34

Niedobór magnezu jest związany z do 50% większym ryzykiem wystąpienia migotania przedsionków, a także z przerostem lewej komory, nagłą śmiercią sercowo-naczyniową i ogólną śmiertelnością.35 Magnez zapobiega występowaniu migotania przedsionków po operacji serca.36

Liczne badania kliniczne wykazały, że niskie stężenie potasu w surowicy jest związane z wysokim przedoperacyjnym ryzykiem migotania przedsionków.37 Zaburzenia potasu są głównym problemem w cukrzycowej kwasicy ketonowej i mogą potencjalnie prowadzić do śmiertelnych arytmii.38

Wysokie spożycie sodu w diecie może niezależnie zwiększać ryzyko nowych epizodów migotania przedsionków, co nasila zwłóknienie i stan zapalny w przedsionku, choć mechanizm pozostaje nieznany.39

Kanały jonowe i ich rola w arytmogenezie

Kanały jonowe odgrywają kluczową rolę w utrzymaniu prawidłowego rytmu serca. Zmiany w ekspresji lub funkcji kanałów jonowych mogą prowadzić do zaburzeń elektrycznych, które inicjują i podtrzymują arytmie.40

Przyczynienie się do utrwalenia migotania przedsionków jest spowodowane przebudową elektryczną, w której kanały wapniowe, sodowe i potasowe mogą odnosić się do zmian w ekspresji białka kanału jonowego, rozwoju zwłóknienia, transkrypcji genów i redystrybucji kanału jonowego.41

W prawidłowym sercu z migotaniem przedsionków zwiększone uwalnianie wapnia z siateczki sarkoplazmatycznej i zwiększona wrażliwość na wapń mogą prowadzić do gromadzenia się wewnątrzkomórkowego wapnia i powodować down-regulację kanałów wapniowych typu L. To zmniejsza czas trwania potencjału czynnościowego i okres refrakcji, sprzyjając tym samym przewodzeniu fal nawrotnych.42

W niedawnym badaniu opublikowanym w Circulation Research ustalono bezpośredni związek między zagrażającymi życiu arytmiami a mutacją C122Y w kanale potasowym Kir2.1. Badanie wykazuje, że mutacja C122Y w Kir2.1 ma podwójny efekt: powoduje reorganizację kanału Kir2.1, która destabilizuje jego wiązanie z fosfolipidem PIP2, kluczowym składnikiem sygnalizacji lipidowej błony komórkowej, a także zakłóca ekspresję białka tworzącego kanał NaV1.5, upośledzając jego funkcję.43

Rola zaburzeń przewodzenia w patogenezie arytmii

Zaburzenia przewodzenia są jednym z głównych mechanizmów leżących u podstaw arytmii serca. Mogą one wynikać z bloku przewodzenia lub zjawiska reentry, które prowadzi do podtrzymywania szybkich i nieprawidłowych rytmów.44

Bloki przewodzenia

Bloki przewodzenia występują, gdy impulsy przedsionkowe są przewodzone z opóźnieniem lub wcale nie są przewodzone, gdy impuls elektryczny dociera do tkanki, która nie jest pobudliwa lub znajduje się w okresie refrakcji.45 Bloki przewodzenia mogą występować na różnych poziomach układu przewodzącego serca:

46

Bloki przedsionkowo-komorowe (AVB) odnoszą się do nieprawidłowości w układzie przewodzącym serca w węźle przedsionkowo-komorowym, co ogranicza pulsację dolnej komory serca. AVB są głównie spowodowane nieprawidłowym przewodzeniem elektrycznym między komorami a przedsionkami, zwykle występującym podczas ataków migotania przedsionków.47

Blok przedsionkowo-komorowy II stopnia (II AVB) jest jednym z częstych powikłań u pacjentów z migotaniem przedsionków, a elektrokardiogram (EKG) zwykle pokazuje odstęp R-R wynoszący 1,5 s i wysoką częstość rytmu komór. W praktyce klinicznej II AVB nie tylko wpływa na funkcję serca pacjenta i obniża jego jakość życia, ale może również prowadzić do powikłań, takich jak zatorowość, tachykardia i kardiomiopatia, zagrażając życiu pacjenta.48

Mobitz I (zjawisko Wenckebacha) jest zwykle spowodowany odwracalnym blokiem przewodzenia na poziomie węzła AV. Upośledzonych komórek węzła AV mają tendencję do stopniowego męczenia się, aż nie będą w stanie przewodzić impulsu. Jest to różne od komórek układu Hisa-Purkinjego, które mają tendencję do nagłego i nieoczekiwanego uszkodzenia (czyli powodują blok Mobitz II).49

Reentry i predyspozycje anatomiczne

Reentry jest głównym mechanizmem odpowiedzialnym za tachyarytmie wymagające leczenia. Większość przypadków trzepotania przedsionków jest spowodowana przez reentry, a reentry ma podstawową rolę w rozwoju migotania przedsionków.50

Mechanizmy reentry mogą być związane z anatomicznymi lub funkcjonalnymi przeszkodami w sercu. Klasyczne reentry anatomiczne występuje, gdy impulsy krążą wokół stałej przeszkody anatomicznej, takiej jak blizna po zawale, otwór owalny, zastawka lub inna struktura serca. Reentry funkcjonalne może wystąpić bez jasno określonej przeszkody anatomicznej, a zamiast tego opiera się na różnicach w właściwościach elektrofizjologicznych tkanek.51

Przykłady kliniczne reentry obejmują:52

  • Nawrotny częstoskurcz przedsionkowo-komorowy związany z dodatkową drogą przewodzenia (droga dodatkowa Kent)
  • Nawrotny częstoskurcz węzłowy przedsionkowo-komorowy (mechanizm: wolne szybkie włókna obecne w węźle AV prowadzące do reentry)
  • Trzepotanie przedsionków
  • Częstoskurcz komorowy po zawale mięśnia sercowego

53

W przypadku pacjentów z zespołem WPW (Wolff-Parkinson-White) obecna jest dodatkowa droga przedsionkowo-komorowa (rodzaj drogi omijającej nazywanej pęczkiem Kenta). U tych pacjentów występuje zwiększone ryzyko tachyarytmii z powodu możliwości reentry przez dodatkową drogę.54

Rola czynników genetycznych w patogenezie arytmii

Badania genetyczne zidentyfikowały specyficzne związki, szczególnie w przypadkach rodzinnego migotania przedsionków.55 Mutacje genetyczne mogą wpływać na funkcję kanałów jonowych, białek strukturalnych i innych komponentów komórek serca, prowadząc do zwiększonej podatności na arytmie.

Dziedziczne zespoły arytmogenne

Istnieje wiele dziedzicznych zespołów, które predysponują do wystąpienia zaburzeń rytmu serca:

  • Zespół długiego QT (LQTS) – zaburzenie, w którym komory serca kurczą się i zwalniają zbyt wolno, co czasami prowadzi do omdleń (syncope) lub zatrzymania krążenia.56
  • Zespół Brugadów – mechanizmy arytmogenezy w zespole Brugadów można wyjaśnić heterogenicznym skróceniem czasu trwania potencjału czynnościowego na nasierdziu prawej komory.57
  • Katecholaminergiczny polimorficzny częstoskurcz komorowy (CPVT) – może być spowodowany mutacją receptora rianodynowego typu 2 (RyR2) lub kalsekwestryny (CSQ2).58
  • Zespół Andersena-Tawila – badania wykazały, że mutacja C122Y w kanale potasowym Kir2.1 ma podwójny efekt: powoduje reorganizację kanału Kir2.1 oraz zakłóca ekspresję białka tworzącego kanał NaV1.5.59

Mutacje kanałów jonowych

Mutacje genów kodujących kanały jonowe są częstą przyczyną dziedzicznych arytmii. Na przykład:

  • Mutacje kanału HCN4, który jest częścią kanałów przenoszących prąd If, mogą powodować rodzinną bradykardię.60
  • Mutacja A450V w genie HCN4 odpowiada za rodzinną bradykardię zatokową u niespokrewnionych probandów pochodzenia marokańsko-żydowskiego.61
  • Mutacje w kanałach sodowych, potasowych i wapniowych mogą prowadzić do zespołu długiego QT, zespołu Brugadów i innych dziedzicznych arytmii.62

Wyniki niedawnego badania opublikowanego w Circulation Research wspierają hipotezę, że mechanizmy molekularne zwiększające podatność na arytmie i nagłą śmierć sercową w zespole Andersena-Tawila typu 1 (ATS1) zależą od konkretnej mutacji, więc leczenie farmakologiczne i postępowanie kliniczne powinny być dostosowane do każdego indywidualnego pacjenta.63

Rola czynników środowiskowych i współistniejących chorób

Zaburzenia rytmu serca mogą być wywołane przez różnorodne stany i substancje wpływające na fizjologię i funkcję elektryczną serca. Śmiertelne arytmie, które powodują nagłe zatrzymanie krążenia, nie są wyjątkiem.64

Choroby współistniejące

Wiele chorób może przyczyniać się do rozwoju zaburzeń rytmu serca:

  • Choroba niedokrwienna serca – niedokrwienie mięśnia sercowego może prowadzić do zaburzeń przewodzenia i arytmii.65
  • Niewydolność serca – jest najczęstszą przyczyną hospitalizacji z powodu chorób sercowo-naczyniowych i nakłada ogromne obciążenie na system opieki zdrowotnej i społeczeństwo.66
  • Kardiomiopatia – zmiany strukturalne w sercu mogą tworzyć podłoże do arytmii.67
  • Zaburzenia endokrynologiczne – zaburzenia endokrynologiczne mogą prowadzić do arytmii serca, co może mieć poważne konsekwencje dla zdrowia jednostki, w tym nagłą śmierć sercową.68
  • Cukrzyca – może przyczyniać się do różnych typów arytmii serca, ale migotanie przedsionków jest najczęściej zgłaszaną arytmią związaną z cukrzycą.69
  • Niedoczynność tarczycy – może prowadzić do zmniejszenia pojemności minutowej serca nawet o 30-40%, co można przypisać zmniejszeniu zarówno objętości wyrzutowej, jak i częstości akcji serca. Dodatkowo niedoczynność tarczycy może powodować bloki przewodzenia o różnym stopniu.70
  • Nadczynność tarczycy – problemy sercowe wywołane nadczynnością tarczycy mogą obejmować tachykardię zatokową, podwyższone napięcie zespołu QRS oraz przedwczesne skurcze przedsionkowe i komorowe. Około 6-12% pacjentów z nadczynnością tarczycy doświadcza napadowego częstoskurczu przedsionkowego i migotania przedsionków.71

Czynniki związane ze stylem życia

Styl życia może znacząco wpływać na ryzyko wystąpienia arytmii:

  • Alkohol – nadmierne spożycie alkoholu może wyzwalać arytmie.72
  • Kofeina – nadmierne spożycie kofeiny może wyzwalać arytmie u niektórych osób.73
  • Palenie tytoniu – historia palenia jest jednym z czynników wpływających na kombinację migotania przedsionków z blokiem przedsionkowo-komorowym II stopnia.74
  • Stres – zaburzenie równowagi układu wegetatywnego (stres, lęk, wstrząs, kompensacja innego stanu patologicznego) może przyczyniać się do arytmii.75

Rola układu immunologicznego i zapalenia w patogenezie arytmii

Coraz więcej dowodów wskazuje na istotną rolę układu immunologicznego i stanów zapalnych w patogenezie zaburzeń rytmu serca.76 Mechanizmy immunopatogenetyczne zaburzeń rytmu serca i przewodzenia zostały zidentyfikowane w zespole chorego węzła zatokowego, bradyarytmiach i zespole nadwrażliwej zatoki szyjnej.77

Rola zapalenia

Zapalenie może inicjować lub nasilać arytmie, zmieniając właściwości elektrofizjologiczne komórek serca, takie jak ekspresja kanałów jonowych, potencjał błonowy, gospodarka wapniowa i sprzężenie złącza szczelinowego. Zapalenie może również powodować zmiany strukturalne w tkance sercowej, takie jak apoptoza, przerost i zwłóknienie.78

Z drugiej strony, arytmie mogą wywoływać lub zaostrzać zapalenie poprzez uszkodzenie serca przez napięcie mechaniczne, niedokrwienie-reperfuzję lub stres oksydacyjny.79

Istnieje kilka przyczyn zapalenia ogólnoustrojowego, w tym sepsa, uraz, operacja i przewlekłe choroby.80 Zapalenie ogólnoustrojowe może wpływać na arytmogenność poprzez kilka mechanizmów:

  1. Stres oksydacyjny i uszkodzenie komórek serca, które mogą prowadzić do zmniejszonego przewodzenia elektrycznego i zwiększonej podatności na obwody reentry.81
  2. Zaburzenie równowagi autonomicznego układu nerwowego (ANS).82
  3. Wpływ na poziomy elektrolitów (potas, wapń, magnez), które są niezbędne dla prawidłowego potencjału czynnościowego komór.83
  4. Aktywacja układu krzepnięcia i zwiększenie ryzyka zakrzepicy, co może prowadzić do zawału mięśnia sercowego i niedokrwienia.84

Lokalne zapalenie serca

Konkretne infekcje, w tym infekcje bakteryjne, grzybicze lub wirusowe, a także zaburzenia autoimmunologiczne, mogą prowadzić do miejscowego zapalenia.85 Lokalne zapalenie może wpływać na rytm serca poprzez:

  1. Przebudowę strukturalną tkanki sercowo-naczyniowej, w tym procesy takie jak martwica, apoptoza i zwłóknienie.86
  2. Zapalenie zwojów lub nerwów sercowych, co może zmieniać regulację autonomicznego układu nerwowego serca.87
  3. Bezpośrednie uszkodzenie komórek serca, upośledzając ich zdolność do gospodarki wapniowej, zwiększając ich automatyczność lub zwiększając ich podatność na katecholaminy.88
  4. Ucisk lub infiltrację układu przewodzącego serca, w tym węzła zatokowo-przedsionkowego, węzła przedsionkowo-komorowego i układu Hisa-Purkinjego, co może prowadzić do bloku serca lub bradyarytmii.89

Stany takie jak zapalenie wsierdzia, zapalenie mięśnia sercowego lub zapalenie osierdzia mogą wynikać z miejscowego zapalenia, które dotyczy konkretnych komponentów serca.90

Nowe koncepcje w patogenezie arytmii

Obecnie prowadzone są intensywne badania nad nowymi mechanizmami i koncepcjami w patogenezie zaburzeń rytmu serca, co może prowadzić do rozwoju innowacyjnych metod diagnostycznych i terapeutycznych.

Dysregulacja immunometaboliczna

Normalne sprzężenie immunometaboliczne pomiędzy retikulum endoplazmatycznym (ER) a mitochondriami jest istotnym warunkiem prawidłowego rytmu serca. Stres ER i stres oksydacyjny mitochondriów mogą wywoływać wyzwania immunometaboliczne, które mogą powodować stan zapalny, lipotoksyczność i apoptozę komórek, prowadząc do choroby wieńcowej i wynikających z niej arytmii.91

W patogenezie chorób sercowo-naczyniowych i wynikających z nich arytmii, urazy immunologiczne i zaburzenia metaboliczne występują jednocześnie i są ze sobą powiązane, tworząc nieprawidłowo funkcjonującą sieć immunometaboliczną.92

Zaburzenia immunometaboliczne obejmują dysregulację wielu organelli podczas uszkodzeń serca i następującej po nich arytmii. Stres ER i stres oksydacyjny mitochondriów stanowią punkt przecięcia uszkodzenia immunologicznego i zaburzeń metabolicznych, reprezentując w wysokim stopniu nieprawidłowe funkcje sieci immunometabolicznej w arytmogenezie.93

Rola rytmu dobowego i kortyzolu

Badania prowadzone przez Imperial College London wykazały, że potencjalnie śmiertelne zaburzenia rytmu serca (arytmia komorowa) są bardziej prawdopodobne rano, po przebudzeniu z nocnego snu, i są związane z naturalnym wzrostem poziomu hormonu stresu – kortyzolu, który osiąga szczyt we krwi rano.9495

W badaniu na myszach wykazano, że kortyzol wiąże się z określonym receptorem w komórkach serca. Receptor przemieszcza się do jądra, gdzie wpływa na geny regulujące kanały jonowe w błonie komórkowej, które kontrolują uderzenia serca. Gdy aktywność kanałów jonowych się zmienia, serce staje się znacznie bardziej podatne, ponieważ łatwiej jest regularne impulsy elektryczne, które powodują regularne uderzenia serca, rozpaść się na bardziej chaotyczną aktywność lub arytmię.96

Odkrycie to tłumaczy, dlaczego arytmie komorowe występują częściej we wczesnych godzinach porannych i może prowadzić do rozwoju nowych metod leczenia.97 Jak zauważyła główna badaczka Alicia DSouza z National Heart and Lung Institute (HNLI) Imperial College: „Nasze serca są efektywnie różnymi narządami w różnych porach dnia. Są bardziej podatne wcześnie rano z powodu starożytnych rytmów dobowych, które ewoluowały przez miliony lat.”9899

Rola hipoksji i citrullinacji

Niskie poziomy tlenu w sercu od dawna są znane jako czynnik wywołujący zagrażające życiu arytmie, a nawet nagłą śmierć. Najnowsze badania pokazują, że w ciągu kilku sekund, przy niskich poziomach tlenu (hipoksja), białko nazywane małym modyfikatorem podobnym do ubikwityny (SUMO) jest powiązane z wewnętrzną częścią kanałów sodowych, które są odpowiedzialne za rozpoczęcie każdego uderzenia serca.100

Jeśli kanały sodowe ponownie się otwierają i wytwarzają późne prądy sodowe, jak zaobserwowano w tym badaniu przy niskich poziomach tlenu, potencjał czynnościowy jest wydłużony i nowa aktywność elektryczna może rozpocząć się, zanim serce zdąży się zregenerować, co grozi niebezpiecznymi, zdezorganizowanymi rytmami.101

Inne badania pokazują, że PAD2 (peptidyloarginina deiminaza 2) odgrywa kluczową rolę w patogenezie arytmii wywołanych wstrząsem krwotocznym poprzez regulację aktywności SERCA2a poprzez citrullinację. Inhibicja PAD2 może stanowić nowe podejście terapeutyczne do łagodzenia dysfunkcji serca i poprawy przeżywalności u pacjentów z urazowym wstrząsem krwotocznym.102

Wpływ leków i substancji na arytmogenezę

Wiele leków i substancji może wpływać na funkcję elektryczną serca i przyczyniać się do rozwoju zaburzeń rytmu serca.103

Leki przeciwarytmiczne a proarytmia

Leki przeciwarytmiczne, które są stosowane do leczenia zaburzeń rytmu serca, mogą paradoksalnie również wywoływać arytmie.104 Ten paradoksalny efekt znany jest jako proarytmia.

Leki, które hamują prądy potasowe lub które zwiększają prądy dokomórkowe, predysponują do rozwoju wczesnych następczych depolaryzacji (EAD).105 Jest to szczególnie istotne w przypadku leków klasy IA i III, które wydłużają okres repolaryzacji.

Inne leki i substancje wpływające na rytm serca

Wiele różnych substancji może wpływać na rytm serca:106

  • Substancje arytmogenne (leki, kofeina, adrenalina, alkohol, digoksyna, diuretyki, leki przeciwarytmiczne)
  • Niektóre leki przeciwcukrzycowe mogą powodować wydłużenie odstępu QT, albo w wyniku działania leku wywołującego hipoglikemię, albo jako bezpośredni skutek uboczny107
  • Stosowanie konopii – zaburzenia używania konopii wśród pacjentów z niewydolnością serca mogą zwiększać prawdopodobieństwo wystąpienia wstrząsu kardiogennego, zawału mięśnia sercowego i arytmii108

Suplementy i nutraceutyki w zapobieganiu arytmiom

Niektóre suplementy diety mogą mieć korzystny wpływ na zapobieganie i leczenie zaburzeń rytmu serca:

  • Koenzym Q10 (CoQ10) – suplementacja CoQ10 może zmniejszyć śmiertelność z przyczyn sercowo-naczyniowych i zmniejszyć sztywność tętnic oraz nadciśnienie. Niektóre badania sugerują, że ma działanie przeciwarytmiczne, co oznacza, że może korygować zbyt szybkie lub nieregularne bicie serca.109
  • Magnez – jest ważnym minerałem do regulacji różnych funkcji organizmu, w tym tych, które pomagają ustanowić regularny rytm serca. Retrospektywne badanie z 2020 roku sugerowało, że magnez w połączeniu ze standardową terapią pomógł obniżyć szybkie rytmy serca u osób z migotaniem przedsionków.110
  • Witamina C – przegląd z 2022 roku sugeruje, że witamina C może być korzystna w leczeniu migotania przedsionków po operacji serca i może zmniejszyć nawroty po kardiowersji.111
  • Imbir – badanie z 2021 roku sugeruje, że imbir ma różne działania kardioprotekcyjne, w tym działanie przeciwnadciśnieniowe, przeciwpłytkowe i przeciwhiperlipidemiczne. Badanie z 2016 roku sugeruje, że 100 miligramów na kilogram masy ciała imbiru jako codzienny suplement doustny przez 15 dni znacząco obniżyło częstość występowania arytmii u szczurów.112

Suplementy mogą pomóc wyrównać nierównowagę we krwi i przywrócić rytmy serca do oczekiwanych wzorców. Problemy z przewodnictwem elektrycznym, leki, stres lub wysiłek fizyczny, czy nierównowaga we krwi mogą powodować arytmie.113

Implikacje kliniczne dla leczenia zaburzeń rytmu serca

Zrozumienie mechanizmów leżących u podstaw arytmii ma kluczowe znaczenie dla opracowania odpowiednich strategii diagnostycznych i terapeutycznych. Leczenie zaburzeń rytmu serca obejmuje różne modalności, w zależności od rodzaju i nasilenia arytmii.114

Podejście terapeutyczne oparte na mechanizmach

Arytmie spowodowane nieprawidłową automatycznością mogą być leczone lekami, które zmniejszają automatyczność, takimi jak beta-blokery czy blokery kanału wapniowego. Propranolol, na przykład, jest stosowany w leczeniu stanów, które powodują nieregularne bicie serca (arytmię), jak migotanie przedsionków. Propranolol działa poprzez zmianę sposobu, w jaki organizm reaguje na niektóre impulsy nerwowe, w tym w sercu. Spowalnia częstość akcji serca i ułatwia sercu pompowanie krwi po ciele.115

Arytmie spowodowane aktywnością wyzwalaną mogą być leczone lekami, które zmniejszają wewnątrzkomórkowe stężenie wapnia lub które skracają czas trwania potencjału czynnościowego.

Arytmie oparte na mechanizmie reentry mogą być leczone poprzez przerwanie obiegu ponownego wejścia przy użyciu leków antyarytmicznych, ablacji lub urządzeń takich jak rozruszniki serca i kardiowertery-defibrylatory (ICD).116

Spersonalizowana medycyna w leczeniu zaburzeń rytmu serca

Rezultaty badań z Circulation Research wspierają hipotezę, że mechanizmy molekularne zwiększające podatność na arytmie i nagłą śmierć sercową w zespole Andersena-Tawila typu 1 (ATS1) zależą od konkretnej mutacji, więc leczenie farmakologiczne i postępowanie kliniczne powinny być dostosowane do każdego indywidualnego pacjenta.117

To podejście podkreśla znaczenie personalizacji leczenia arytmii, biorąc pod uwagę specyficzne mechanizmy leżące u podstaw zaburzeń rytmu u każdego pacjenta.

Nowe kierunki terapeutyczne

Odkrycie związku między poziomem kortyzolu a arytmiami porannymi podnosi perspektywę nowych metod leczenia w tej dziedzinie.118119

Badania nad patogenezą zaburzeń rytmu serca związanych z zapaleniem doprowadziły do nowych podejść terapeutycznych. Leki przeciwzapalne, takie jak kortykosteroidy, NLPZ, kolchicyna, statyny i leki biologiczne, mogą być stosowane w leczeniu kardiomiopatii zapalnych, które zwiększają ryzyko arytmii, takich jak sarkoidoza serca, zapalenie mięśnia sercowego i reumatyczna choroba serca.120

Informacje uzyskane dzięki nowym badaniom oferują nowe cele dla leków zapobiegających późnemu prądowi i arytmii związanej z zawałami serca, przewlekłą niewydolnością serca i innymi zagrażającymi życiu stanami serca z niskim poziomem tlenu.121

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  1. 10.04.2026
  2. www.leksykon.com.pl

Materiały źródłowe

  • #1 Overview of Basic Mechanisms of Cardiac Arrhythmia
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3164530/
    A cardiac arrhythmia simply defined is a variation from the normal heart rate and/or rhythm that is not physiologically justified. Recent years have witnessed important advances in our understanding of the electrophysiologic mechanisms underlying the development of a variety of cardiac arrhythmias. The mechanisms responsible for cardiac arrhythmias are generally divided into 2 major categories: (1) enhanced or abnormal impulse formation (ie, focal activity) and (2) conduction disturbances (ie, reentry). […] Abnormal automaticity includes both reduced automaticity, which causes bradycardia, and increased automaticity, which causes tachycardia. Arrhythmias caused by abnormal automaticity can result from diverse mechanisms. Alterations in sinus rate can be accompanied by shifts of the origin of the dominant pacemaker within the sinus node or to subsidiary pacemaker sites elsewhere in the atria. Impulse conduction out of the SA mode can be impaired or blocked as a result of disease or increased vagal activity leading to development of bradycardia. AV junctional rhythms occur when AV junctional pacemakers located either in the AV node or in the His bundle accelerate to exceed the rate of SA node, or when the SA nodal activation rate was too slow to suppress the AV junctional pacemaker.
  • #2 Mechanisms of Cardiac Arrhythmias – Revista Española de Cardiología (English Edition)
    https://www.revespcardiol.org/en-mechanisms-cardiac-arrhythmias-articulo-S1885585711006086
    Cardiac arrhythmias are prevalent among humans across all age ranges and may occur in the setting of underlying heart disease as well as in structurally normal hearts. While arrhythmias are widely varied in their clinical presentations, they possess shared electrophysiologic properties at the cellular level. The 3 main mechanisms responsible for cardiac arrhythmias are automaticity, triggered activity, and reentry. Although identifying the specific mechanism may at times be challenging for the clinician and require invasive electrophysiologic study, differentiating and understanding the underlying mechanism may be critical to the development of an appropriate diagnosis and treatment strategy. […] Understanding the mechanisms of arrhythmias is helpful to the appropriate management and treatment of all arrhythmia types. Since the mechanisms that lead to clinical arrhythmias are frequently due to abnormalities beyond the tissue level, it is also essential to understand what occurs at the cellular level.
  • #3 Mechanisms of Cardiac Arrhythmias – Revista Española de Cardiología (English Edition)
    https://www.revespcardiol.org/en-mechanisms-of-cardiac-arrhythmias-articulo-S1885585711006086
    Cardiac arrhythmias are prevalent among humans across all age ranges and may occur in the setting of underlying heart disease as well as in structurally normal hearts. While arrhythmias are widely varied in their clinical presentations, they possess shared electrophysiologic properties at the cellular level. The 3 main mechanisms responsible for cardiac arrhythmias are automaticity, triggered activity, and reentry. Although identifying the specific mechanism may at times be challenging for the clinician and require invasive electrophysiologic study, differentiating and understanding the underlying mechanism may be critical to the development of an appropriate diagnosis and treatment strategy. […] Understanding the mechanisms of arrhythmias is helpful to the appropriate management and treatment of all arrhythmia types. Since the mechanisms that lead to clinical arrhythmias are frequently due to abnormalities beyond the tissue level, it is also essential to understand what occurs at the cellular level.
  • #4 Mechanisms of cardiac arrhythmias: from automaticity to re-entry (reentry) – The Cardiovascular
    https://ecgwaves.com/topic/mechanisms-cardiac-arrhythmias-automaticity-reentry-triggered-activity/
    Cardiac arrhythmias can be subdivided into the following categories: Bradyarrhythmias (bradycardia): arrhythmias commonly due to dysfunctional automaticity in pacemaker cells or blocking of impulses somewhere along the conduction system. Supraventricular tachyarrhythmias (tachycardia): rapid arrhythmias due to impulses originating from the atria. Ventricular tachyarrhythmias (tachycardia): rapid arrhythmias due to impulses originating from the ventricles. […] The mechanisms underlying cardiac arrhythmias are being unraveled at an accelerating pace, making arrhythmology a field of intense research activity. […] Arrhythmias arise if the impulse formation is abnormal, if the impulse transmission is abnormal, or if both these are abnormal. […] Abnormal impulse formation can cause arrhythmias by the following two mechanisms: Increased or abnormal automaticity, Triggered activity.
  • #5 Mechanism of arrythmias | PPT
    https://www.slideshare.net/slideshow/mechanism-of-arrythmias/29637225
    1. Cardiac arrhythmias can be caused by disorders of impulse formation, disorders of impulse conduction, or a combination of the two. […] 2. Disorders of impulse formation include abnormalities in automaticity and triggered activity. […] 3. Abnormal automaticity occurs when an ectopic pacemaker fires at an inappropriate rate, taking over control of the heart rhythm from the normal sinus node. […] 4. Triggered activity is initiated by afterdepolarizations following an action potential. […] 5. Disorders of impulse conduction include conduction block and reentry, which is when an impulse circles back and reactivates tissue that is still recovering, leading to sustained, rapid rhythms. […] 6. The mechanisms responsible for arrhythmias are generally divided into Disorders of impulse formation, Disorders of impulse conduction, Combinations of both cardiac.
  • #6 Overview of Basic Mechanisms of Cardiac Arrhythmia
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3164530/
    A cardiac arrhythmia simply defined is a variation from the normal heart rate and/or rhythm that is not physiologically justified. Recent years have witnessed important advances in our understanding of the electrophysiologic mechanisms underlying the development of a variety of cardiac arrhythmias. The mechanisms responsible for cardiac arrhythmias are generally divided into 2 major categories: (1) enhanced or abnormal impulse formation (ie, focal activity) and (2) conduction disturbances (ie, reentry). […] Abnormal automaticity includes both reduced automaticity, which causes bradycardia, and increased automaticity, which causes tachycardia. Arrhythmias caused by abnormal automaticity can result from diverse mechanisms. Alterations in sinus rate can be accompanied by shifts of the origin of the dominant pacemaker within the sinus node or to subsidiary pacemaker sites elsewhere in the atria. Impulse conduction out of the SA mode can be impaired or blocked as a result of disease or increased vagal activity leading to development of bradycardia. AV junctional rhythms occur when AV junctional pacemakers located either in the AV node or in the His bundle accelerate to exceed the rate of SA node, or when the SA nodal activation rate was too slow to suppress the AV junctional pacemaker.
  • #7 Overview of Basic Mechanisms of Cardiac Arrhythmia
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3164530/
    Bradycardia can occur in structurally normal hearts because of genetic mutations that result in abnormalities of either membrane clock or Ca clock mechanisms of automaticity. One example is the mutation of hyperpolarization-activated nucleotide-gated channel (HCN4), which is part of the channels that carry If. Mutations of the HCN4 may cause familial bradycardia as well. […] Common diseases, such as heart failure and atrial fibrillation, may be associated with significant SA node dysfunction. Malfunction of both membrane voltage and Ca clocks might be associated with both of these common diseases. Zicha and colleagues reported that down-regulation of HCN4 expression contributes to heart failure-induced sinus node dysfunction. An A450 V missense loss of function mutation in HCN4 has recently been shown to underlie familial sinus bradycardia in several unrelated probands of Moroccan Jewish descent.
  • #8 Mechanism of arrythmias | PPT
    https://www.slideshare.net/slideshow/mechanism-of-arrythmias/29637225
    1. Cardiac arrhythmias can be caused by disorders of impulse formation, disorders of impulse conduction, or a combination of the two. […] 2. Disorders of impulse formation include abnormalities in automaticity and triggered activity. […] 3. Abnormal automaticity occurs when an ectopic pacemaker fires at an inappropriate rate, taking over control of the heart rhythm from the normal sinus node. […] 4. Triggered activity is initiated by afterdepolarizations following an action potential. […] 5. Disorders of impulse conduction include conduction block and reentry, which is when an impulse circles back and reactivates tissue that is still recovering, leading to sustained, rapid rhythms. […] 6. The mechanisms responsible for arrhythmias are generally divided into Disorders of impulse formation, Disorders of impulse conduction, Combinations of both cardiac.
  • #9 Mechanisms of Cardiac Arrhythmias – Revista Española de Cardiología (English Edition)
    https://www.revespcardiol.org/en-mechanisms-of-cardiac-arrhythmias-articulo-S1885585711006086
    The mechanisms responsible for cardiac arrhythmias may be divided into disorders of impulse formation, disorders of impulse conduction or a combination of both. […] The hallmark of normal automaticity is overdrive suppression. Overdriving a latent pacemaker cell faster than its intrinsic rate decreases the slope of phase 4, mediated mostly by enhanced activity of the Na/K exchange pump. […] An important distinction between enhanced normal and abnormal induced automaticity is that the latter is less sensitive to overdrive suppression, although there are situations where it may be observed. […] Triggered activity (TA) is defined by impulse initiation caused by afterdepolarizations (membrane potential oscillations that occur during or immediately following a preceding AP). […] A DAD is an oscillation in membrane voltage that occurs after completion of repolarization of the AP (during phase 4).
  • #10 Mechanisms of Cardiac Arrhythmias – Revista Española de Cardiología (English Edition)
    https://www.revespcardiol.org/en-mechanisms-of-cardiac-arrhythmias-articulo-S1885585711006086
    The mechanisms responsible for cardiac arrhythmias may be divided into disorders of impulse formation, disorders of impulse conduction or a combination of both. […] The hallmark of normal automaticity is overdrive suppression. Overdriving a latent pacemaker cell faster than its intrinsic rate decreases the slope of phase 4, mediated mostly by enhanced activity of the Na/K exchange pump. […] An important distinction between enhanced normal and abnormal induced automaticity is that the latter is less sensitive to overdrive suppression, although there are situations where it may be observed. […] Triggered activity (TA) is defined by impulse initiation caused by afterdepolarizations (membrane potential oscillations that occur during or immediately following a preceding AP). […] A DAD is an oscillation in membrane voltage that occurs after completion of repolarization of the AP (during phase 4).
  • #11 Mechanisms of Cardiac Arrhythmias – Revista Española de Cardiología (English Edition)
    https://www.revespcardiol.org/en-mechanisms-cardiac-arrhythmias-articulo-S1885585711006086
    Abnormal automaticity is thought to play a role in cases of elevated extracellular potassium, low intracellular pH, and catecholamine excess. […] Triggered activity (TA) is defined by impulse initiation caused by afterdepolarizations (membrane potential oscillations that occur during or immediately following a preceding AP). […] Delayed Afterdepolarization-Induced Triggered Activity is an oscillation in membrane voltage that occurs after completion of repolarization of the AP (during phase 4). […] Early afterdepolarization-triggered arrhythmias are rate dependent, and in general the EAD amplitude increases at a slow rate. […] Reentry has been divided in 2 main groups: anatomical or classic reentry, where the circuit is determined by anatomical structures, and functional reentry, which in turn includes different mechanisms.
  • #12 Mechanisms of Cardiac Arrhythmias – Revista Española de Cardiología (English Edition)
    https://www.revespcardiol.org/en-mechanisms-cardiac-arrhythmias-articulo-S1885585711006086
    Abnormal automaticity is thought to play a role in cases of elevated extracellular potassium, low intracellular pH, and catecholamine excess. […] Triggered activity (TA) is defined by impulse initiation caused by afterdepolarizations (membrane potential oscillations that occur during or immediately following a preceding AP). […] Delayed Afterdepolarization-Induced Triggered Activity is an oscillation in membrane voltage that occurs after completion of repolarization of the AP (during phase 4). […] Early afterdepolarization-triggered arrhythmias are rate dependent, and in general the EAD amplitude increases at a slow rate. […] Reentry has been divided in 2 main groups: anatomical or classic reentry, where the circuit is determined by anatomical structures, and functional reentry, which in turn includes different mechanisms.
  • #13 Mechanism of arrythmias | PPT
    https://www.slideshare.net/slideshow/mechanism-of-arrythmias/29637225
    7. Automaticity is the property of a fiber to initiate an impulse spontaneously, without need for prior stimulation. […] 8. Ectopic pacemakers are usually suppressed by overdrive suppression by the more rapidly firing SA node or by concealed conduction from neighboring fibers. […] 9. Triggered activity is initiated by after-depolarizations, which are depolarizing oscillations in membrane voltage induced by one or more preceding action potentials. […] 10. Early after-depolarizations (EADs), arise from a reduced level of membrane potential during phases 2 and 3 of the cardiac action potential. […] 11. Late or delayed after-depolarizations (DADs), occur after completion of repolarization, generally at a more negative membrane potential than that from which EADs arise. […] 12. Disorder of Impulse Conduction can be conduction block or re-entry. […] 13. Atrial flutter is caused by a large reentrant circuit in the wall of the right atrium. […] 14. Atrial fibrillation is caused by numerous wavelets of depolarization spreading throughout the atria simultaneously, leading to an absence of coordinated atrial contraction.
  • #14 Mechanisms of Cardiac Arrhythmias – Revista Española de Cardiología (English Edition)
    https://www.revespcardiol.org/en-mechanisms-of-cardiac-arrhythmias-articulo-S1885585711006086
    The mechanisms responsible for cardiac arrhythmias may be divided into disorders of impulse formation, disorders of impulse conduction or a combination of both. […] The hallmark of normal automaticity is overdrive suppression. Overdriving a latent pacemaker cell faster than its intrinsic rate decreases the slope of phase 4, mediated mostly by enhanced activity of the Na/K exchange pump. […] An important distinction between enhanced normal and abnormal induced automaticity is that the latter is less sensitive to overdrive suppression, although there are situations where it may be observed. […] Triggered activity (TA) is defined by impulse initiation caused by afterdepolarizations (membrane potential oscillations that occur during or immediately following a preceding AP). […] A DAD is an oscillation in membrane voltage that occurs after completion of repolarization of the AP (during phase 4).
  • #15 Overview of Basic Mechanisms of Cardiac Arrhythmia
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3164530/
    EADs are typically observed in cardiac tissues exposed to injury, altered electrolytes, hypoxia, acidosis, catecholamines, and pharmacologic agents, including antiarrhythmic drugs. Ventricular hypertrophy and heart failure also predispose to the development of EADs. EAD characteristics vary as a function of animal species, tissue or cell type, and the method by which the EAD is elicited. Although specific mechanisms of EAD induction can differ, a critical prolongation of repolarization accompanies most, but not all, EADs. Drugs that inhibit potassium currents or which augment inward currents predispose to the development of EADs. […] An example of DAD-induced arrhythmia is the catecholaminergic polymorphic ventricular tachycardia (CPVT), which may be caused by the mutation of either the type 2 ryanodine receptor (RyR2) or the calsequestrin (CSQ2). The principal mechanism underlying these arrhythmias is the leaky ryanodine receptor, which is aggravated during catecholamine stimulation. A typical clinical phenotype of CPVT is bidirectional ventricular tachycardia, which is also seen in digitalis toxicity.
  • #16 Overview of Basic Mechanisms of Cardiac Arrhythmia
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3164530/
    EADs are typically observed in cardiac tissues exposed to injury, altered electrolytes, hypoxia, acidosis, catecholamines, and pharmacologic agents, including antiarrhythmic drugs. Ventricular hypertrophy and heart failure also predispose to the development of EADs. EAD characteristics vary as a function of animal species, tissue or cell type, and the method by which the EAD is elicited. Although specific mechanisms of EAD induction can differ, a critical prolongation of repolarization accompanies most, but not all, EADs. Drugs that inhibit potassium currents or which augment inward currents predispose to the development of EADs. […] An example of DAD-induced arrhythmia is the catecholaminergic polymorphic ventricular tachycardia (CPVT), which may be caused by the mutation of either the type 2 ryanodine receptor (RyR2) or the calsequestrin (CSQ2). The principal mechanism underlying these arrhythmias is the leaky ryanodine receptor, which is aggravated during catecholamine stimulation. A typical clinical phenotype of CPVT is bidirectional ventricular tachycardia, which is also seen in digitalis toxicity.
  • #17 Mechanisms of Cardiac Arrhythmias – Revista Española de Cardiología (English Edition)
    https://www.revespcardiol.org/en-mechanisms-of-cardiac-arrhythmias-articulo-S1885585711006086
    The EADs are oscillatory potentials that occur during the AP plateau (phase 2 EADs) or during the late repolarization (phase 3 EADs). […] Reentry has been divided in 2 main groups: anatomical or classic reentry, where the circuit is determined by anatomical structures, and functional reentry, which in turn includes different mechanisms. […] Prerequisites for reentry include: A substrate: the presence of joined myocardial tissue with different electrophysiological properties, conduction, and refractoriness. […] The classic reentry mechanism is based on an inexcitable anatomical obstacle surrounded by a circular pathway in which the wavefront can reenter, creating fixed and stable reentrant circuits. […] In functional reentry, the circuit is not determined by anatomic obstacles; it is defined by dynamic heterogeneities in the electrophysiologic properties of the involving tissue. […] The predominant mechanisms underlying most VTs are abnormal automaticity, TA, and reentry. The latter is the most frequent mechanism causing VT.
  • #18 Overview of Basic Mechanisms of Cardiac Arrhythmia
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3164530/
    EADs are typically observed in cardiac tissues exposed to injury, altered electrolytes, hypoxia, acidosis, catecholamines, and pharmacologic agents, including antiarrhythmic drugs. Ventricular hypertrophy and heart failure also predispose to the development of EADs. EAD characteristics vary as a function of animal species, tissue or cell type, and the method by which the EAD is elicited. Although specific mechanisms of EAD induction can differ, a critical prolongation of repolarization accompanies most, but not all, EADs. Drugs that inhibit potassium currents or which augment inward currents predispose to the development of EADs. […] An example of DAD-induced arrhythmia is the catecholaminergic polymorphic ventricular tachycardia (CPVT), which may be caused by the mutation of either the type 2 ryanodine receptor (RyR2) or the calsequestrin (CSQ2). The principal mechanism underlying these arrhythmias is the leaky ryanodine receptor, which is aggravated during catecholamine stimulation. A typical clinical phenotype of CPVT is bidirectional ventricular tachycardia, which is also seen in digitalis toxicity.
  • #19 Overview of Basic Mechanisms of Cardiac Arrhythmia
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3164530/
    EADs are typically observed in cardiac tissues exposed to injury, altered electrolytes, hypoxia, acidosis, catecholamines, and pharmacologic agents, including antiarrhythmic drugs. Ventricular hypertrophy and heart failure also predispose to the development of EADs. EAD characteristics vary as a function of animal species, tissue or cell type, and the method by which the EAD is elicited. Although specific mechanisms of EAD induction can differ, a critical prolongation of repolarization accompanies most, but not all, EADs. Drugs that inhibit potassium currents or which augment inward currents predispose to the development of EADs. […] An example of DAD-induced arrhythmia is the catecholaminergic polymorphic ventricular tachycardia (CPVT), which may be caused by the mutation of either the type 2 ryanodine receptor (RyR2) or the calsequestrin (CSQ2). The principal mechanism underlying these arrhythmias is the leaky ryanodine receptor, which is aggravated during catecholamine stimulation. A typical clinical phenotype of CPVT is bidirectional ventricular tachycardia, which is also seen in digitalis toxicity.
  • #20 Overview of Basic Mechanisms of Cardiac Arrhythmia
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3164530/
    In 2003, Burashnikov and Antzelevitch described a novel mechanism giving rise to triggered activity, termed late phase 3 EAD, which combines properties of both EAD and DAD, but has its own unique character. Late phase 3 EAD-induced triggered extrasystoles represent a new concept of arrhythmogenesis in which abbreviated repolarization permits normal SR calcium release to induce an EAD-mediated closely coupled triggered response, particularly under conditions permitting intracellular calcium loading. […] Reentry is fundamentally different from automaticity or triggered activity in the mechanism by which it initiates and sustains cardiac arrhythmias. Circus movement reentry occurs when an activation wavefront propagates around an anatomic or functional obstacle or core, and reexcites the site of origin. In this type of reentry, all cells take turns in recovering from excitation so that they are ready to be excited again when the next wavefront arrives. […] The mechanisms of arrhythmogenesis in BrS can be explained by the heterogeneous shortening of the APD on the right ventricular epicardium.
  • #21 Overview of Basic Mechanisms of Cardiac Arrhythmia
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3164530/
    In 2003, Burashnikov and Antzelevitch described a novel mechanism giving rise to triggered activity, termed late phase 3 EAD, which combines properties of both EAD and DAD, but has its own unique character. Late phase 3 EAD-induced triggered extrasystoles represent a new concept of arrhythmogenesis in which abbreviated repolarization permits normal SR calcium release to induce an EAD-mediated closely coupled triggered response, particularly under conditions permitting intracellular calcium loading. […] Reentry is fundamentally different from automaticity or triggered activity in the mechanism by which it initiates and sustains cardiac arrhythmias. Circus movement reentry occurs when an activation wavefront propagates around an anatomic or functional obstacle or core, and reexcites the site of origin. In this type of reentry, all cells take turns in recovering from excitation so that they are ready to be excited again when the next wavefront arrives. […] The mechanisms of arrhythmogenesis in BrS can be explained by the heterogeneous shortening of the APD on the right ventricular epicardium.
  • #22 Cardiac arrhythmias pathophysiology | PPT
    https://www.slideshare.net/slideshow/cardiac-arrhythmias-pathophysiology/237187702
    Conversely, there may be enhanced automaticity of SA node leading to sinus tachycardia. […] Triggered activity (or after-depolarization) occur when a normal AP triggers extra-abnormal depolarisations. […] Two major forms of triggered rhythms are recognised: „delayed after-depolarization (DAD)” „early after-depolarisation (EAD)”. […] The third type of electrical disturbance of the heart involves defects in impulse conduction which can result from either one or combination of any of the three mechanisms: (a) conduction block, (b) re-entry phenomenon and (c) accessory tract pathways. […] It has been estimated that 80 to 90% of Clinical arrhythmias occur due to re entry phenomenon. […] In these patients an accessory atrioventricular pathway (a sort of bypass tract called bundle of Kent) is present.
  • #23 Mechanisms of Cardiac Arrhythmias – Revista Española de Cardiología (English Edition)
    https://www.revespcardiol.org/en-mechanisms-cardiac-arrhythmias-articulo-S1885585711006086
    Abnormal automaticity is thought to play a role in cases of elevated extracellular potassium, low intracellular pH, and catecholamine excess. […] Triggered activity (TA) is defined by impulse initiation caused by afterdepolarizations (membrane potential oscillations that occur during or immediately following a preceding AP). […] Delayed Afterdepolarization-Induced Triggered Activity is an oscillation in membrane voltage that occurs after completion of repolarization of the AP (during phase 4). […] Early afterdepolarization-triggered arrhythmias are rate dependent, and in general the EAD amplitude increases at a slow rate. […] Reentry has been divided in 2 main groups: anatomical or classic reentry, where the circuit is determined by anatomical structures, and functional reentry, which in turn includes different mechanisms.
  • #24 Mechanisms of Cardiac Arrhythmias – Revista Española de Cardiología (English Edition)
    https://www.revespcardiol.org/en-mechanisms-of-cardiac-arrhythmias-articulo-S1885585711006086
    The EADs are oscillatory potentials that occur during the AP plateau (phase 2 EADs) or during the late repolarization (phase 3 EADs). […] Reentry has been divided in 2 main groups: anatomical or classic reentry, where the circuit is determined by anatomical structures, and functional reentry, which in turn includes different mechanisms. […] Prerequisites for reentry include: A substrate: the presence of joined myocardial tissue with different electrophysiological properties, conduction, and refractoriness. […] The classic reentry mechanism is based on an inexcitable anatomical obstacle surrounded by a circular pathway in which the wavefront can reenter, creating fixed and stable reentrant circuits. […] In functional reentry, the circuit is not determined by anatomic obstacles; it is defined by dynamic heterogeneities in the electrophysiologic properties of the involving tissue. […] The predominant mechanisms underlying most VTs are abnormal automaticity, TA, and reentry. The latter is the most frequent mechanism causing VT.
  • #25 Mechanisms of Cardiac Arrhythmias – Revista Española de Cardiología (English Edition)
    https://www.revespcardiol.org/en-mechanisms-cardiac-arrhythmias-articulo-S1885585711006086
    Abnormal automaticity is thought to play a role in cases of elevated extracellular potassium, low intracellular pH, and catecholamine excess. […] Triggered activity (TA) is defined by impulse initiation caused by afterdepolarizations (membrane potential oscillations that occur during or immediately following a preceding AP). […] Delayed Afterdepolarization-Induced Triggered Activity is an oscillation in membrane voltage that occurs after completion of repolarization of the AP (during phase 4). […] Early afterdepolarization-triggered arrhythmias are rate dependent, and in general the EAD amplitude increases at a slow rate. […] Reentry has been divided in 2 main groups: anatomical or classic reentry, where the circuit is determined by anatomical structures, and functional reentry, which in turn includes different mechanisms.
  • #26 Mechanisms of Cardiac Arrhythmias – Revista Española de Cardiología (English Edition)
    https://www.revespcardiol.org/en-mechanisms-of-cardiac-arrhythmias-articulo-S1885585711006086
    The EADs are oscillatory potentials that occur during the AP plateau (phase 2 EADs) or during the late repolarization (phase 3 EADs). […] Reentry has been divided in 2 main groups: anatomical or classic reentry, where the circuit is determined by anatomical structures, and functional reentry, which in turn includes different mechanisms. […] Prerequisites for reentry include: A substrate: the presence of joined myocardial tissue with different electrophysiological properties, conduction, and refractoriness. […] The classic reentry mechanism is based on an inexcitable anatomical obstacle surrounded by a circular pathway in which the wavefront can reenter, creating fixed and stable reentrant circuits. […] In functional reentry, the circuit is not determined by anatomic obstacles; it is defined by dynamic heterogeneities in the electrophysiologic properties of the involving tissue. […] The predominant mechanisms underlying most VTs are abnormal automaticity, TA, and reentry. The latter is the most frequent mechanism causing VT.
  • #27 Mechanisms of Cardiac Arrhythmias – Revista Española de Cardiología (English Edition)
    https://www.revespcardiol.org/en-mechanisms-cardiac-arrhythmias-articulo-S1885585711006086
    Prerequisites for reentry include: A substrate: the presence of joined myocardial tissue with different electrophysiological properties, conduction, and refractoriness. […] The classic reentry mechanism is based on an inexcitable anatomical obstacle surrounded by a circular pathway in which the wavefront can reenter, creating fixed and stable reentrant circuits. […] Clinical examples: AV reentrant tachycardia associated with a bypass tract, AV nodal reentrant tachycardia, atrial flutter, bundle branch reentry VT, post-infarction VT. […] The predominant mechanisms underlying most VTs are abnormal automaticity, TA, and reentry. The latter is the most frequent mechanism causing VT.
  • #28 Mechanisms of Cardiac Arrhythmias – Revista Española de Cardiología (English Edition)
    https://www.revespcardiol.org/en-mechanisms-of-cardiac-arrhythmias-articulo-S1885585711006086
    The EADs are oscillatory potentials that occur during the AP plateau (phase 2 EADs) or during the late repolarization (phase 3 EADs). […] Reentry has been divided in 2 main groups: anatomical or classic reentry, where the circuit is determined by anatomical structures, and functional reentry, which in turn includes different mechanisms. […] Prerequisites for reentry include: A substrate: the presence of joined myocardial tissue with different electrophysiological properties, conduction, and refractoriness. […] The classic reentry mechanism is based on an inexcitable anatomical obstacle surrounded by a circular pathway in which the wavefront can reenter, creating fixed and stable reentrant circuits. […] In functional reentry, the circuit is not determined by anatomic obstacles; it is defined by dynamic heterogeneities in the electrophysiologic properties of the involving tissue. […] The predominant mechanisms underlying most VTs are abnormal automaticity, TA, and reentry. The latter is the most frequent mechanism causing VT.
  • #29 Mechanisms of Cardiac Arrhythmias – Revista Española de Cardiología (English Edition)
    https://www.revespcardiol.org/en-mechanisms-cardiac-arrhythmias-articulo-S1885585711006086
    Prerequisites for reentry include: A substrate: the presence of joined myocardial tissue with different electrophysiological properties, conduction, and refractoriness. […] The classic reentry mechanism is based on an inexcitable anatomical obstacle surrounded by a circular pathway in which the wavefront can reenter, creating fixed and stable reentrant circuits. […] Clinical examples: AV reentrant tachycardia associated with a bypass tract, AV nodal reentrant tachycardia, atrial flutter, bundle branch reentry VT, post-infarction VT. […] The predominant mechanisms underlying most VTs are abnormal automaticity, TA, and reentry. The latter is the most frequent mechanism causing VT.
  • #30 Mechanisms of Cardiac Arrhythmias – Revista Española de Cardiología (English Edition)
    https://www.revespcardiol.org/en-mechanisms-of-cardiac-arrhythmias-articulo-S1885585711006086
    The EADs are oscillatory potentials that occur during the AP plateau (phase 2 EADs) or during the late repolarization (phase 3 EADs). […] Reentry has been divided in 2 main groups: anatomical or classic reentry, where the circuit is determined by anatomical structures, and functional reentry, which in turn includes different mechanisms. […] Prerequisites for reentry include: A substrate: the presence of joined myocardial tissue with different electrophysiological properties, conduction, and refractoriness. […] The classic reentry mechanism is based on an inexcitable anatomical obstacle surrounded by a circular pathway in which the wavefront can reenter, creating fixed and stable reentrant circuits. […] In functional reentry, the circuit is not determined by anatomic obstacles; it is defined by dynamic heterogeneities in the electrophysiologic properties of the involving tissue. […] The predominant mechanisms underlying most VTs are abnormal automaticity, TA, and reentry. The latter is the most frequent mechanism causing VT.
  • #31 Overview of Arrhythmias – Cardiovascular Disorders – Merck Manual Professional Edition
    https://www.merckmanuals.com/professional/cardiovascular-disorders/overview-of-arrhythmias-and-conduction-disorders/overview-of-arrhythmias
    Under certain conditions, typically precipitated by a premature beat, reentry can cause continuous circulation of an activation wavefront, causing a tachyarrhythmia. […] However, 3 conditions favor reentry: Shortening of tissue refractoriness (eg, by sympathetic stimulation), Lengthening of the conduction pathway (eg, by hypertrophy or abnormal conduction pathways), Slowing of impulse conduction (eg, by ischemia).
  • #32 Atrial fibrillation | Nature Reviews Disease Primers
    https://www.nature.com/articles/s41572-022-00347-9
    Atrial fibrillation (AF) is the most common cardiac arrhythmia despite substantial efforts to understand the pathophysiology of the condition and develop improved treatments. […] Research has revealed that defects in specific molecular pathways underlie AF pathogenesis, resulting in electrical conduction disorders that drive AF. […] The severity of this so-called electropathology correlates with the stage of AF disease progression and determines the response to AF treatment. […] Therefore, unravelling the molecular mechanisms underlying electropathology is expected to fuel the development of innovative personalized diagnostic tools and mechanism-based therapies. […] Currently, various treatment modalities targeting AF-related electropathology, including lifestyle changes, pharmaceutical and nutraceutical therapy, substrate-based ablative therapy, and neuromodulation, are available to maintain sinus rhythm and might offer a novel holistic strategy to treat AF.
  • #33 Electrolyte’s imbalance role in atrial fibrillation: Pharmacological management | International Journal of Arrhythmia | Full Text
    https://arrhythmia.biomedcentral.com/articles/10.1186/s42444-022-00065-z
    The contribution of the perpetuation of atrial fibrillation is caused by electrical remodeling in which calcium, sodium and potassium channels could refer to changes in the ion channel protein expression, development of fibrosis, gene transcription and ion channel redistribution. […] Calcium and magnesium could influence the risk of atrial fibrillation which is the leading cause of cardiac death, heart failure and ischemic stroke. […] The elevated serum concentration of calcium had a higher range of in-patients mortality, increased total cost of hospitalization and increased length of hospital stay as compared to those without hypercalcemia in atrial fibrillation patients. […] Moreover, chloride channels could affect homeostasis, atrial myocardial metabolism which may participate in the development of atrial fibrillation.
  • #34 Electrolyte’s imbalance role in atrial fibrillation: Pharmacological management | International Journal of Arrhythmia | Full Text
    https://arrhythmia.biomedcentral.com/articles/10.1186/s42444-022-00065-z
    The contribution of the perpetuation of atrial fibrillation is caused by electrical remodeling in which calcium, sodium and potassium channels could refer to changes in the ion channel protein expression, development of fibrosis, gene transcription and ion channel redistribution. […] Calcium and magnesium could influence the risk of atrial fibrillation which is the leading cause of cardiac death, heart failure and ischemic stroke. […] The elevated serum concentration of calcium had a higher range of in-patients mortality, increased total cost of hospitalization and increased length of hospital stay as compared to those without hypercalcemia in atrial fibrillation patients. […] Moreover, chloride channels could affect homeostasis, atrial myocardial metabolism which may participate in the development of atrial fibrillation.
  • #35 Electrolyte’s imbalance role in atrial fibrillation: Pharmacological management | International Journal of Arrhythmia | Full Text
    https://arrhythmia.biomedcentral.com/articles/10.1186/s42444-022-00065-z
    Up to a 50% risk of incidence of AF are higher in which left ventricular hypertrophy, sudden cardiovascular death and overall mortality relate to a low serum magnesium level. […] Additionally, magnesium prevents the occurrence of AF after cardiac surgery, whereas greater levels of serum phosphorus in the large population-based study and the related calciumphosphorus products were linked with a greater incidence of AF. […] Numerous clinical studies had shown the high preoperative risk of AF that is linked with lower serum potassium levels. […] The conventional risk factor of increased risk of new onset of AF events could independently link with high dietary sodium intake which enhances the fibrosis and inflammation in the atrium but the mechanism remains unknown. […] This review concludes that electrolytes imbalance plays a significant role in the pathogenesis of atrial fibrillation.
  • #36 Electrolyte’s imbalance role in atrial fibrillation: Pharmacological management | International Journal of Arrhythmia | Full Text
    https://arrhythmia.biomedcentral.com/articles/10.1186/s42444-022-00065-z
    Up to a 50% risk of incidence of AF are higher in which left ventricular hypertrophy, sudden cardiovascular death and overall mortality relate to a low serum magnesium level. […] Additionally, magnesium prevents the occurrence of AF after cardiac surgery, whereas greater levels of serum phosphorus in the large population-based study and the related calciumphosphorus products were linked with a greater incidence of AF. […] Numerous clinical studies had shown the high preoperative risk of AF that is linked with lower serum potassium levels. […] The conventional risk factor of increased risk of new onset of AF events could independently link with high dietary sodium intake which enhances the fibrosis and inflammation in the atrium but the mechanism remains unknown. […] This review concludes that electrolytes imbalance plays a significant role in the pathogenesis of atrial fibrillation.
  • #37 Electrolyte’s imbalance role in atrial fibrillation: Pharmacological management | International Journal of Arrhythmia | Full Text
    https://arrhythmia.biomedcentral.com/articles/10.1186/s42444-022-00065-z
    Up to a 50% risk of incidence of AF are higher in which left ventricular hypertrophy, sudden cardiovascular death and overall mortality relate to a low serum magnesium level. […] Additionally, magnesium prevents the occurrence of AF after cardiac surgery, whereas greater levels of serum phosphorus in the large population-based study and the related calciumphosphorus products were linked with a greater incidence of AF. […] Numerous clinical studies had shown the high preoperative risk of AF that is linked with lower serum potassium levels. […] The conventional risk factor of increased risk of new onset of AF events could independently link with high dietary sodium intake which enhances the fibrosis and inflammation in the atrium but the mechanism remains unknown. […] This review concludes that electrolytes imbalance plays a significant role in the pathogenesis of atrial fibrillation.
  • #38
    https://journals.lww.com/bjem/fulltext/2023/02030/a_review_of_arrhythmias_in_endocrinology.3.aspx
    Potassium imbalance is a major problem in diabetic ketoacidosis and can potentially lead to deadly arrhythmias. […] Certain anti-diabetic drugs may cause QT prolongation, either as a result of the drugs effect of hypoglycemia or as a direct side effect. […] Hypothyroidism can lead to a reduction in cardiac output of up to 30%40%, which can be attributed to a decrease in both stroke volume and heart rate. Additionally, hypothyroidism can cause varying degrees of conduction blocks. […] Most rhythm and conduction abnormalities identified in hypothyroidism can be quickly resolved with the start of levothyroxine medication in the proper dosage. […] In hypothyroidism, the expression of hepatic low-density lipoprotein receptors declines, which results in decreased cholesterol clearance and the development of hyperlipidemia.
  • #39 Electrolyte’s imbalance role in atrial fibrillation: Pharmacological management | International Journal of Arrhythmia | Full Text
    https://arrhythmia.biomedcentral.com/articles/10.1186/s42444-022-00065-z
    Up to a 50% risk of incidence of AF are higher in which left ventricular hypertrophy, sudden cardiovascular death and overall mortality relate to a low serum magnesium level. […] Additionally, magnesium prevents the occurrence of AF after cardiac surgery, whereas greater levels of serum phosphorus in the large population-based study and the related calciumphosphorus products were linked with a greater incidence of AF. […] Numerous clinical studies had shown the high preoperative risk of AF that is linked with lower serum potassium levels. […] The conventional risk factor of increased risk of new onset of AF events could independently link with high dietary sodium intake which enhances the fibrosis and inflammation in the atrium but the mechanism remains unknown. […] This review concludes that electrolytes imbalance plays a significant role in the pathogenesis of atrial fibrillation.
  • #40 Atrial fibrillation | Nature Reviews Disease Primers
    https://www.nature.com/articles/s41572-022-00347-9
    Atrial fibrillation (AF) is the most common cardiac arrhythmia despite substantial efforts to understand the pathophysiology of the condition and develop improved treatments. […] Research has revealed that defects in specific molecular pathways underlie AF pathogenesis, resulting in electrical conduction disorders that drive AF. […] The severity of this so-called electropathology correlates with the stage of AF disease progression and determines the response to AF treatment. […] Therefore, unravelling the molecular mechanisms underlying electropathology is expected to fuel the development of innovative personalized diagnostic tools and mechanism-based therapies. […] Currently, various treatment modalities targeting AF-related electropathology, including lifestyle changes, pharmaceutical and nutraceutical therapy, substrate-based ablative therapy, and neuromodulation, are available to maintain sinus rhythm and might offer a novel holistic strategy to treat AF.
  • #41 Electrolyte’s imbalance role in atrial fibrillation: Pharmacological management | International Journal of Arrhythmia | Full Text
    https://arrhythmia.biomedcentral.com/articles/10.1186/s42444-022-00065-z
    The contribution of the perpetuation of atrial fibrillation is caused by electrical remodeling in which calcium, sodium and potassium channels could refer to changes in the ion channel protein expression, development of fibrosis, gene transcription and ion channel redistribution. […] Calcium and magnesium could influence the risk of atrial fibrillation which is the leading cause of cardiac death, heart failure and ischemic stroke. […] The elevated serum concentration of calcium had a higher range of in-patients mortality, increased total cost of hospitalization and increased length of hospital stay as compared to those without hypercalcemia in atrial fibrillation patients. […] Moreover, chloride channels could affect homeostasis, atrial myocardial metabolism which may participate in the development of atrial fibrillation.
  • #42 Atrial fibrillation – Wikipedia
    https://en.wikipedia.org/wiki/Atrial_fibrillation
    An important theory is that the regular impulses produced by the sinus node for a normal heartbeat are overwhelmed by rapid electrical discharges produced in the atria and adjacent parts of the pulmonary veins. […] In a heart with AF, the increased calcium release from the sarcoplasmic reticulum and increased calcium sensitivity can lead to an accumulation of intracellular calcium and causes downregulation of L-type calcium channels. This reduces the duration of action potential and the refractory period, thus favoring the conduction of re-entrant waves.
  • #43 New mechanism discovered for the life-threatening arrhythmias in Andersen-Tawil syndrome | EurekAlert!
    https://www.eurekalert.org/news-releases/1040441
    The study, published in Circulation Research, establishes a direct link between these life-threatening arrhythmias and the C122Y mutation in the Kir2.1 potassium channel. […] The study demonstrates that a specific genetic mutation (C122Y) in the Kir2.1 potassium channel alters the function not only of Kir2.1 but also of the main cardiac sodium channel NaV1.5, thus establishing a direct link with the life-threatening arrhythmias associated with ATS1. […] The study reveals that the C122Y mutation in Kir2.1 has a dual effect: it causes a reorganization of the Kir2.1 channel that destabilizes its binding to the phospholipid PIP2, a key lipid-signaling component of the cell membrane, and also disrupts the expression of the protein that forms the NaV1.5 channel, impairing its function. […] Dr. Jalife underscored the importance of the interaction between these channels for cardiac health, explaining that any alteration that disturbs the function of one or both channels can trigger life-threatening arrhythmias.
  • #44 Mechanism of arrythmias | PPT
    https://www.slideshare.net/slideshow/mechanism-of-arrythmias/29637225
    7. Automaticity is the property of a fiber to initiate an impulse spontaneously, without need for prior stimulation. […] 8. Ectopic pacemakers are usually suppressed by overdrive suppression by the more rapidly firing SA node or by concealed conduction from neighboring fibers. […] 9. Triggered activity is initiated by after-depolarizations, which are depolarizing oscillations in membrane voltage induced by one or more preceding action potentials. […] 10. Early after-depolarizations (EADs), arise from a reduced level of membrane potential during phases 2 and 3 of the cardiac action potential. […] 11. Late or delayed after-depolarizations (DADs), occur after completion of repolarization, generally at a more negative membrane potential than that from which EADs arise. […] 12. Disorder of Impulse Conduction can be conduction block or re-entry. […] 13. Atrial flutter is caused by a large reentrant circuit in the wall of the right atrium. […] 14. Atrial fibrillation is caused by numerous wavelets of depolarization spreading throughout the atria simultaneously, leading to an absence of coordinated atrial contraction.
  • #45 Arrhythmias – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK558923/
    Mechanism: Accessory pathway present outside of the AV node-Bundle of Kent. […] Mechanism: Slow fast fibers present in AV node peri-nodal tissue leading to re-entry. […] Mechanism: Multiple reentrant wavelets due to atrial ectopy from muscle fibers near the proximal part of the pulmonary vein. […] Mechanism: Presence of damaged fibers in ischemic heart disease leading to re-entry of current leading to disorganized high-frequency excitation. […] Mechanism: It is usually precipitated by premature ventricular contraction leading to the R on T phenomenon. […] Bradyarrhythmia is defined as a heart rate below 60 beats per minute (bpm) and comprises several rhythm disorders, including atrioventricular (A-V) blocks and sinus node disorders. […] Mechanism: Atrial impulses are conducted with a delay or not at all when an electrical impulse reaches a tissue that not excitable or is in a refractory period. […] Mechanism: Senescence of the SA node, an ischemic event involving the SA node leading to impulse generation at a slower rate. […] Mechanism: Subaortic outflow tract obstruction from abnormal hypertrophy of the septal region of the heart, leading to precipitation of ventricular arrhythmias.
  • #46 Overview of Arrhythmias – Cardiovascular Disorders – Merck Manual Professional Edition
    https://www.merckmanuals.com/professional/cardiovascular-disorders/overview-of-arrhythmias-and-conduction-disorders/overview-of-arrhythmias
    The heart beats in a regular, coordinated way because electrical impulses generated and spread by myocytes with unique electrical properties trigger a sequence of organized myocardial contractions. Arrhythmias and conduction disorders are caused by abnormalities in the generation or conduction of these electrical impulses or both. […] Rhythm disturbances result from abnormalities of impulse formation, impulse conduction, or both. […] Bradyarrhythmias result from decreased intrinsic pacemaker function or blocks in conduction, principally within the AV node or the His-Purkinje system. […] Most tachyarrhythmias are caused by reentry; some result from enhanced normal automaticity or from abnormal mechanisms of automaticity. […] Reentry is the circular propagation of an impulse around 2 interconnected pathways with different conduction characteristics and refractory periods.
  • #47 Analysis of the independent risk factors of second-degree atrioventric | IJGM
    https://www.dovepress.com/analysis-of-the-independent-risk-factors-of-second-degree-atrioventric-peer-reviewed-fulltext-article-IJGM
    Atrial fibrillation (AF) refers to arrhythmia caused by abnormal electrical activity in the upper chamber of the heart, which significantly reduces the efficiency of the heart in delivering blood to the ventricles, thereby increasing the risk of thrombosis and subsequent cerebral infarction. […] Atrioventricular block (AVB) refers to an abnormality in the conduction system of the heart at the atrioventricular node, which limits the pulsation of the lower ventricle of the heart. AVB is mainly caused by abnormal electrical conduction between the ventricles and atria, usually occurring during atrial fibrillation attacks. […] Second-degree AVB (II AVB) is one of the common complications in AF patients, with the electrocardiogram (ECG) commonly shows an R-R interval of 1.5 s and a high ventricular heart rate.
  • #48 Analysis of the independent risk factors of second-degree atrioventric | IJGM
    https://www.dovepress.com/analysis-of-the-independent-risk-factors-of-second-degree-atrioventric-peer-reviewed-fulltext-article-IJGM
    However, in clinical practice, II AVB not only affects the patients heart function and reduces their quality of life, but may also leads to complications such as thromboembolism, tachycardia, and cardiomyopathy, endangering the patients life. […] The pathogenesis of AF is relatively complex, and increasing evidence suggests that the occurrence of AF is related to sudden cardiac death, cerebral infarction, and congestive heart failure. […] AVB is an abnormal conduction along the atrioventricular node or Hipper system, and different etiologies may lead to different outcomes. […] The results showed that smoking history, LAD, R-R interval, and ventricular rate were all influencing factors of AF combined with II AVB. […] The R-R interval exceeding 1.5 seconds and the appearance of escape rhythm are important features of atrial fibrillation.
  • #49 AV Block: 2nd degree, Mobitz I (Wenckebach Phenomenon) • LITFL
    https://litfl.com/av-block-2nd-degree-mobitz-i-wenckebach-phenomenon/
    Mobitz I is usually due to reversible conduction block at the level of the AV node. […] Malfunctioning AV nodal cells tend to progressively fatigue until they fail to conduct an impulse. This is different to cells of the His-Purkinje system which tend to fail suddenly and unexpectedly (i.e. producing a Mobitz II block).
  • #50 Mechanisms of cardiac arrhythmias: from automaticity to re-entry (reentry) – The Cardiovascular
    https://ecgwaves.com/topic/mechanisms-cardiac-arrhythmias-automaticity-reentry-triggered-activity/
    The sinoatrial node serves as the primary pacemaker of the heart simply because it possesses the fastest automaticity. […] The automaticity in the sinoatrial node increases during physical exercise. […] An action potential may induce an after-depolarization, which is a depolarization occurring either during or after the repolarization phase. […] Normal impulse transmission implies that the depolarizing wave spreads rapidly, uniformly and unhindered through the myocardium. […] It is fundamental to understand how re-entry occurs, as this mechanism is responsible for the majority of arrhythmias requiring treatment. […] Re-entry is the most common cause of supraventricular and ventricular arrhythmias that require treatment. Most cases of atrial flutter are due to re-entry and re-entry has a fundamental role in the development of atrial fibrillation. […] The re-entry circuit will terminate if the wavefront encounters refractory tissue (i.e. cells that cannot be depolarized).
  • #51 Mechanisms of Cardiac Arrhythmias – Revista Española de Cardiología (English Edition)
    https://www.revespcardiol.org/en-mechanisms-of-cardiac-arrhythmias-articulo-S1885585711006086
    The EADs are oscillatory potentials that occur during the AP plateau (phase 2 EADs) or during the late repolarization (phase 3 EADs). […] Reentry has been divided in 2 main groups: anatomical or classic reentry, where the circuit is determined by anatomical structures, and functional reentry, which in turn includes different mechanisms. […] Prerequisites for reentry include: A substrate: the presence of joined myocardial tissue with different electrophysiological properties, conduction, and refractoriness. […] The classic reentry mechanism is based on an inexcitable anatomical obstacle surrounded by a circular pathway in which the wavefront can reenter, creating fixed and stable reentrant circuits. […] In functional reentry, the circuit is not determined by anatomic obstacles; it is defined by dynamic heterogeneities in the electrophysiologic properties of the involving tissue. […] The predominant mechanisms underlying most VTs are abnormal automaticity, TA, and reentry. The latter is the most frequent mechanism causing VT.
  • #52 Mechanisms of Cardiac Arrhythmias – Revista Española de Cardiología (English Edition)
    https://www.revespcardiol.org/en-mechanisms-cardiac-arrhythmias-articulo-S1885585711006086
    Prerequisites for reentry include: A substrate: the presence of joined myocardial tissue with different electrophysiological properties, conduction, and refractoriness. […] The classic reentry mechanism is based on an inexcitable anatomical obstacle surrounded by a circular pathway in which the wavefront can reenter, creating fixed and stable reentrant circuits. […] Clinical examples: AV reentrant tachycardia associated with a bypass tract, AV nodal reentrant tachycardia, atrial flutter, bundle branch reentry VT, post-infarction VT. […] The predominant mechanisms underlying most VTs are abnormal automaticity, TA, and reentry. The latter is the most frequent mechanism causing VT.
  • #53 Arrhythmias – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK558923/
    Mechanism: Accessory pathway present outside of the AV node-Bundle of Kent. […] Mechanism: Slow fast fibers present in AV node peri-nodal tissue leading to re-entry. […] Mechanism: Multiple reentrant wavelets due to atrial ectopy from muscle fibers near the proximal part of the pulmonary vein. […] Mechanism: Presence of damaged fibers in ischemic heart disease leading to re-entry of current leading to disorganized high-frequency excitation. […] Mechanism: It is usually precipitated by premature ventricular contraction leading to the R on T phenomenon. […] Bradyarrhythmia is defined as a heart rate below 60 beats per minute (bpm) and comprises several rhythm disorders, including atrioventricular (A-V) blocks and sinus node disorders. […] Mechanism: Atrial impulses are conducted with a delay or not at all when an electrical impulse reaches a tissue that not excitable or is in a refractory period. […] Mechanism: Senescence of the SA node, an ischemic event involving the SA node leading to impulse generation at a slower rate. […] Mechanism: Subaortic outflow tract obstruction from abnormal hypertrophy of the septal region of the heart, leading to precipitation of ventricular arrhythmias.
  • #54 Cardiac arrhythmias pathophysiology | PPT
    https://www.slideshare.net/slideshow/cardiac-arrhythmias-pathophysiology/237187702
    Conversely, there may be enhanced automaticity of SA node leading to sinus tachycardia. […] Triggered activity (or after-depolarization) occur when a normal AP triggers extra-abnormal depolarisations. […] Two major forms of triggered rhythms are recognised: „delayed after-depolarization (DAD)” „early after-depolarisation (EAD)”. […] The third type of electrical disturbance of the heart involves defects in impulse conduction which can result from either one or combination of any of the three mechanisms: (a) conduction block, (b) re-entry phenomenon and (c) accessory tract pathways. […] It has been estimated that 80 to 90% of Clinical arrhythmias occur due to re entry phenomenon. […] In these patients an accessory atrioventricular pathway (a sort of bypass tract called bundle of Kent) is present.
  • #55 Atrial Fibrillation
    https://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/cardiology/atrial-fibrillation/
    Atrial fibrillation (AF) is a common heart rhythm disorder caused by degeneration of the electrical impulses in the upper cardiac chambers (atria) resulting in a change from an organized heart rhythm to a rapid, chaotic rhythm. The resulting arrhythmia is often rapid and irregular with no discernible pattern (known as irregularly irregular). The disrupted rhythm occurs because of the unpredictable conduction of disordered impulses across the electrical bridge, called the atrioventricular (AV) node, to the lower cardiac chambers (ventricles). The arrhythmia also results in ineffectual atrial contractions affecting cardiac output and vulnerability to blood clot (thrombus) formation that can result in stroke events. […] Considerable research has been devoted to the mechanisms and pathogenesis of AF. Genetic studies have identified specific associations, particularly in the cases of familial AF. Achieving a complete understanding of AF is limited by the complexity of this disorder and the heterogeneous patient population it affects.
  • #56 Heart Conduction System (Cardiac Conduction)
    https://my.clevelandclinic.org/health/body/21648-heart-conduction-system
    Several different conditions can affect your hearts electrical system. Cardiac conduction problems cause issues with your hearts rhythm. […] Some common heart rhythm disorders include: […] Arrhythmia. An irregular heart rhythm, including atrial fibrillation (Afib). […] Bundle branch block. A block in the Purkinje fibers on one side of your heart, causing arrhythmia. […] Heart block. Impaired electrical signals between your hearts atria and ventricles. […] Long QT syndrome (LQTS). Your ventricles contract and release too slowly, sometimes leading to fainting (syncope) or cardiac arrest. […] Premature ventricular contractions. A too-early heartbeat in your ventricles, causing heart palpitations or a skipped heartbeat. […] Cardiac arrest. A severe malfunction in your hearts rhythm that causes your heart to stop. Without immediate treatment, this is fatal.
  • #57 Overview of Basic Mechanisms of Cardiac Arrhythmia
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3164530/
    In 2003, Burashnikov and Antzelevitch described a novel mechanism giving rise to triggered activity, termed late phase 3 EAD, which combines properties of both EAD and DAD, but has its own unique character. Late phase 3 EAD-induced triggered extrasystoles represent a new concept of arrhythmogenesis in which abbreviated repolarization permits normal SR calcium release to induce an EAD-mediated closely coupled triggered response, particularly under conditions permitting intracellular calcium loading. […] Reentry is fundamentally different from automaticity or triggered activity in the mechanism by which it initiates and sustains cardiac arrhythmias. Circus movement reentry occurs when an activation wavefront propagates around an anatomic or functional obstacle or core, and reexcites the site of origin. In this type of reentry, all cells take turns in recovering from excitation so that they are ready to be excited again when the next wavefront arrives. […] The mechanisms of arrhythmogenesis in BrS can be explained by the heterogeneous shortening of the APD on the right ventricular epicardium.
  • #58 Overview of Basic Mechanisms of Cardiac Arrhythmia
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3164530/
    EADs are typically observed in cardiac tissues exposed to injury, altered electrolytes, hypoxia, acidosis, catecholamines, and pharmacologic agents, including antiarrhythmic drugs. Ventricular hypertrophy and heart failure also predispose to the development of EADs. EAD characteristics vary as a function of animal species, tissue or cell type, and the method by which the EAD is elicited. Although specific mechanisms of EAD induction can differ, a critical prolongation of repolarization accompanies most, but not all, EADs. Drugs that inhibit potassium currents or which augment inward currents predispose to the development of EADs. […] An example of DAD-induced arrhythmia is the catecholaminergic polymorphic ventricular tachycardia (CPVT), which may be caused by the mutation of either the type 2 ryanodine receptor (RyR2) or the calsequestrin (CSQ2). The principal mechanism underlying these arrhythmias is the leaky ryanodine receptor, which is aggravated during catecholamine stimulation. A typical clinical phenotype of CPVT is bidirectional ventricular tachycardia, which is also seen in digitalis toxicity.
  • #59 New mechanism discovered for the life-threatening arrhythmias in Andersen-Tawil syndrome | EurekAlert!
    https://www.eurekalert.org/news-releases/1040441
    The study, published in Circulation Research, establishes a direct link between these life-threatening arrhythmias and the C122Y mutation in the Kir2.1 potassium channel. […] The study demonstrates that a specific genetic mutation (C122Y) in the Kir2.1 potassium channel alters the function not only of Kir2.1 but also of the main cardiac sodium channel NaV1.5, thus establishing a direct link with the life-threatening arrhythmias associated with ATS1. […] The study reveals that the C122Y mutation in Kir2.1 has a dual effect: it causes a reorganization of the Kir2.1 channel that destabilizes its binding to the phospholipid PIP2, a key lipid-signaling component of the cell membrane, and also disrupts the expression of the protein that forms the NaV1.5 channel, impairing its function. […] Dr. Jalife underscored the importance of the interaction between these channels for cardiac health, explaining that any alteration that disturbs the function of one or both channels can trigger life-threatening arrhythmias.
  • #60 Overview of Basic Mechanisms of Cardiac Arrhythmia
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3164530/
    Bradycardia can occur in structurally normal hearts because of genetic mutations that result in abnormalities of either membrane clock or Ca clock mechanisms of automaticity. One example is the mutation of hyperpolarization-activated nucleotide-gated channel (HCN4), which is part of the channels that carry If. Mutations of the HCN4 may cause familial bradycardia as well. […] Common diseases, such as heart failure and atrial fibrillation, may be associated with significant SA node dysfunction. Malfunction of both membrane voltage and Ca clocks might be associated with both of these common diseases. Zicha and colleagues reported that down-regulation of HCN4 expression contributes to heart failure-induced sinus node dysfunction. An A450 V missense loss of function mutation in HCN4 has recently been shown to underlie familial sinus bradycardia in several unrelated probands of Moroccan Jewish descent.
  • #61 Overview of Basic Mechanisms of Cardiac Arrhythmia
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3164530/
    Bradycardia can occur in structurally normal hearts because of genetic mutations that result in abnormalities of either membrane clock or Ca clock mechanisms of automaticity. One example is the mutation of hyperpolarization-activated nucleotide-gated channel (HCN4), which is part of the channels that carry If. Mutations of the HCN4 may cause familial bradycardia as well. […] Common diseases, such as heart failure and atrial fibrillation, may be associated with significant SA node dysfunction. Malfunction of both membrane voltage and Ca clocks might be associated with both of these common diseases. Zicha and colleagues reported that down-regulation of HCN4 expression contributes to heart failure-induced sinus node dysfunction. An A450 V missense loss of function mutation in HCN4 has recently been shown to underlie familial sinus bradycardia in several unrelated probands of Moroccan Jewish descent.
  • #62 New mechanism discovered for the life-threatening arrhythmias in Andersen-Tawil syndrome | EurekAlert!
    https://www.eurekalert.org/news-releases/1040441
    The study, published in Circulation Research, establishes a direct link between these life-threatening arrhythmias and the C122Y mutation in the Kir2.1 potassium channel. […] The study demonstrates that a specific genetic mutation (C122Y) in the Kir2.1 potassium channel alters the function not only of Kir2.1 but also of the main cardiac sodium channel NaV1.5, thus establishing a direct link with the life-threatening arrhythmias associated with ATS1. […] The study reveals that the C122Y mutation in Kir2.1 has a dual effect: it causes a reorganization of the Kir2.1 channel that destabilizes its binding to the phospholipid PIP2, a key lipid-signaling component of the cell membrane, and also disrupts the expression of the protein that forms the NaV1.5 channel, impairing its function. […] Dr. Jalife underscored the importance of the interaction between these channels for cardiac health, explaining that any alteration that disturbs the function of one or both channels can trigger life-threatening arrhythmias.
  • #63 New mechanism discovered for the life-threatening arrhythmias in Andersen-Tawil syndrome | EurekAlert!
    https://www.eurekalert.org/news-releases/1040441
    The discovery that a mutation considered 'monogenic’ disrupts not only the ion channel directly affected by the mutation, but also a complementary channel is important. […] The results of the new Circulation Research study support the hypothesis that the molecular mechanisms that increase susceptibility to arrhythmias and sudden cardiac death in ATS1 depend on the specific mutation, so that pharmacological treatment and clinical management should be tailored to each individual patient.
  • #64 What Is Cardiac Arrhythmia? Types, Causes & Diagnosis – Avive AED
    https://www.avive.life/blog/arrhythmias-and-sudden-cardiac-arrest
    Sudden Cardiac Arrest (SCA) is an unexpected loss of heart function due to an underlying arrhythmia. During cardiac arrest, the heart is no longer able to pump oxygen to the brain or body. […] When someone suffers SCA, their heart is likely in either pulseless ventricular tachycardia or ventricular fibrillation. […] While many cardiac arrhythmias are not immediately dangerous, both of these lethal ventricular rhythms will lead to death within minutes if left untreated. […] Arrhythmias are caused by a diverse range of conditions and substances that affect the physiology and electrical function of the heart. The lethal arrhythmias that cause Sudden Cardiac Arrests are no different. […] Based on the type and severity of the arrhythmia, treatment can take many different forms. Some treatment options include:
  • #65 Heart arrhythmia – Symptoms and causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/heart-arrhythmia/symptoms-causes/syc-20350668
    A heart arrhythmia (uh-RITH-me-uh) is an irregular heartbeat. A heart arrhythmia occurs when the electrical signals that tell the heart to beat don’t work properly. The heart may beat too fast or too slow. Or the pattern of the heartbeat may be inconsistent. […] A heart arrhythmia may feel like a fluttering, pounding or racing heartbeat. Some heart arrhythmias are harmless. Others may cause life-threatening symptoms. […] Heart arrhythmia treatment may include medicines, devices such as pacemakers, or a procedure or surgery. The goals of treatment are to control or get rid of fast, slow or otherwise irregular heartbeats. A heart-healthy lifestyle can help prevent heart damage that can trigger some heart arrhythmias. […] But some things can change how electrical signals travel through the heart and cause arrhythmias. They include: A heart attack or scarring from a previous heart attack. Blocked arteries in the heart, called coronary artery disease. Changes to the heart’s structure, such as from cardiomyopathy.
  • #66 IJMS | Special Issue : Pathogenesis of Cardiac Arrhythmias and Heart Failure
    https://www.mdpi.com/journal/ijms/special_issues/cardiac_arrhythmias
    Cardiac arrhythmias are any of a group of conditions in which the electrical activity of the heart is irregular or is faster or slower than normal. Up to 50% of patients die suddenly at the first manifestation of cardiac diseases; the majority of these patients die of ventricular fibrillation, a lethal cardiac arrhythmia. Heart failure, a syndrome characterized by inadequate systemic perfusion owing to reduced cardiac pumping, is the most common cause of hospitalization of cardiovascular diseases and imposes a great burden on the healthcare system and society. […] Understanding the pathogenesis of cardiac arrhythmias and heart failure is critical to the development of diagnostic, treatment and preventive strategies. The current understanding of electrophysiological mechanisms of cardiac arrhythmias includes automaticity, triggered activity and reentry, and an understanding of pathogenetic mechanisms of heart failure includes a multitude of biomechanical, hemodynamic, hormonal and pathologic stimuli. However, the molecular pathways of cardiac arrhythmias and heart failure are still elusive, and novel molecular defects and pathways remain to be identified for screening, molecular diagnosis, drug-target development, and personalized medicine.
  • #67 Heart arrhythmia – Symptoms and causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/heart-arrhythmia/symptoms-causes/syc-20350668
    A heart arrhythmia (uh-RITH-me-uh) is an irregular heartbeat. A heart arrhythmia occurs when the electrical signals that tell the heart to beat don’t work properly. The heart may beat too fast or too slow. Or the pattern of the heartbeat may be inconsistent. […] A heart arrhythmia may feel like a fluttering, pounding or racing heartbeat. Some heart arrhythmias are harmless. Others may cause life-threatening symptoms. […] Heart arrhythmia treatment may include medicines, devices such as pacemakers, or a procedure or surgery. The goals of treatment are to control or get rid of fast, slow or otherwise irregular heartbeats. A heart-healthy lifestyle can help prevent heart damage that can trigger some heart arrhythmias. […] But some things can change how electrical signals travel through the heart and cause arrhythmias. They include: A heart attack or scarring from a previous heart attack. Blocked arteries in the heart, called coronary artery disease. Changes to the heart’s structure, such as from cardiomyopathy.
  • #68
    https://journals.lww.com/bjem/fulltext/2023/02030/a_review_of_arrhythmias_in_endocrinology.3.aspx
    Endocrine disorders can lead to cardiac arrhythmias, which can have serious implications for an individuals health, including sudden cardiac death. The pathophysiology of arrhythmias in endocrine disorders is a multifaceted process that includes alterations in hormone levels, disruptions in electrolyte levels, and changes to the hearts structure. Tachycardia and bradycardia are common rhythm abnormalities caused by defects in the cardiac conduction system or autonomic nervous system, metabolic disorders, and medication use. Therefore, it is crucial to identify and manage underlying endocrinopathies in patients with rhythm or conduction abnormalities. […] The onset of arrhythmias can be easily triggered in healthy hearts due to hormonal changes and electrolyte imbalances. Nonetheless, specific endocrine conditions can induce alterations in the hearts structure, which could potentially establish a long-lasting foundation for arrhythmias.
  • #69
    https://journals.lww.com/bjem/fulltext/2023/02030/a_review_of_arrhythmias_in_endocrinology.3.aspx
    Identifying and managing underlying endocrinopathies is critical in patients who present with rhythm or conduction abnormalities, given the strong association between endocrine disorders and cardiac arrhythmias. Effective management of endocrine disorders can aid in preventing and treating cardiac arrhythmias. […] While diabetes can contribute to various types of cardiac arrhythmias, atrial fibrillation is the most commonly reported arrhythmia associated with diabetes. […] Diabetes has been associated with decreased heart rate variability, and both type 1 and type 2 diabetes have been shown to cause longer QT intervals. […] The likelihood of bradycardia, atrial ectopy, and ventricular arrhythmias is increased by hypoglycemia, especially at night, according to studies using continuous glucose monitoring and 24-h Holter monitoring.
  • #70
    https://journals.lww.com/bjem/fulltext/2023/02030/a_review_of_arrhythmias_in_endocrinology.3.aspx
    Potassium imbalance is a major problem in diabetic ketoacidosis and can potentially lead to deadly arrhythmias. […] Certain anti-diabetic drugs may cause QT prolongation, either as a result of the drugs effect of hypoglycemia or as a direct side effect. […] Hypothyroidism can lead to a reduction in cardiac output of up to 30%40%, which can be attributed to a decrease in both stroke volume and heart rate. Additionally, hypothyroidism can cause varying degrees of conduction blocks. […] Most rhythm and conduction abnormalities identified in hypothyroidism can be quickly resolved with the start of levothyroxine medication in the proper dosage. […] In hypothyroidism, the expression of hepatic low-density lipoprotein receptors declines, which results in decreased cholesterol clearance and the development of hyperlipidemia.
  • #71
    https://journals.lww.com/bjem/fulltext/2023/02030/a_review_of_arrhythmias_in_endocrinology.3.aspx
    The role of oral T3 supplementation and the risks of arrhythmias have not been extensively studied in the existing literature. […] Heart problems brought on by hyperthyroidism might include sinus tachycardia, elevated QRS complex voltage, and premature atrial and ventricular beats. […] Around 6%12% of patients with hyperthyroidism experience paroxysmal atrial tachycardia and atrial fibrillation. […] Patients who have structural or ischemic heart disease, long-standing atrial fibrillation, or who are older, are at a higher risk of developing persistent atrial fibrillation. […] The risk of stroke is reduced in those with chronic atrial fibrillation and hyperthyroidism compared to people without the condition, despite the fact that hyperthyroidism is associated with coagulation problems.
  • #72 Arrhythmia: Symptoms & Treatment
    https://my.clevelandclinic.org/health/diseases/16749-arrhythmia
    If you have an arrhythmia, you should limit the amount of alcohol and caffeine you consume. Both of these can trigger arrhythmias. […] There are many ways for your heartbeat to be irregular. Some of these irregular heartbeats, called arrhythmias, dont cause symptoms. It’s important to see your healthcare provider if you do notice symptoms like extreme fatigue or heart palpitations.
  • #73 Arrhythmia: Symptoms & Treatment
    https://my.clevelandclinic.org/health/diseases/16749-arrhythmia
    If you have an arrhythmia, you should limit the amount of alcohol and caffeine you consume. Both of these can trigger arrhythmias. […] There are many ways for your heartbeat to be irregular. Some of these irregular heartbeats, called arrhythmias, dont cause symptoms. It’s important to see your healthcare provider if you do notice symptoms like extreme fatigue or heart palpitations.
  • #74 Analysis of the independent risk factors of second-degree atrioventric | IJGM
    https://www.dovepress.com/analysis-of-the-independent-risk-factors-of-second-degree-atrioventric-peer-reviewed-fulltext-article-IJGM
    However, in clinical practice, II AVB not only affects the patients heart function and reduces their quality of life, but may also leads to complications such as thromboembolism, tachycardia, and cardiomyopathy, endangering the patients life. […] The pathogenesis of AF is relatively complex, and increasing evidence suggests that the occurrence of AF is related to sudden cardiac death, cerebral infarction, and congestive heart failure. […] AVB is an abnormal conduction along the atrioventricular node or Hipper system, and different etiologies may lead to different outcomes. […] The results showed that smoking history, LAD, R-R interval, and ventricular rate were all influencing factors of AF combined with II AVB. […] The R-R interval exceeding 1.5 seconds and the appearance of escape rhythm are important features of atrial fibrillation.
  • #75 Heart rhythm disorders – WikiLectures
    https://www.wikilectures.eu/w/Heart_rhythm_disorders
    Heart rhythm disorders (arytmie, dysrytmie) is a collective name for disorders of heart rate, heart rhythm, propagation of excitement in the heart or their combination. […] According to the pathogenetic mechanisms leading to individual arrhythmias, we distinguish: disorders of excitability; conduction disorders; combined disorders. […] The most common cause of arrhythmia is CHD (ischemia, hypoxia, acidosis, reperfusion injury). […] Ionic disorders (hypokalemia, hypomagnesia, hyperkalemia hypercalcemia); acid-base balance disorders; myocardial disorders: dilation or hypertrophy of the heart (cardiomyopathy, e.g. right ventricular cardiomyopathy is directly referred to as arrhythmogenic right ventricular dysplasia); inflammation (myocarditis); congenital and acquired heart defects. […] Disturbance of the balance of the vegetative nervous system (stress, anxiety shock, compensation of another pathological condition); arrhythmogenic substances (drugs, caffeine, adrenaline alcohol, digoxin, diuretics, antiarrhythmics); other diseases (endocrinopathy – thyrotoxicosis); cardiovascular autonomic neuropathy.
  • #76 Pathological basis of cardiac arrhythmias: vicious cycle of immune-metabolic dysregulation
    https://www.oatext.com/pathological-basis-of-cardiac-arrhythmias-vicious-cycle-of-immune-metabolic-dysregulation.php
    Recently, the association of immunometabolic disorders with the occurrence of arrhythmias has emerged as a new horizon of studies; however, the underlying mechanism for immunometabolic disorder-associated arrhythmias remains poorly understood. In this paper, we review current evidence supporting the involvement of vicious cycle of immune-metabolic dysregulation in the pathogenesis of arrhythmias. […] In the pathogenesis of these CVDs, immunologic injury and metabolic disorders are essential factors that constitute the immunometabolic basis of cardiac arrhythmias. […] The immunopathogenesis of cardiac rhythm and conduction disorders have been identified in sick sinus syndrome, bradyarrhythmias, and hypersensitive carotid sinus syndrome. […] These facts support the proposal that autoimmunity and inflammation take part in electrical and structural remodeling of left atrium and predispose patients with autoimmune and inflammatory diseases to increased risk of arrhythmia.
  • #77 Pathological basis of cardiac arrhythmias: vicious cycle of immune-metabolic dysregulation
    https://www.oatext.com/pathological-basis-of-cardiac-arrhythmias-vicious-cycle-of-immune-metabolic-dysregulation.php
    Recently, the association of immunometabolic disorders with the occurrence of arrhythmias has emerged as a new horizon of studies; however, the underlying mechanism for immunometabolic disorder-associated arrhythmias remains poorly understood. In this paper, we review current evidence supporting the involvement of vicious cycle of immune-metabolic dysregulation in the pathogenesis of arrhythmias. […] In the pathogenesis of these CVDs, immunologic injury and metabolic disorders are essential factors that constitute the immunometabolic basis of cardiac arrhythmias. […] The immunopathogenesis of cardiac rhythm and conduction disorders have been identified in sick sinus syndrome, bradyarrhythmias, and hypersensitive carotid sinus syndrome. […] These facts support the proposal that autoimmunity and inflammation take part in electrical and structural remodeling of left atrium and predispose patients with autoimmune and inflammatory diseases to increased risk of arrhythmia.
  • #78 Inflammation and arrhythmogenesis: a narrative review of the complex relationship | International Journal of Arrhythmia | Full Text
    https://arrhythmia.biomedcentral.com/articles/10.1186/s42444-024-00110-z
    Arrhythmias can be initiated or exacerbated by inflammation, which can change the electrophysiological properties of cardiac cells, such as ion channel expression, membrane potential, calcium handling, and gap junction coupling. […] Apoptosis, hypertrophy, and fibrosis are examples of structural changes that inflammation may cause in cardiac tissue. […] On the other hand, arrhythmias may cause or worsen inflammation by injuring the heart through mechanical strain, ischemiareperfusion, or oxidative stress. […] The aim of this narrative review is to clarify the intricate connection between inflammation and arrhythmogenesis, highlighting the numerous ways that both localized and systemic inflammation can affect the onset and course of different cardiac arrhythmias. […] There are several causes of systemic inflammation, including sepsis, trauma, surgery, and long-term illnesses.
  • #79 Inflammation and arrhythmogenesis: a narrative review of the complex relationship | International Journal of Arrhythmia | Full Text
    https://arrhythmia.biomedcentral.com/articles/10.1186/s42444-024-00110-z
    Arrhythmias can be initiated or exacerbated by inflammation, which can change the electrophysiological properties of cardiac cells, such as ion channel expression, membrane potential, calcium handling, and gap junction coupling. […] Apoptosis, hypertrophy, and fibrosis are examples of structural changes that inflammation may cause in cardiac tissue. […] On the other hand, arrhythmias may cause or worsen inflammation by injuring the heart through mechanical strain, ischemiareperfusion, or oxidative stress. […] The aim of this narrative review is to clarify the intricate connection between inflammation and arrhythmogenesis, highlighting the numerous ways that both localized and systemic inflammation can affect the onset and course of different cardiac arrhythmias. […] There are several causes of systemic inflammation, including sepsis, trauma, surgery, and long-term illnesses.
  • #80 Inflammation and arrhythmogenesis: a narrative review of the complex relationship | International Journal of Arrhythmia | Full Text
    https://arrhythmia.biomedcentral.com/articles/10.1186/s42444-024-00110-z
    Arrhythmias can be initiated or exacerbated by inflammation, which can change the electrophysiological properties of cardiac cells, such as ion channel expression, membrane potential, calcium handling, and gap junction coupling. […] Apoptosis, hypertrophy, and fibrosis are examples of structural changes that inflammation may cause in cardiac tissue. […] On the other hand, arrhythmias may cause or worsen inflammation by injuring the heart through mechanical strain, ischemiareperfusion, or oxidative stress. […] The aim of this narrative review is to clarify the intricate connection between inflammation and arrhythmogenesis, highlighting the numerous ways that both localized and systemic inflammation can affect the onset and course of different cardiac arrhythmias. […] There are several causes of systemic inflammation, including sepsis, trauma, surgery, and long-term illnesses.
  • #81 Inflammation and arrhythmogenesis: a narrative review of the complex relationship | International Journal of Arrhythmia | Full Text
    https://arrhythmia.biomedcentral.com/articles/10.1186/s42444-024-00110-z
    First, oxidative stress and cardiac cell damage from systemic inflammation might result in decreased electrical conduction and heightened vulnerability to reentry circuits. […] Second, the autonomic nervous system (ANS) might have its equilibrium upset by systemic inflammation. […] Third, since potassium, calcium, and magnesium are necessary for a proper ventricular action potential, systemic inflammation may have an impact on these electrolyte levels. […] Fourth, systemic inflammation has the potential to trigger the coagulation system and raise the risk of thromboembolism, both of which can result in myocardial infarction and ischemia. […] Systemic inflammatory markers were found to have high correlations with the development of atrial fibrillation/flutter (AF), ventricular arrhythmia (VA), and bradyarrhythmia in a research including 478,524 participants from the UK Biobank cohort.
  • #82 Inflammation and arrhythmogenesis: a narrative review of the complex relationship | International Journal of Arrhythmia | Full Text
    https://arrhythmia.biomedcentral.com/articles/10.1186/s42444-024-00110-z
    First, oxidative stress and cardiac cell damage from systemic inflammation might result in decreased electrical conduction and heightened vulnerability to reentry circuits. […] Second, the autonomic nervous system (ANS) might have its equilibrium upset by systemic inflammation. […] Third, since potassium, calcium, and magnesium are necessary for a proper ventricular action potential, systemic inflammation may have an impact on these electrolyte levels. […] Fourth, systemic inflammation has the potential to trigger the coagulation system and raise the risk of thromboembolism, both of which can result in myocardial infarction and ischemia. […] Systemic inflammatory markers were found to have high correlations with the development of atrial fibrillation/flutter (AF), ventricular arrhythmia (VA), and bradyarrhythmia in a research including 478,524 participants from the UK Biobank cohort.
  • #83 Inflammation and arrhythmogenesis: a narrative review of the complex relationship | International Journal of Arrhythmia | Full Text
    https://arrhythmia.biomedcentral.com/articles/10.1186/s42444-024-00110-z
    First, oxidative stress and cardiac cell damage from systemic inflammation might result in decreased electrical conduction and heightened vulnerability to reentry circuits. […] Second, the autonomic nervous system (ANS) might have its equilibrium upset by systemic inflammation. […] Third, since potassium, calcium, and magnesium are necessary for a proper ventricular action potential, systemic inflammation may have an impact on these electrolyte levels. […] Fourth, systemic inflammation has the potential to trigger the coagulation system and raise the risk of thromboembolism, both of which can result in myocardial infarction and ischemia. […] Systemic inflammatory markers were found to have high correlations with the development of atrial fibrillation/flutter (AF), ventricular arrhythmia (VA), and bradyarrhythmia in a research including 478,524 participants from the UK Biobank cohort.
  • #84 Inflammation and arrhythmogenesis: a narrative review of the complex relationship | International Journal of Arrhythmia | Full Text
    https://arrhythmia.biomedcentral.com/articles/10.1186/s42444-024-00110-z
    First, oxidative stress and cardiac cell damage from systemic inflammation might result in decreased electrical conduction and heightened vulnerability to reentry circuits. […] Second, the autonomic nervous system (ANS) might have its equilibrium upset by systemic inflammation. […] Third, since potassium, calcium, and magnesium are necessary for a proper ventricular action potential, systemic inflammation may have an impact on these electrolyte levels. […] Fourth, systemic inflammation has the potential to trigger the coagulation system and raise the risk of thromboembolism, both of which can result in myocardial infarction and ischemia. […] Systemic inflammatory markers were found to have high correlations with the development of atrial fibrillation/flutter (AF), ventricular arrhythmia (VA), and bradyarrhythmia in a research including 478,524 participants from the UK Biobank cohort.
  • #85 Inflammation and arrhythmogenesis: a narrative review of the complex relationship | International Journal of Arrhythmia | Full Text
    https://arrhythmia.biomedcentral.com/articles/10.1186/s42444-024-00110-z
    Specific infections include bacterial, fungal, or viral infections as well as autoimmune disorders can result in localized inflammation. […] First, there is a chance that localized inflammation will cause structural remodeling in cardiovascular tissue, in addition to processes like necrosis, apoptosis, and fibrosis. […] Second, localized inflammation may result in inflammation of the ganglia or cardiac nerves, which may change how the heart’s autonomic nervous system regulates itself. […] Third, localized inflammation may directly harm the heart’s cells, impairing their ability to handle calcium, boosting their automaticity, or making them more susceptible to catecholamines. […] Fourth, localized inflammation may compress or infiltrate the cardiac conduction system, including the His-Purkinje system, the atrioventricular node, and the sinoatrial node, which may result in heart block or bradyarrhythmias.
  • #86 Inflammation and arrhythmogenesis: a narrative review of the complex relationship | International Journal of Arrhythmia | Full Text
    https://arrhythmia.biomedcentral.com/articles/10.1186/s42444-024-00110-z
    Specific infections include bacterial, fungal, or viral infections as well as autoimmune disorders can result in localized inflammation. […] First, there is a chance that localized inflammation will cause structural remodeling in cardiovascular tissue, in addition to processes like necrosis, apoptosis, and fibrosis. […] Second, localized inflammation may result in inflammation of the ganglia or cardiac nerves, which may change how the heart’s autonomic nervous system regulates itself. […] Third, localized inflammation may directly harm the heart’s cells, impairing their ability to handle calcium, boosting their automaticity, or making them more susceptible to catecholamines. […] Fourth, localized inflammation may compress or infiltrate the cardiac conduction system, including the His-Purkinje system, the atrioventricular node, and the sinoatrial node, which may result in heart block or bradyarrhythmias.
  • #87 Inflammation and arrhythmogenesis: a narrative review of the complex relationship | International Journal of Arrhythmia | Full Text
    https://arrhythmia.biomedcentral.com/articles/10.1186/s42444-024-00110-z
    Specific infections include bacterial, fungal, or viral infections as well as autoimmune disorders can result in localized inflammation. […] First, there is a chance that localized inflammation will cause structural remodeling in cardiovascular tissue, in addition to processes like necrosis, apoptosis, and fibrosis. […] Second, localized inflammation may result in inflammation of the ganglia or cardiac nerves, which may change how the heart’s autonomic nervous system regulates itself. […] Third, localized inflammation may directly harm the heart’s cells, impairing their ability to handle calcium, boosting their automaticity, or making them more susceptible to catecholamines. […] Fourth, localized inflammation may compress or infiltrate the cardiac conduction system, including the His-Purkinje system, the atrioventricular node, and the sinoatrial node, which may result in heart block or bradyarrhythmias.
  • #88 Inflammation and arrhythmogenesis: a narrative review of the complex relationship | International Journal of Arrhythmia | Full Text
    https://arrhythmia.biomedcentral.com/articles/10.1186/s42444-024-00110-z
    Specific infections include bacterial, fungal, or viral infections as well as autoimmune disorders can result in localized inflammation. […] First, there is a chance that localized inflammation will cause structural remodeling in cardiovascular tissue, in addition to processes like necrosis, apoptosis, and fibrosis. […] Second, localized inflammation may result in inflammation of the ganglia or cardiac nerves, which may change how the heart’s autonomic nervous system regulates itself. […] Third, localized inflammation may directly harm the heart’s cells, impairing their ability to handle calcium, boosting their automaticity, or making them more susceptible to catecholamines. […] Fourth, localized inflammation may compress or infiltrate the cardiac conduction system, including the His-Purkinje system, the atrioventricular node, and the sinoatrial node, which may result in heart block or bradyarrhythmias.
  • #89 Inflammation and arrhythmogenesis: a narrative review of the complex relationship | International Journal of Arrhythmia | Full Text
    https://arrhythmia.biomedcentral.com/articles/10.1186/s42444-024-00110-z
    Specific infections include bacterial, fungal, or viral infections as well as autoimmune disorders can result in localized inflammation. […] First, there is a chance that localized inflammation will cause structural remodeling in cardiovascular tissue, in addition to processes like necrosis, apoptosis, and fibrosis. […] Second, localized inflammation may result in inflammation of the ganglia or cardiac nerves, which may change how the heart’s autonomic nervous system regulates itself. […] Third, localized inflammation may directly harm the heart’s cells, impairing their ability to handle calcium, boosting their automaticity, or making them more susceptible to catecholamines. […] Fourth, localized inflammation may compress or infiltrate the cardiac conduction system, including the His-Purkinje system, the atrioventricular node, and the sinoatrial node, which may result in heart block or bradyarrhythmias.
  • #90 Inflammation and arrhythmogenesis: a narrative review of the complex relationship | International Journal of Arrhythmia | Full Text
    https://arrhythmia.biomedcentral.com/articles/10.1186/s42444-024-00110-z
    Conditions like endocarditis, myocarditis, or pericarditis may result from localized inflammation that targets specific heart components. […] The following are the consequences of inflammation-induced arrhythmogenesis in the electrocardiogram (ECG): Inflammation can impact cardiomyocytes’ ion channel function, resulting in a delayed repolarization and a prolonged action potential duration (APD). […] Inflammation can also result in transmural and regional variations in the electrical characteristics of the heart tissue, including dispersion of repolarization, refractoriness, and conduction velocity. […] When there is inflammation, the heart’s tissue may be less able to adjust to variations in heart rate, which may occur during stress or exercise. […] Atrial fibrillation (AF), ventricular tachycardia (VT), and sudden cardiac death (SCD) are a few arrhythmias that can be prevented or treated by reducing inflammation.
  • #91 Pathological basis of cardiac arrhythmias: vicious cycle of immune-metabolic dysregulation
    https://www.oatext.com/pathological-basis-of-cardiac-arrhythmias-vicious-cycle-of-immune-metabolic-dysregulation.php
    Cardiac arrhythmias are a major type of cardiovascular diseases and account for high morbidity and mortality. The occurrence of cardiac arrhythmias is closely associated with abnormal neurohumoral regulation of heart rhythmicity and the pathogenesis of many cardiovascular diseases, particularly coronary artery disease (CAD). Normal immunometabolic coupling between endoplasmic reticulum (ER) and mitochondria is an essential condition for normal heart rhythm. ER stress and mitochondrial oxidative stress evoked immunometabolic challenges can cause inflammation, lipotoxicity and cell apoptosis, leading to CAD and the ensuing arrhythmias. These disorders are associated with activation of inducible nitric oxide synthase, protein tyrosine nitration, malfunctioned chaperone, abnormal calcium signaling through mitochondria-associated ER membrane, disruption of oxidative phosphorylation, and activation of inflammatory and apoptotic pathways. In this review, we highlight the mechanisms underlying arrhythmias, specifically involving disorders in immuno-metabolic network and the underlying signaling process.
  • #92 Pathological basis of cardiac arrhythmias: vicious cycle of immune-metabolic dysregulation
    https://www.oatext.com/pathological-basis-of-cardiac-arrhythmias-vicious-cycle-of-immune-metabolic-dysregulation.php
    The cellular type of immunological injury is associated with the activation of cytotoxic T-lymphocytes/cells. […] In the pathogenesis of CVDs and the resultant arrhythmias, immunologic injuries and metabolic disorders occur simultaneously and are intertwined to form a malfunctioned immunometabolic network. […] Together with a previous review, the facts presented above allow us to propose that accumulation of harmful lipids or generation of signaling intermediates can interfere with immune regulation in cardiac tissues and vice versa; they can form a vicious cycle of immune-metabolic dysregulation and in turn hurt cardiac functions. Thus, in studying on the pathogenesis of arrhythmias and therapeutic approaches, the immune states and metabolic conditions should be considered in an intact immunometabolic network.
  • #93 Pathological basis of cardiac arrhythmias: vicious cycle of immune-metabolic dysregulation
    https://www.oatext.com/pathological-basis-of-cardiac-arrhythmias-vicious-cycle-of-immune-metabolic-dysregulation.php
    Immunometabolic disorders involve dysregulation of multiple organelles during cardiac injuries and the ensuing arrhythmia. ER stress and mitochondrial oxidative stress intersect immune injury and metabolic disorder, thereby highly representing malfunctions of immunometabolic network in arrhythmogenesis. […] It is important to note that ER stress can propagate through inactivation of inositol-requiring enzyme-1, the key ER regulator, through nitrosylation due to excessively produced NO following increased iNOS activity. […] We propose that ER is an important immunometabolic hub in the cardiac pathogenesis and the ensuing arrhythmias. […] ROS is a natural byproduct of the normal metabolism of oxygen including peroxides, superoxide, hydroxyl radical, and singlet oxygen. In diabetic cardiomyopathy and I/R, cardiac production of ROS can increase dramatically, resulting in oxidative stress and significant cellular damage.
  • #94 Why heart rhythm problems tend to happen early in the morning | Imperial News | Imperial College London
    https://www.imperial.ac.uk/news/252500/why-heart-rhythm-problems-tend-happen/
    Researchers have uncovered why people are more likely to have heart arrhythmia first thing in the morning. […] Many studies have shown that potentially lethal heart rhythm disturbances (ventricular arrhythmia) are more likely to occur in the morning, when people wake after a nights sleep, but until now the trigger mechanism has not been fully understood. […] Now, research led by Imperial College London have revealed that these heart disturbances are linked to the natural surge of the stress hormone, cortisol, which peaks in our blood first thing in the morning. […] In a study in mice, they found that cortisol binds to a specific receptor in heart cells. The receptor moves to the nucleus where it influences the genes regulating ion channels in the cell membrane, which control heart beats. As the activity of the ion channels changes, the heart becomes much more vulnerable, since it is easier for the regular electrical impulses, which cause regular heart beats, to break down into more chaotic activity or arrhythmia.
  • #95 Why heart rhythm disturbances are more likely early in the morning – BHF
    https://www.bhf.org.uk/what-we-do/news-from-the-bhf/news-archive/2024/april/why-heart-rhythm-disturbances-are-more-likely-to-happen-early-in-the-morning
    Research funded by us has revealed for the first time a mechanism explaining why potentially lethal heart rhythm disturbances are more likely to occur in the morning, when people wake after a nights sleep. […] These disturbances, known as ventricular arrhythmias, are linked to the natural surge of the stress hormone cortisol, which peaks in our blood first thing in the morning. […] As the activity of the genes change, electrical impulses to the heart become less regular and more chaotic, leading to abnormal heart rhythms, or arrhythmia. […] Ventricular arrhythmias can strike at any time and, if left untreated, can lead to a loss of consciousness, sudden cardiac arrest, and death. […] Identifying a rise in cortisol as the culprit could allow us to explore new treatment options that could reduce arrhythmias in those most at risk.
  • #96 Why heart rhythm problems tend to happen early in the morning | Imperial News | Imperial College London
    https://www.imperial.ac.uk/news/252500/why-heart-rhythm-problems-tend-happen/
    Researchers have uncovered why people are more likely to have heart arrhythmia first thing in the morning. […] Many studies have shown that potentially lethal heart rhythm disturbances (ventricular arrhythmia) are more likely to occur in the morning, when people wake after a nights sleep, but until now the trigger mechanism has not been fully understood. […] Now, research led by Imperial College London have revealed that these heart disturbances are linked to the natural surge of the stress hormone, cortisol, which peaks in our blood first thing in the morning. […] In a study in mice, they found that cortisol binds to a specific receptor in heart cells. The receptor moves to the nucleus where it influences the genes regulating ion channels in the cell membrane, which control heart beats. As the activity of the ion channels changes, the heart becomes much more vulnerable, since it is easier for the regular electrical impulses, which cause regular heart beats, to break down into more chaotic activity or arrhythmia.
  • #97 Why heart rhythm problems tend to happen early in the morning | Imperial News | Imperial College London
    https://www.imperial.ac.uk/news/252500/why-heart-rhythm-problems-tend-happen/
    The discovery of the link also raises the prospect of new treatments in this field. […] Lead researcher Alicia DSouza from Imperials National Heart and Lung Institute (HNLI) says: Our hearts are effectively different organs at different times of the day. They are more vulnerable first thing in the morning because of ancient circadian rhythms, which have evolved over millions of years. […] Ventricular arrhythmias can strike at any time and, if left untreated, can lead to a loss of consciousness, sudden cardiac arrest, and death. […] This intriguing study in mice reveals a possible solution to the mystery of why ventricular arrhythmias are more common in the morning. Identifying a rise in cortisol as the culprit could allow us to explore new treatment options that could reduce arrhythmias in those most at risk.
  • #98 Why heart rhythm problems tend to happen early in the morning | Imperial News | Imperial College London
    https://www.imperial.ac.uk/news/252500/why-heart-rhythm-problems-tend-happen/
    The discovery of the link also raises the prospect of new treatments in this field. […] Lead researcher Alicia DSouza from Imperials National Heart and Lung Institute (HNLI) says: Our hearts are effectively different organs at different times of the day. They are more vulnerable first thing in the morning because of ancient circadian rhythms, which have evolved over millions of years. […] Ventricular arrhythmias can strike at any time and, if left untreated, can lead to a loss of consciousness, sudden cardiac arrest, and death. […] This intriguing study in mice reveals a possible solution to the mystery of why ventricular arrhythmias are more common in the morning. Identifying a rise in cortisol as the culprit could allow us to explore new treatment options that could reduce arrhythmias in those most at risk.
  • #99 Why heart rhythm disturbances are more likely early in the morning – BHF
    https://www.bhf.org.uk/what-we-do/news-from-the-bhf/news-archive/2024/april/why-heart-rhythm-disturbances-are-more-likely-to-happen-early-in-the-morning
    The discovery of the link also raises the prospect of new treatments in this field. […] Our hearts are effectively different organs at different times of the day. They are more vulnerable first thing in the morning because of ancient circadian rhythms, which have evolved over millions of years. […] This study is the latest in a series in which Dr DSouza and Professor Mark Boyett from the University of Bradford have been exploring why the electrical activity of the heart shows an important day-night rhythm and why the heart is vulnerable to different arrhythmias at different times of the day or night.
  • #100 Azthena logo with the word Azthena
    https://www.news-medical.net/news/20200218/Study-reveals-underlying-mechanism-for-life-threatening-cardiac-arrhythmias.aspx
    Low oxygen levels in the heart have long been known to produce life-threatening arrhythmias, even sudden death. Until now, it was not clear how. […] Our research shows that within seconds, at low levels of oxygen (hypoxia), a protein called small ubiquitin-like modifier (SUMO) is linked to the inside of the sodium channels which are responsible for starting each heartbeat. […] If sodium channels re-open and produce late sodium currents, as observed in this study with low oxygen levels, the action potential is prolonged and new electrical activity can begin before the heart has recovered risking dangerous, disorganized rhythms. […] This new research shows how rapid SUMOylation of cell surface cardiac sodium channels causes late sodium current in response to hypoxia, a challenge that confronts many people with heart disease. […] The information, gained through the current study, offers new targets for therapeutics to prevent late current and arrhythmia associated with heart attacks, chronic heart failure and other life-threatening low oxygen cardiac conditions.
  • #101 Azthena logo with the word Azthena
    https://www.news-medical.net/news/20200218/Study-reveals-underlying-mechanism-for-life-threatening-cardiac-arrhythmias.aspx
    Low oxygen levels in the heart have long been known to produce life-threatening arrhythmias, even sudden death. Until now, it was not clear how. […] Our research shows that within seconds, at low levels of oxygen (hypoxia), a protein called small ubiquitin-like modifier (SUMO) is linked to the inside of the sodium channels which are responsible for starting each heartbeat. […] If sodium channels re-open and produce late sodium currents, as observed in this study with low oxygen levels, the action potential is prolonged and new electrical activity can begin before the heart has recovered risking dangerous, disorganized rhythms. […] This new research shows how rapid SUMOylation of cell surface cardiac sodium channels causes late sodium current in response to hypoxia, a challenge that confronts many people with heart disease. […] The information, gained through the current study, offers new targets for therapeutics to prevent late current and arrhythmia associated with heart attacks, chronic heart failure and other life-threatening low oxygen cardiac conditions.
  • #102
    https://journals.lww.com/jtrauma/fulltext/9900/pad2_disturbs_cardiomyocyte_calcium_homeostasis_by.974.aspx
    In conclusion, we find that PAD2 plays a critical role in the pathogenesis of hemorrhagic shock-induced arrhythmias by regulating SERCA2a activity through citrullination. PAD2 inhibition may represent a novel therapeutic approach for mitigating cardiac dysfunction and improving survival rates in patients with traumatic hemorrhagic shock.
  • #103 Arrhythmias: MedlinePlus Medical EncyclopediaLock
    https://medlineplus.gov/ency/article/001101.htm
    An arrhythmia is a disorder of the heart rate (pulse) or heart rhythm. The heart can beat too fast (tachycardia), too slow (bradycardia), or irregularly. […] Arrhythmias are caused by problems with the heart’s electrical conduction system. […] Abnormal extra signals may occur. […] Electrical signals may be blocked or slowed. […] Electrical signals travel in new or different pathways through the heart. […] Some common causes of abnormal heartbeats are: […] Arrhythmias may also be caused by some substances or drugs, including: […] Some of the more common abnormal heart rhythms are: […] When an arrhythmia is serious, you may need urgent treatment to restore a normal rhythm. […] Medicines called anti-arrhythmic drugs may be used: […] Other treatments to prevent or treat abnormal heart rhythms include: […] The outcome depends on several factors:
  • #104 Palpitations – Cardiovascular Disorders – Merck Manual Professional Edition
    https://www.merckmanuals.com/professional/cardiovascular-disorders/symptoms-of-cardiovascular-disorders/palpitations
    Many arrhythmias that cause palpitations have no adverse physiologic consequences of their own (ie, independent of the underlying disorder). However, bradyarrhythmias, tachyarrhythmias, and heart blocks can be unpredictable and may adversely affect cardiac output and cause hypotension or death. Ventricular tachycardia sometimes degenerates to ventricular fibrillation. […] Most antiarrhythmic medications themselves can cause arrhythmias.
  • #105 Overview of Basic Mechanisms of Cardiac Arrhythmia
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3164530/
    EADs are typically observed in cardiac tissues exposed to injury, altered electrolytes, hypoxia, acidosis, catecholamines, and pharmacologic agents, including antiarrhythmic drugs. Ventricular hypertrophy and heart failure also predispose to the development of EADs. EAD characteristics vary as a function of animal species, tissue or cell type, and the method by which the EAD is elicited. Although specific mechanisms of EAD induction can differ, a critical prolongation of repolarization accompanies most, but not all, EADs. Drugs that inhibit potassium currents or which augment inward currents predispose to the development of EADs. […] An example of DAD-induced arrhythmia is the catecholaminergic polymorphic ventricular tachycardia (CPVT), which may be caused by the mutation of either the type 2 ryanodine receptor (RyR2) or the calsequestrin (CSQ2). The principal mechanism underlying these arrhythmias is the leaky ryanodine receptor, which is aggravated during catecholamine stimulation. A typical clinical phenotype of CPVT is bidirectional ventricular tachycardia, which is also seen in digitalis toxicity.
  • #106 Heart rhythm disorders – WikiLectures
    https://www.wikilectures.eu/w/Heart_rhythm_disorders
    Heart rhythm disorders (arytmie, dysrytmie) is a collective name for disorders of heart rate, heart rhythm, propagation of excitement in the heart or their combination. […] According to the pathogenetic mechanisms leading to individual arrhythmias, we distinguish: disorders of excitability; conduction disorders; combined disorders. […] The most common cause of arrhythmia is CHD (ischemia, hypoxia, acidosis, reperfusion injury). […] Ionic disorders (hypokalemia, hypomagnesia, hyperkalemia hypercalcemia); acid-base balance disorders; myocardial disorders: dilation or hypertrophy of the heart (cardiomyopathy, e.g. right ventricular cardiomyopathy is directly referred to as arrhythmogenic right ventricular dysplasia); inflammation (myocarditis); congenital and acquired heart defects. […] Disturbance of the balance of the vegetative nervous system (stress, anxiety shock, compensation of another pathological condition); arrhythmogenic substances (drugs, caffeine, adrenaline alcohol, digoxin, diuretics, antiarrhythmics); other diseases (endocrinopathy – thyrotoxicosis); cardiovascular autonomic neuropathy.
  • #107
    https://journals.lww.com/bjem/fulltext/2023/02030/a_review_of_arrhythmias_in_endocrinology.3.aspx
    Potassium imbalance is a major problem in diabetic ketoacidosis and can potentially lead to deadly arrhythmias. […] Certain anti-diabetic drugs may cause QT prolongation, either as a result of the drugs effect of hypoglycemia or as a direct side effect. […] Hypothyroidism can lead to a reduction in cardiac output of up to 30%40%, which can be attributed to a decrease in both stroke volume and heart rate. Additionally, hypothyroidism can cause varying degrees of conduction blocks. […] Most rhythm and conduction abnormalities identified in hypothyroidism can be quickly resolved with the start of levothyroxine medication in the proper dosage. […] In hypothyroidism, the expression of hepatic low-density lipoprotein receptors declines, which results in decreased cholesterol clearance and the development of hyperlipidemia.
  • #108 Society for Cardiovascular Angiography and Interventions
    https://www.healio.com/news/cardiology/20250506/cannabis-use-disorder-among-those-with-heart-failure-may-increase-mi-shock-arrhythmias
    Among patients with heart failure, those with cannabis use disorder had elevated odds for cardiogenic shock, MI and arrhythmias, researchers reported at the Society for Cardiovascular Angiography and Interventions Scientific Sessions. […] After adjustment for demographics, compared with nonusers, patients with cannabis use disorder had lower odds of mortality (adjusted OR = 0.51; 95% CI, 0.35-0.77; P.01) and respiratory failure (aOR = 0.75; 95% CI, 0.69-0.83; P.001) but higher odds of cardiogenic shock (aOR = 1.27; 95% CI, 1.08-1.49; P.01), MI (aOR = 1.5; 95% CI, 1.27-1.77; P.01) and arrhythmias (aOR = 1.48; 95% CI, 1.21-1.97; P.01), Ishaq and colleagues found. […] The negative cardiac effects are associated with the frequency of use, Ishaq told Healio. The more you are using it, the worse prognosis you are going to have in terms of MI, arrhythmias, cardiogenic shock, etc.
  • #109 What supplements should you take for arrhythmia?
    https://www.medicalnewstoday.com/articles/supplements-for-arrhythmia-types-benefits-side-effects
    A doctor may recommend several dietary supplements, including magnesium, vitamin C, or coenzyme Q10 (Co Q10), to help a person with arrhythmia. […] When the heart does not beat with a typical rhythm and speed, health experts call this an arrhythmia. […] The most common is a fast pace with an irregular rhythm, which doctors call atrial fibrillation (AFib). […] Co Q10 supplementation may reduce mortality due to cardiovascular causes and decrease arterial stiffness and hypertension (high blood pressure). […] Some research suggests it has an antiarrhythmic effect, meaning it could correct a heartbeat that is too fast or irregular. However, further research is necessary to investigate this. […] Magnesium is an important mineral for regulating various bodily functions, including those that help establish a regular heart rhythm.
  • #110 What supplements should you take for arrhythmia?
    https://www.medicalnewstoday.com/articles/supplements-for-arrhythmia-types-benefits-side-effects
    A 2020 retrospective study suggested magnesium, in combination with standard therapy, helped lower fast heart rates in people with AFib. […] Some research in a 2022 review suggests magnesium supplementation may help prevent AFib. However, the authors highlight the need for further research. […] According to a 2022 overview of systematic reviews, WXKL may be safe and effective in AFib treatment. However, more research is necessary to strengthen this conclusion. […] A 2021 study suggests ginger has various cardioprotective effects, including antihypertensive effects, which help lower blood pressure, antiplatelet effects, which help prevent heart attack and stroke, and antihyperlipidemia effects, which reduce the buildup of fats in the blood. […] A 2016 study suggests that 100 milligrams per kilogram of body weight of ginger as a daily oral supplement over 15 days significantly lowered the incidence of arrhythmia in rats.
  • #111 What supplements should you take for arrhythmia?
    https://www.medicalnewstoday.com/articles/supplements-for-arrhythmia-types-benefits-side-effects
    A 2022 review suggests that vitamin C may be beneficial in treating AFib after heart surgery and may reduce recurrence after cardioversion. […] Supplements may help level out blood imbalances and restore heart rhythms to expected patterns. […] Electrical conduction problems, medications, stress or exertion, or blood imbalances can cause arrhythmias.
  • #112 What supplements should you take for arrhythmia?
    https://www.medicalnewstoday.com/articles/supplements-for-arrhythmia-types-benefits-side-effects
    A 2020 retrospective study suggested magnesium, in combination with standard therapy, helped lower fast heart rates in people with AFib. […] Some research in a 2022 review suggests magnesium supplementation may help prevent AFib. However, the authors highlight the need for further research. […] According to a 2022 overview of systematic reviews, WXKL may be safe and effective in AFib treatment. However, more research is necessary to strengthen this conclusion. […] A 2021 study suggests ginger has various cardioprotective effects, including antihypertensive effects, which help lower blood pressure, antiplatelet effects, which help prevent heart attack and stroke, and antihyperlipidemia effects, which reduce the buildup of fats in the blood. […] A 2016 study suggests that 100 milligrams per kilogram of body weight of ginger as a daily oral supplement over 15 days significantly lowered the incidence of arrhythmia in rats.
  • #113 What supplements should you take for arrhythmia?
    https://www.medicalnewstoday.com/articles/supplements-for-arrhythmia-types-benefits-side-effects
    A 2022 review suggests that vitamin C may be beneficial in treating AFib after heart surgery and may reduce recurrence after cardioversion. […] Supplements may help level out blood imbalances and restore heart rhythms to expected patterns. […] Electrical conduction problems, medications, stress or exertion, or blood imbalances can cause arrhythmias.
  • #114 Atrial fibrillation | Nature Reviews Disease Primers
    https://www.nature.com/articles/s41572-022-00347-9
    Atrial fibrillation (AF) is the most common cardiac arrhythmia despite substantial efforts to understand the pathophysiology of the condition and develop improved treatments. […] Research has revealed that defects in specific molecular pathways underlie AF pathogenesis, resulting in electrical conduction disorders that drive AF. […] The severity of this so-called electropathology correlates with the stage of AF disease progression and determines the response to AF treatment. […] Therefore, unravelling the molecular mechanisms underlying electropathology is expected to fuel the development of innovative personalized diagnostic tools and mechanism-based therapies. […] Currently, various treatment modalities targeting AF-related electropathology, including lifestyle changes, pharmaceutical and nutraceutical therapy, substrate-based ablative therapy, and neuromodulation, are available to maintain sinus rhythm and might offer a novel holistic strategy to treat AF.
  • #115 Propranolol: medicine for heart problems, anxiety and migraine – NHS
    https://www.nhs.uk/medicines/propranolol/
    Propranolol is used to treat conditions that cause an irregular heartbeat (arrhythmia), like atrial fibrillation. […] Propranolol can help reduce your symptoms if you have too much thyroid hormone in your body (thyrotoxicosis). […] Propranolol slows down your heart rate and makes it easier for your heart to pump blood around your body. […] Propranolol works by changing the way your body responds to some nerve impulses, including in the heart. It slows down your heart rate and makes it easier for your heart to pump blood around your body. […] Propranolol treats the physical symptoms of anxiety for example, it stops your heart beating too fast. […] You have shortness of breath with a cough which gets worse when you exercise (like walking up stairs), swollen ankles or legs, chest pain, or an irregular heartbeat these are signs of heart problems. […] Heart rhythm problems (arrhythmia)
  • #116 Arrhythmia: Symptoms & Treatment
    https://my.clevelandclinic.org/health/diseases/16749-arrhythmia
    In addition to medicine, some people need therapies to treat or eliminate irregular heart rhythms. […] A cardiologist may insert certain devices during a procedure in the electrophysiology lab. Devices to treat a heart arrhythmia include permanent pacemakers and implantable cardioverter defibrillators (ICD). […] People with arrhythmias may require heart surgery for any of these reasons: to treat heart disease that may be causing the arrhythmia, including valve surgery or coronary artery bypass surgery. […] Depending on the type of cardiac arrhythmia you have, you may have mild or severe symptoms or none at all. You may not need treatment, but some people need medicine or a procedure. With heart arrhythmia treatment, many people can live full lives. […] Harmless arrhythmias go away and come back in response to what triggers them. However, people with other types of arrhythmias especially those that put you at risk for cardiac arrest need treatment for the rest of their lives.
  • #117 New mechanism discovered for the life-threatening arrhythmias in Andersen-Tawil syndrome | EurekAlert!
    https://www.eurekalert.org/news-releases/1040441
    The discovery that a mutation considered 'monogenic’ disrupts not only the ion channel directly affected by the mutation, but also a complementary channel is important. […] The results of the new Circulation Research study support the hypothesis that the molecular mechanisms that increase susceptibility to arrhythmias and sudden cardiac death in ATS1 depend on the specific mutation, so that pharmacological treatment and clinical management should be tailored to each individual patient.
  • #118 Why heart rhythm problems tend to happen early in the morning | Imperial News | Imperial College London
    https://www.imperial.ac.uk/news/252500/why-heart-rhythm-problems-tend-happen/
    The discovery of the link also raises the prospect of new treatments in this field. […] Lead researcher Alicia DSouza from Imperials National Heart and Lung Institute (HNLI) says: Our hearts are effectively different organs at different times of the day. They are more vulnerable first thing in the morning because of ancient circadian rhythms, which have evolved over millions of years. […] Ventricular arrhythmias can strike at any time and, if left untreated, can lead to a loss of consciousness, sudden cardiac arrest, and death. […] This intriguing study in mice reveals a possible solution to the mystery of why ventricular arrhythmias are more common in the morning. Identifying a rise in cortisol as the culprit could allow us to explore new treatment options that could reduce arrhythmias in those most at risk.
  • #119 Why heart rhythm disturbances are more likely early in the morning – BHF
    https://www.bhf.org.uk/what-we-do/news-from-the-bhf/news-archive/2024/april/why-heart-rhythm-disturbances-are-more-likely-to-happen-early-in-the-morning
    The discovery of the link also raises the prospect of new treatments in this field. […] Our hearts are effectively different organs at different times of the day. They are more vulnerable first thing in the morning because of ancient circadian rhythms, which have evolved over millions of years. […] This study is the latest in a series in which Dr DSouza and Professor Mark Boyett from the University of Bradford have been exploring why the electrical activity of the heart shows an important day-night rhythm and why the heart is vulnerable to different arrhythmias at different times of the day or night.
  • #120 Inflammation and arrhythmogenesis: a narrative review of the complex relationship | International Journal of Arrhythmia | Full Text
    https://arrhythmia.biomedcentral.com/articles/10.1186/s42444-024-00110-z
    These consist of corticosteroids, NSAIDs, colchicine, statins, and biologics, among others. […] They may be used to treat inflammatory cardiomyopathies that increase the risk of arrhythmias, such as cardiac sarcoidosis, myocarditis, and rheumatic heart disease. […] By modifying the electrophysiological characteristics of cardiac cells, such as ion channel function, calcium handling, and gap junction coupling, they may also have anti-arrhythmic effects. […] The kind, etiology, and severity of the arrhythmias, as well as the patient’s features and comorbidities, may all affect how effective certain treatment techniques are.
  • #121 Azthena logo with the word Azthena
    https://www.news-medical.net/news/20200218/Study-reveals-underlying-mechanism-for-life-threatening-cardiac-arrhythmias.aspx
    Low oxygen levels in the heart have long been known to produce life-threatening arrhythmias, even sudden death. Until now, it was not clear how. […] Our research shows that within seconds, at low levels of oxygen (hypoxia), a protein called small ubiquitin-like modifier (SUMO) is linked to the inside of the sodium channels which are responsible for starting each heartbeat. […] If sodium channels re-open and produce late sodium currents, as observed in this study with low oxygen levels, the action potential is prolonged and new electrical activity can begin before the heart has recovered risking dangerous, disorganized rhythms. […] This new research shows how rapid SUMOylation of cell surface cardiac sodium channels causes late sodium current in response to hypoxia, a challenge that confronts many people with heart disease. […] The information, gained through the current study, offers new targets for therapeutics to prevent late current and arrhythmia associated with heart attacks, chronic heart failure and other life-threatening low oxygen cardiac conditions.