Wczesne skurcze komorowe
Patofizjologia i mechanizm

Wczesne skurcze komorowe (PVCs) są najczęstszymi zaburzeniami rytmu serca pochodzenia komorowego, występującymi u 12-20% populacji. Patofizjologia PVCs obejmuje trzy główne mechanizmy: automatyzm, re-entry oraz aktywność wyzwalaną (EADs i DADs). Automatyzm wiąże się ze spontaniczną depolaryzacją ektopową, często modulowaną przez zaburzenia elektrolitowe (hipokaliemia, hipomagnezemia, hiperkalcemia), niedokrwienie i katecholaminy. Re-entry wymaga obecności dwóch dróg przewodzenia z jednokierunkowym blokiem, typowo w obszarach bliznowatych po zawale mięśnia sercowego, co jest częstsze u pacjentów ze strukturalną chorobą serca. Aktywność wyzwalana, najczęstsza w idiopatycznych PVCs z drogi odpływu prawej komory (RVOT), związana jest z zaburzeniami gospodarki wapniowej i zwiększonym stężeniem cAMP. Zaburzenia kanałów jonowych (m.in. zmniejszenie Ito, IK1, ICaL) oraz dysregulacja autonomiczna również odgrywają istotną rolę w patogenezie PVCs i ich potencjalnym wpływie na funkcję lewej komory.

Mechanizmy powstawania wczesnych skurczów komorowych

Wczesne skurcze komorowe (Premature Ventricular Contractions, PVCs) są najczęstszymi zaburzeniami rytmu serca pochodzenia komorowego, występującymi u około 12-20% populacji ogólnej. Pomimo powszechności występowania, dokładna patofizjologia PVCs pozostaje nie w pełni wyjaśniona. Obecnie wyróżnia się trzy główne mechanizmy odpowiedzialne za powstawanie wczesnych skurczów komorowych: automatyzm, pobudzenie nawrotne (re-entry) oraz aktywność wyzwalana (triggered activity)123.

Automatyzm

Automatyzm jako mechanizm powstawania PVCs polega na spontanicznym wytworzeniu nowego ogniska depolaryzacji w tkance komorowej, poza fizjologicznym układem przewodzącym4. W warunkach prawidłowych komórki robocze mięśnia sercowego nie wykazują właściwości automatycznych, jednak w pewnych warunkach mogą one nabyć zdolność do spontanicznej depolaryzacji5.

Wzmożony automatyzm może być spowodowany zaburzeniami elektrolitowymi (szczególnie hipokaliemią, hipomagnezemią czy hiperkalcemią), niedokrwieniem mięśnia sercowego, podwyższonym poziomem amin katecholowych (w wyniku stresu, wysiłku fizycznego lub lęku) lub zapaleniem mięśnia sercowego67. Charakterystyczną cechą PVCs powstających w mechanizmie automatyzmu jest występowanie parasystolii, gdzie ektopiczne ognisko wykazuje regularne wyładowania niezależne od rytmu zatokowego8.

W klasycznym obrazie parasystolii, PVCs występują w dokładnych wielokrotnościach cyklu ogniska ektopowego i mogą pojawiać się w całym okresie pobudliwości cyklu sercowego. Blok przewodzenia chroniący ognisko parasystoliczne przed pobudzeniem z zewnątrz musi mieć charakter funkcjonalny, co oznacza, że mimo bloku może zachodzić pewien stopień interakcji elektrotonicznych, pozwalających na modulację ogniska parasystolicznego przez front aktywacji z rytmu zatokowego9.

Re-entry (pobudzenie nawrotne)

Mechanizm re-entry wymaga obecności dwóch różnych dróg przewodzenia z jednokierunkowym blokiem, często związanym z obecnością blizn, zwłóknienia lub nieprawidłowego przewodzenia w określonych regionach mięśnia sercowego10. Re-entry zazwyczaj występuje, gdy wolno przewodząca tkanka (np. niedokrwiony lub bliznowaty mięsień sercowy) sąsiaduje z tkanką o normalnej przewodności1112.

Podłoże arytmogenne dla PVCs u pacjentów po przebytym zawale mięśnia sercowego jest dobrze opisane jako związane z blizną pobudzenie nawrotne o stałym interwale sprzężenia (w przypadkach jednokształtnych PVCs)13. Ten mechanizm jest częstszy u pacjentów ze strukturalną chorobą serca niż u osób bez takiej patologii14.

Charakterystyczną cechą PVCs powstających w mechanizmie re-entry jest niższa zmienność interwału sprzężenia, co sugeruje, że pobudzenie nawrotne może być prawdopodobnym mechanizmem u pacjentów z idiopatycznymi PVCs oraz u chorych z kardiomiopatią rozstrzeniową o nieischemicznym podłożu15.

Triggered activity (aktywność wyzwalana)

Aktywność wyzwalana to mechanizm, w którym następcze depolaryzacje wywołane przez poprzedzający impuls mogą prowadzić do przedwczesnej aktywacji, jeśli osiągną potencjał progowy, co skutkuje powstaniem PVCs1617. Następcze depolaryzacje mogą występować albo podczas (wczesne następcze depolaryzacje, EADs) albo po (późne następcze depolaryzacje, DADs) zakończeniu repolaryzacji18.

Wczesne następcze depolaryzacje (EADs) są najczęściej odpowiedzialne za PVCs związane z bradykardią, ale mogą również występować w przebiegu niedokrwienia i zaburzeń elektrolitowych19. Z kolei późne następcze depolaryzacje (DADs) są zazwyczaj związane ze zwiększonym stężeniem wapnia wewnątrzkomórkowego, co może być spowodowane toksycznością glikozydów naparstnicy, hiperkalcemią, ekspozycją na katecholaminy i zaburzeniami wewnątrzkomórkowego transportu wapnia uwarunkowanymi genetycznie20.

Uważa się, że mechanizm aktywności wyzwalanej jest najczęstszym patofizjologicznym podłożem idiopatycznych PVCs, zwłaszcza tych pochodzących z drogi odpływu prawej komory (RVOT)21. Idiopatyczne zaburzenia rytmu serca wywodzące się z dróg odpływu komór są uważane za spowodowane przez katecholaminy, cykliczny monofosforan adenozyny (cAMP) i zależne od wapnia późne następcze depolaryzacje22.

Szczegółowe mechanizmy na poziomie komórek i tkanek

Zaburzenia gospodarki wapniowej

Zaburzenia wewnątrzkomórkowej gospodarki wapniowej odgrywają istotną rolę w patogenezie PVCs, szczególnie w mechanizmie aktywności wyzwalanej23. W modelu świńskim kardiomiopatii indukowanej przez PVCs (PVICM) zaobserwowano zmniejszoną ekspresję wapniowej ATPazy retikulum sarkoplazmatycznego (SERCA2a) oraz zwiększoną ekspresję receptora ryanodynowego typu 2 (RyR2), wymiennika sodowo-wapniowego (NCX1), kinazy białkowej zależnej od wapnia/kalmoduliny II alfa (CaMKII-α) i fosfolambanu (PLN)24.

Nadmierna regulacja białka hamującego PLN pogłębia zaburzenia sprzężenia elektromechanicznego kardiomiocytów. Zmiany w kanałach jonowych mogą prowadzić do nieprawidłowej repolaryzacji kardiomiocytów, zwiększając ryzyko złośliwych arytmii25. W badaniach eksperymentalnych zauważono, że PVCs prowadzą do wydłużenia czasu trwania potencjału czynnościowego komórek mięśnia sercowego oraz zmniejszenia gęstości przejściowych prądów potasowych wychodzących (Ito), prostujących prądów potasowych wchodzących (IK1) i prądów wapniowych typu L (ICaL), którym towarzyszy zmniejszona ekspresja związanych z nimi podjednostek kanałów jonowych26.

Dysfunkcja układu autonomicznego

Układ autonomiczny odgrywa istotną rolę w patogenezie, podtrzymywaniu i zakłócaniu arytmii komorowych27. Analiza 24-godzinnego elektrokardiogramu pod kątem zmienności rytmu serca u pacjentów z idiopatycznymi PVCs wykazała, że aktywność autonomiczna jest zaangażowana w występowanie PVCs28.

Mechanizm związku między stresem/lękiem a ektopią komorową polega na zwiększonej aktywności współczulnego układu nerwowego (SNE)29. Wpływ PVCs na funkcję lewej komory może wynikać z dysregulacji autonomicznej, a nie tylko z dyssynchronii mechanicznej30.

Interesujące powiązanie między chorobami górnego odcinka przewodu pokarmowego a PVCs może być wyjaśnione rolą nerwu błędnego, który przyczynia się do tworzenia splotu przełykowego, unerwia mięśnie gładkie przełyku i wydziela gałęzie sercowe, regulując częstość akcji serca poprzez przywspółczulny układ nerwowy31.

Dyssynchronia elektromehaniczna

Dyssynchronia komorowa jest ostrym efektem PVCs, który może przyczyniać się do rozwoju kardiomiopatii32. Częste PVCs mogą powodować kardiomiopatię poprzez złożone przejściowe zmiany w wewnątrzkomórkowym wapniu i prądach jonowych błony komórkowej, dynamice częstości akcji serca, parametrach hemodynamicznych oraz stymulacji i hamowaniu autonomicznym mięśnia sercowego i obwodowych naczyń krwionośnych33.

Mechanizm upośledzonej funkcji lewej komory nie jest w pełni zrozumiały. Niektórzy autorzy opisali dyssynchronię jako główną przyczynę, podczas gdy inni sugerowali nieregularny rytm, rozprzężenie przedsionkowo-komorowe i mechaniczną bradykardię34. Czas trwania zespołu QRS PVCs jest jednym z najbardziej niezależnych czynników predykcyjnych rozwoju kardiomiopatii indukowanej przez PVCs35.

Czynniki genetyczne i molekularne

Na poziomie molekularnym, jednym z wyjaśnień mechanizmu PVCs jest zwiększona ilość cyklicznego AMP (cAMP) w komorowych miocytach sercowych, prowadząca do zwiększonego przepływu jonów wapnia do komórki36. Czynniki genetyczne mogą również odgrywać rolę, co sugerują różnice w mechanizmach arytmii u pacjentów z rodzinną kardiomiopatią rozstrzeniową (grupa mutacji PLN/LMNA), którzy wykazują wysoką zmienność interwału sprzężenia, wskazującą na mechanizm inny niż re-entry lub aktywność wyzwalana37.

Istnieją dowody na związek między PVCs a stanami zapalnymi. Podwyższony poziom białka C-reaktywnego o wysokiej czułości (hs-CRP) był niezależnym predyktorem PVCs w populacji chińskiej, szczególnie u mężczyzn, i był związany z przyszłym występowaniem PVCs u uczestników bez historii zawału mięśnia sercowego lub udaru38.

Czynniki wyzwalające i predysponujące

Strukturalne choroby serca

Istniejące uszkodzenie mięśnia sercowego może również prowokować PVCs. Blizna mięśnia sercowego, która pojawia się po zawale mięśnia sercowego, a także po chirurgicznej naprawie wrodzonych wad serca, może zakłócać system przewodzenia serca i może również drażnić otaczające żywotne miocyty komorowe, zwiększając prawdopodobieństwo ich spontanicznej depolaryzacji39.

Choroby serca zwiększające ryzyko PVCs obejmują nadciśnienie tętnicze, zawał serca, chorobę wieńcową, kardiomiopatię rozstrzeniową, kardiomiopatię przerostową, wrodzone wady serca i niewydolność serca40. U osób ze strukturalną chorobą serca re-entry jest najczęstszym mechanizmem ze względu na obecność tkanki o różnych cechach elektrofizjologicznych w porównaniu ze zdrowym mięśniem sercowym (najczęściej obszary włóknienia), co pozwala fali depolaryzacji na wystarczające spowolnienie, aby dotrzeć do obszaru mięśnia sercowego, który nie jest już refrakcyjny, prowadząc tym samym do jednego lub kilku dodatkowych pobudzeń41.

Zaburzenia elektrolitowe

Zaburzenia elektrolitowe, takie jak niski poziom potasu lub magnezu albo wysoki poziom wapnia, mogą być czynnikami wyzwalającymi PVCs4243. Nieprawidłowe stężenia elektrolitów mogą wpływać na potencjał błonowy kardiomiocytów i zmieniać ich właściwości elektrofizjologiczne, predysponując do arytmii44.

Czynniki hormonalne i stres

Podwyższony poziom adrenaliny w organizmie z powodu stresu lub niepokoju może przyczyniać się do występowania PVCs45. Nadczynność tarczycy to kolejny stan endokrynologiczny, który może być związany z PVCs46.

Leki i substancje

Niektóre leki, w tym leki przeciwhistaminowe i leki na przeziębienie, mogą wywoływać PVCs47. Cilostazol, inhibitor fosfodiesterazy III, został powiązany z występowaniem PVCs u pacjentów z historią zawału mięśnia sercowego48.

Nadmierne spożycie alkoholu, tytoniu lub substancji niedozwolonych również może zwiększać ryzyko PVCs49. Kofeina jest często wymieniana jako potencjalny czynnik wyzwalający, chociaż badania dotyczące jej wpływu są niejednoznaczne50.

Kliniczne konsekwencje mechanizmów patofizjologicznych

Kardiomiopatia indukowana przez PVCs

Częste PVCs mogą prowadzić do potencjalnie odwracalnej formy kardiomiopatii u pacjentów bez strukturalnej choroby serca51. Chociaż dokładny mechanizm patofizjologiczny kardiomiopatii indukowanej przez PVCs (PVICM) nie został jeszcze w pełni wyjaśniony, badania na modelach zwierzęcych sugerują, że nieprawidłowe zarządzanie wapniem i przebudowa serca mogą być kluczowymi mechanizmami leżącymi u podstaw rozwoju kardiomiopatii52.

Obciążenie PVCs (PVC burden) niezbędne do wywołania kardiomiopatii jest określane jako więcej niż 5-10% wszystkich dziennych uderzeń serca w nieznanym przedziale czasowym53. Jednakże nie wszyscy pacjenci z częstymi PVCs rozwiną kardiomiopatię. W rzeczywistości niektórzy pacjenci z wysokim obciążeniem PVCs nigdy nie wykazują żadnej dysfunkcji lewej komory, dlatego podjęto próby znalezienia czynników ryzyka i hipotez przewidujących wystąpienie tego typu kardiomiopatii54.

Kardiomiopatia indukowana przez PVCs jest potencjalnie odwracalnym stanem, w którym dysfunkcja lewej komory może ulec poprawie, a nawet normalizacji dzięki farmakologicznemu tłumieniu lub technikom ablacji55. Badania obserwacyjne wykazały, że redukcja PVCs poprzez zastosowanie leków farmakologicznych, takich jak beta-blokery, amiodaron lub flekainid, lub poprzez ablację cewnikową może poprawić funkcję lewej komory56.

Implikacje dla leczenia

Zrozumienie mechanizmu leżącego u podstaw PVCs jest kluczowe dla wyboru odpowiedniej terapii57. Aktywność wyzwalana, która jest prawdopodobnie najczęstszym mechanizmem idiopatycznych PVCs, może być skutecznie leczona beta-blokerami i antagonistami kanału wapniowego58.

Karwedilol, jeden z najskuteczniejszych beta-blokerów w redukcji tachyarytmii komorowych i śmiertelności u pacjentów z niewydolnością serca, może działać poprzez hamowanie uwalniania wapnia wywołanego przeciążeniem magazynów (SOICR), szczególnie w przypadku aktywności wyzwalanej59.

Flekainid, lek antyarytmiczny klasy IC o właściwościach blokujących kanały sodowe, jest podawany jako monoterapia i wykazuje znaczącą redukcję obciążenia PVCs oraz poprawę objawową, co wspiera potencjalną użyteczność flekainidu jako skutecznej nieinwazyjnej opcji terapeutycznej u odpowiednio wyselekcjonowanych pacjentów60.

U pacjentów z wczesnymi jednokształtnymi ektopami komorowymi, bez wykrycia predyktorów kardiomiopatii arytmogennej (ACM), najskuteczniejsze były leki antyarytmiczne klasy I. U innych pacjentów z wczesnymi i późnymi jednokształtnymi ektopami komorowymi i wykrytymi predyktorami ACM, skuteczne okazały się leki klasy III61.

Ablacja cewnikowa jest bezpieczna i skuteczna oraz może być leczeniem przyczynowym w wielu przypadkach62. Ablacja cewnikowa o częstotliwości radiowej (RFCA) jest szczególnie skuteczna w leczeniu objawowych PVCs pochodzących z drogi odpływu w strukturalnie prawidłowych sercach63.

Znaczenie prognostyczne

PVCs w niektórych przypadkach mogą być pierwszą manifestacją podstawowej strukturalnej choroby serca64. Przez ponad 20 lat akceptowano, że obecność PVCs przy braku strukturalnej choroby serca pociąga za sobą korzystne, łagodne rokowanie, nawet gdy pojawiają się często65.

Jednakże znaczenie prognostyczne PVCs w chorobie niedokrwiennej serca jest mniej łagodne. U pacjentów, którzy przebyli zawał mięśnia sercowego, obecność PVCs wiązała się z trzykrotnie zwiększonym ryzykiem nagłej śmierci66.

PVCs mogą również wyzwalać złośliwe arytmie komorowe u niektórych pacjentów z idiopatycznym migotaniem komór i innymi zespołami67. Ryzyko nagłej śmierci sercowej z powodu złośliwej arytmii komorowej należy rozważyć u pacjentów z chorobą serca, którzy mają częste PVCs68.

Nowe kierunki badań i koncepcje

Mechaniczna indukcja PVCs

Nagłe rozciągnięcie mięśnia sercowego ma wpływ elektrofizjologiczny na mięsień sercowy, zależny od czasu w cyklu sercowym69. Naprężenie mechaniczne zostało wskazane jako czynnik predysponujący pacjentów do arytmii komorowych w różnych chorobach serca, w tym w niedokrwieniu mięśnia sercowego, arytmogennej kardiomiopatii prawej komory i zatrzymaniu akcji serca u pacjentów z wypadaniem zastawki mitralnej70.

Związek PVCs z chorobą przełyku i górnego odcinka przewodu pokarmowego

Zidentyfikowano unikalne powiązanie między chorobami górnego odcinka przewodu pokarmowego a PVCs, proponując podwójny mechanizm działania – przez górny odcinek przewodu pokarmowego i PVCs pośredniczone przez nerw błędny oraz przez bezpośrednie, anatomiczne, zewnętrzne wyzwalanie drogi odpływu prawej komory (RVOT) serca71.

We wszystkich opisanych przypadkach pochodzenie PVCs było zlokalizowane u podstawy drogi odpływu prawej komory (RVOT), a u pacjentów z chorobą górnego odcinka przewodu pokarmowego, którzy mieli skądinąd idiopatyczne obciążenie PVCs, zauważono znaczną redukcję PVCs po interwencjach chirurgicznych lub zabiegowych górnego odcinka przewodu pokarmowego (redukcja o 68,34%, p = 0,024)72.

Związek z migotaniem przedsionków

Związek między PVCs a migotaniem przedsionków (AF) nie jest w pełni zrozumiały. Teoretycznie wsteczne przewodzenie komorowo-przedsionkowe może wystąpić z PVCs, które mogą działać jak przedsionkowe pobudzenia ektopowe. Istnieje więc możliwość, że PVCs mogą zwiększać ryzyko AF poprzez wsteczne przewodzenie komorowo-przedsionkowe73.

Parametry hematologiczne i biomarkery

W analizie związku PVCs z parametrami hematologicznymi stwierdzono, że najważniejszymi czynnikami hematologicznymi związanymi z PVCs były liczba białych krwinek (WBC), płytek krwi (PLT), rozpiętość rozkładu objętości erytrocytów (RDW), rozpiętość rozkładu objętości płytek krwi (PDW) i hematokryt (HCT) u mężczyzn oraz liczba czerwonych krwinek (RBC), płytek krwi (PLT), RDW, średnia objętość krwinki czerwonej (MCV) i mieszane białe krwinki (MXD) u kobiet74.

Chociaż nie ma oczywistego bezpośredniego związku między tymi parametrami a PVCs, według wcześniejszych badań niektóre stany medyczne mogą powodować współwystępowanie wyższych wartości tych parametrów i PVCs. Wykazano, że PVCs mogą być związane z chorobami serca, takimi jak choroba wieńcowa, strukturalna choroba serca, zapalenie mięśnia sercowego i arytmie. Wykazano również, że niektóre z tych parametrów hematologicznych mogą być związane ze zwiększonym ryzykiem różnych chorób serca75.

Ponadto podwyższony poziom białka C-reaktywnego o wysokiej czułości (hs-CRP) był niezależnym predyktorem PVCs w populacji chińskiej, szczególnie u mężczyzn, i był związany z przyszłym PVCs u uczestników bez historii zawału mięśnia sercowego lub udaru76.

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  1. 09.04.2026
  2. www.leksykon.com.pl

Materiały źródłowe

  • #1 Premature Ventricular Complex – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK547713/
    The primary mechanisms thought to result in PVCs include triggered activity, automaticity, and reentry. Identification of the pathophysiological is essential as this informs the management approach. […] Triggered activity arises during the early depolarization phase due to exceeding the cell membrane activation threshold. The PVCs associated with bradycardia are often caused by this mechanism, along with other factors like electrolyte abnormalities, ischemia, and digoxin toxicity. […] Automaticity involves PVCs originating from abnormal cardiomyocyte activity, often showing parasystole. The enhanced automaticity characteristically results from an ectopic ventricular focus that fires spontaneously. […] Though usually linked to sustained arrhythmias, reentry can also cause PVCs. It requires 2 distinct pathways with unidirectional block, often involving scars, fibrosis, or abnormal conduction in specific regions. This mechanism is seen in phenomena like bundle-branch or fascicular PVCs.
  • #2 Premature Ventricular Complexes: Background, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/761148-overview
    Premature ventricular complexes (PVCs) (also known as ventricular premature complexes [VPCs]) are ectopic impulses originating from an area distal to the His Purkinje system. PVCs are the most common ventricular arrhythmia. […] The fundamental underlying etiology of PVCs remain to be determined. […] Very few studies have evaluated the pathophysiology of PVCs in human subjects; most of the information is derived from animal studies. However, what is known is that ventricular monocytes at the cellular level spontaneously depolarize, leading to a cardiac cycle that is an out-of-sync extrasystole. […] The most prevalent PVCs are from the outflow tract and appear to be due to triggered activity from excess calcium and afterdepolarizations. […] Three common mechanisms exist for PVCs: automaticity, reentry, and triggered activity.
  • #3 Premature Ventricular Complexes: Background, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/158939-overview
    Premature ventricular complexes (PVCs) (also known as ventricular premature complexes [VPCs]) are ectopic impulses originating from an area distal to the His Purkinje system. PVCs are the most common ventricular arrhythmia. […] The fundamental underlying etiology of PVCs remain to be determined. […] Very few studies have evaluated the pathophysiology of PVCs in human subjects; most of the information is derived from animal studies. However, what is known is that ventricular monocytes at the cellular level spontaneously depolarize, leading to a cardiac cycle that is an out-of-sync extrasystole. […] The most prevalent PVCs are from the outflow tract and appear to be due to triggered activity from excess calcium and afterdepolarizations. […] Three common mechanisms exist for PVCs: automaticity, reentry, and triggered activity.
  • #4 Premature Ventricular Complexes: Background, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/761148-overview
    Automaticity: This is the development of a new site of depolarization in nonnodal ventricular tissue, which can lead to a PVCs. […] Increased automaticity could be due to electrolyte abnormalities or ischemic myocardium. […] Reentry circuit: Reentry typically occurs when slow-conducting tissue (eg, infarcted myocardium) is present adjacent to normal tissue. […] Triggered activity: After depolarizations triggered by a preceding impulse can lead to premature activation if the threshold is reached, and this can cause a PVC. […] Afterdepolarization can occur either during (early) or after (late) completion of repolarization.
  • #5 Pathophysiological Mechanisms of Premature Ventricular Complexes
    https://pmc.ncbi.nlm.nih.gov/articles/PMC7247859/
    Despite these insights in the potential clinical consequences, the cause of PVCs usually remains obscure as no practical methods exist to directly assess the pathophysiological mechanism in patients. In this review, we aim to provide an overview of the pathophysiological mechanisms of PVCs and focus on characteristics that may aid in their differentiation. […] Automaticity outside the sinus node can cause PVCs via a mechanism called parasystole. […] Ectopic automaticity does not influence the cardiac rhythm under normal conditions as its diastolic depolarization is reset before reaching threshold potential by the activation of the faster sinus node. […] The cycle length of the sinus rhythm and the protected automatic ectopic focus need to allow for the ectopic beat to occur outside the ventricular refractory period.
  • #6 Premature Ventricular Complexes: Background, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/761148-overview
    Automaticity: This is the development of a new site of depolarization in nonnodal ventricular tissue, which can lead to a PVCs. […] Increased automaticity could be due to electrolyte abnormalities or ischemic myocardium. […] Reentry circuit: Reentry typically occurs when slow-conducting tissue (eg, infarcted myocardium) is present adjacent to normal tissue. […] Triggered activity: After depolarizations triggered by a preceding impulse can lead to premature activation if the threshold is reached, and this can cause a PVC. […] Afterdepolarization can occur either during (early) or after (late) completion of repolarization.
  • #7 When to worry about premature ventricular contractions (PVCs)
    https://www.healthline.com/health/arrhythmia/when-to-worry-about-pvc
    According to a 2017 report, having more than 10,000 and up to 20,000 PVCs a day can decrease your hearts function. Doctors refer to this as PVC-induced cardiomyopathy. Its reversible in most patients if the PVCs are treated. […] Some studies say that having more than 1,000 PVCs a day can weaken your left ventricle over several years. This can increase your risk of developing dilated cardiomyopathy, sometimes called an enlarged heart. […] If your doctor has already diagnosed heart disease, PVCs can increase your mortality risk or risk for early death. […] Most doctors dont know exactly what causes PVCs. But some factors can increase your risk of having PVCs, including: anxiety, too much caffeine, irregular electrolyte levels, especially low potassium, low magnesium, or high calcium, lack of sleep, using excess amounts of alcohol, tobacco, or illegal drugs. […] Some medical conditions increase your likelihood of having PVCs. These include: anemia, bundle branch block, cardiomyopathy, hypertension (high blood pressure), hyperthyroidism, mitral valve prolapse, myocardial infarction (heart attack).
  • #8 Premature Ventricular Complex – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK547713/
    The primary mechanisms thought to result in PVCs include triggered activity, automaticity, and reentry. Identification of the pathophysiological is essential as this informs the management approach. […] Triggered activity arises during the early depolarization phase due to exceeding the cell membrane activation threshold. The PVCs associated with bradycardia are often caused by this mechanism, along with other factors like electrolyte abnormalities, ischemia, and digoxin toxicity. […] Automaticity involves PVCs originating from abnormal cardiomyocyte activity, often showing parasystole. The enhanced automaticity characteristically results from an ectopic ventricular focus that fires spontaneously. […] Though usually linked to sustained arrhythmias, reentry can also cause PVCs. It requires 2 distinct pathways with unidirectional block, often involving scars, fibrosis, or abnormal conduction in specific regions. This mechanism is seen in phenomena like bundle-branch or fascicular PVCs.
  • #9 Pathophysiological Mechanisms of Premature Ventricular Complexes
    https://pmc.ncbi.nlm.nih.gov/articles/PMC7247859/
    In this classical description of parasystole, PVCs occur at exact multiples of the cycle length of the ectopic automatic focus and can occur during the whole excitable period of the cardiac cycle. […] The conduction block that protects a parasystolic focus against excitation and reset has to be functional in nature. […] This functional block may still allow a degree of electrotonic interaction and may enable the modulation of a parasystolic focus by the activation front of the sinus rhythm. […] Triggered activity is divided according to their timing in regards to the preceding action potential: the term early afterdepolarizations is used for reactivations during phase 2 or 3 whereas delayed afterdepolarizations occur after completion of the preceding action potential. […] The characteristics of delayed afterdepolarizations and the associated arrhythmias have been studied under many conditions leading to an increased calcium concentrations including digitalis toxicity, hypercalcemia, catecholamine exposure and altered cellular calcium handling through genetic mutations.
  • #10 Premature Ventricular Complex – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK547713/
    The primary mechanisms thought to result in PVCs include triggered activity, automaticity, and reentry. Identification of the pathophysiological is essential as this informs the management approach. […] Triggered activity arises during the early depolarization phase due to exceeding the cell membrane activation threshold. The PVCs associated with bradycardia are often caused by this mechanism, along with other factors like electrolyte abnormalities, ischemia, and digoxin toxicity. […] Automaticity involves PVCs originating from abnormal cardiomyocyte activity, often showing parasystole. The enhanced automaticity characteristically results from an ectopic ventricular focus that fires spontaneously. […] Though usually linked to sustained arrhythmias, reentry can also cause PVCs. It requires 2 distinct pathways with unidirectional block, often involving scars, fibrosis, or abnormal conduction in specific regions. This mechanism is seen in phenomena like bundle-branch or fascicular PVCs.
  • #11 Premature Ventricular Complexes: Background, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/761148-overview
    Automaticity: This is the development of a new site of depolarization in nonnodal ventricular tissue, which can lead to a PVCs. […] Increased automaticity could be due to electrolyte abnormalities or ischemic myocardium. […] Reentry circuit: Reentry typically occurs when slow-conducting tissue (eg, infarcted myocardium) is present adjacent to normal tissue. […] Triggered activity: After depolarizations triggered by a preceding impulse can lead to premature activation if the threshold is reached, and this can cause a PVC. […] Afterdepolarization can occur either during (early) or after (late) completion of repolarization.
  • #12 Premature Ventricular Complexes: Background, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/158939-overview
    Automaticity: This is the development of a new site of depolarization in nonnodal ventricular tissue, which can lead to a PVCs. […] Reentry circuit: Reentry typically occurs when slow-conducting tissue (eg, infarcted myocardium) is present adjacent to normal tissue. […] Triggered activity: After depolarizations triggered by a preceding impulse can lead to premature activation if the threshold is reached, and this can cause a PVC. Afterdepolarization can occur either during (early) or after (late) completion of repolarization. Early afterdepolarizations commonly are responsible for bradycardia associated PVCs, but they also can be present with ischemia and electrolyte abnormalities.
  • #13
    https://link.springer.com/article/10.1007/s10840-017-0309-8
    The arrhythmogenic substrate for PVCs in patients with prior myocardial infarction (post-MI group) is well-described as being scar-related re-entry with a fixed CI (in cases of monomorphic PVC/VT). […] The majority of the patients in the NIDCM group exhibited similar CI variability as the patients of the post-MI and idiopathic VA groups, which suggests that (despite a rather heterogeneous etiological background) the main mechanisms for arrhythmogenesis might essentially be similar to the ones of the previous groups, namely: scar-related micro/macro re-entry or focal-triggered activity with fixed CIs. […] The patients of the familial dilated cardiomyopathy group (PLN/LMNA mutation group) exhibited high CI variability, which indicates that a mechanism different from re-entry or triggered activity might be responsible for PVC generation in this group. This mechanism may be abnormal automaticity, parasystole, or another more complex mechanism.
  • #14 Asymptomatic ventricular extrasystoles
    https://www.escardio.org/Councils/Council-for-Cardiology-Practice-(CCP)/Cardiopractice/asymptomatic-ventricular-extrasystoles
    Premature ventricular contractions (PVCs) are common in clinical practice and may affect both patients with and without previous cardiovascular diseases. […] PVCs can occur in many different conditions, both cardiac and extra-cardiac, they share three pathophysiological mechanisms: re-entry, triggered activity and enhanced electrical automaticity. […] In patients with structural heart disease, re-entry is the most common mechanism. This is due to the presence of tissue with different electrophysiological features than the healthy myocardium (most commonly fibrotic areas), allowing a depolarisation wave to slow down enough to reach an area of the myocardium that is no longer refractory, thus leading to one or several extra beats. […] Considering that PVCs are more prevalent in the presence of structural heart disease, whether diagnosed or undetected, their finding should prompt the physician to pursue an appropriate diagnostic approach to identify or rule out any underlying conditions.
  • #15
    https://link.springer.com/article/10.1007/s10840-017-0309-8
    Coupling interval (CI) variability of premature ventricular contractions (PVCs) is influenced by the underlying arrhythmia mechanism. The aim of this study was to compare CI variability of PVCs in different myocardial disease entities, in order to gain insight into their arrhythmia mechanism. […] Low CI and SD of CI/R-R of idiopathic and NIDCM PVCs suggest that the underlying arrhythmia mechanisms might be re-entry or triggered activity. Abnormal automaticity or modulated parasystole are unlikely mechanisms. High CI variability in PLN/LMNA patients suggests that the re-entry and triggered activity are less likely mechanisms in this group. […] Although the variability of CIs is influenced by several factors (e.g., variation of the preceding cycle length, fluctuations in rhythmic distribution patterns, intermittent parasystole, and precipitancy of another ectopic source), their major determinant is believed to be the underlying arrhythmia mechanism. When PVCs have fixed CIs, then re-entry and triggered activity are among the most probable mechanisms. On the other hand, when PVCs exhibit variable CIs, then increased/abnormal automaticity or parasystole are more likely to be the source of rhythm disturbances.
  • #16 Premature Ventricular Complexes: Background, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/761148-overview
    Automaticity: This is the development of a new site of depolarization in nonnodal ventricular tissue, which can lead to a PVCs. […] Increased automaticity could be due to electrolyte abnormalities or ischemic myocardium. […] Reentry circuit: Reentry typically occurs when slow-conducting tissue (eg, infarcted myocardium) is present adjacent to normal tissue. […] Triggered activity: After depolarizations triggered by a preceding impulse can lead to premature activation if the threshold is reached, and this can cause a PVC. […] Afterdepolarization can occur either during (early) or after (late) completion of repolarization.
  • #17 Premature Ventricular Complexes: Background, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/158939-overview
    Automaticity: This is the development of a new site of depolarization in nonnodal ventricular tissue, which can lead to a PVCs. […] Reentry circuit: Reentry typically occurs when slow-conducting tissue (eg, infarcted myocardium) is present adjacent to normal tissue. […] Triggered activity: After depolarizations triggered by a preceding impulse can lead to premature activation if the threshold is reached, and this can cause a PVC. Afterdepolarization can occur either during (early) or after (late) completion of repolarization. Early afterdepolarizations commonly are responsible for bradycardia associated PVCs, but they also can be present with ischemia and electrolyte abnormalities.
  • #18 Pathophysiological Mechanisms of Premature Ventricular Complexes
    https://pmc.ncbi.nlm.nih.gov/articles/PMC7247859/
    In this classical description of parasystole, PVCs occur at exact multiples of the cycle length of the ectopic automatic focus and can occur during the whole excitable period of the cardiac cycle. […] The conduction block that protects a parasystolic focus against excitation and reset has to be functional in nature. […] This functional block may still allow a degree of electrotonic interaction and may enable the modulation of a parasystolic focus by the activation front of the sinus rhythm. […] Triggered activity is divided according to their timing in regards to the preceding action potential: the term early afterdepolarizations is used for reactivations during phase 2 or 3 whereas delayed afterdepolarizations occur after completion of the preceding action potential. […] The characteristics of delayed afterdepolarizations and the associated arrhythmias have been studied under many conditions leading to an increased calcium concentrations including digitalis toxicity, hypercalcemia, catecholamine exposure and altered cellular calcium handling through genetic mutations.
  • #19 Premature Ventricular Complexes: Background, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/158939-overview
    Automaticity: This is the development of a new site of depolarization in nonnodal ventricular tissue, which can lead to a PVCs. […] Reentry circuit: Reentry typically occurs when slow-conducting tissue (eg, infarcted myocardium) is present adjacent to normal tissue. […] Triggered activity: After depolarizations triggered by a preceding impulse can lead to premature activation if the threshold is reached, and this can cause a PVC. Afterdepolarization can occur either during (early) or after (late) completion of repolarization. Early afterdepolarizations commonly are responsible for bradycardia associated PVCs, but they also can be present with ischemia and electrolyte abnormalities.
  • #20 Pathophysiological Mechanisms of Premature Ventricular Complexes
    https://pmc.ncbi.nlm.nih.gov/articles/PMC7247859/
    In this classical description of parasystole, PVCs occur at exact multiples of the cycle length of the ectopic automatic focus and can occur during the whole excitable period of the cardiac cycle. […] The conduction block that protects a parasystolic focus against excitation and reset has to be functional in nature. […] This functional block may still allow a degree of electrotonic interaction and may enable the modulation of a parasystolic focus by the activation front of the sinus rhythm. […] Triggered activity is divided according to their timing in regards to the preceding action potential: the term early afterdepolarizations is used for reactivations during phase 2 or 3 whereas delayed afterdepolarizations occur after completion of the preceding action potential. […] The characteristics of delayed afterdepolarizations and the associated arrhythmias have been studied under many conditions leading to an increased calcium concentrations including digitalis toxicity, hypercalcemia, catecholamine exposure and altered cellular calcium handling through genetic mutations.
  • #21 Premature Ventricular Complexes | Thoracic Key
    https://thoracickey.com/premature-ventricular-complexes/
    Premature ventricular contractions (PVCs) are increasingly recognized not merely as a marker of structural cardiac disease, but often as a potential cause. […] Initiation of PVCs is dependent on the underlying cardiac substrate and, similar to other arrhythmias, can be explained by reentry, automaticity, or triggered activity. The most likely mechanism of PVCs in patients without structural heart disease is triggered activity. […] The potential for frequent idiopathic PVCs to result in cardiomyopathy has been established on the basis of reversibility of cardiomyopathy with successful elimination of the PVCs demonstrated in observational studies. However, the mechanism responsible for development of cardiomyopathy is still under investigation. […] Potential mechanisms include chronic dyssynchrony and impaired Ca2+ homeostasis, for example, impaired Ca2+ handling or decreased Ca2+ transient.
  • #22 Effect of carvedilol on premature ventricular complexes originating from the ventricular outflow tract | International Journal of Arrhythmia | Full Text
    https://arrhythmia.biomedcentral.com/articles/10.1186/s42444-020-00015-7
    The most common origins of idiopathic VAs are the right and left ventricular outflow tracts. […] The idiopathic VAs are thought to be caused by catecholamine-induced, cyclic adenosine monophosphate-mediated DADs and triggered activity. […] Under this background, we hypothesized that carvedilol, which can reduce triggered activity by inhibiting SOICR, would be effective for OT PVC. […] In our retrospective, pilot study, carvedilol showed good efficacy for suppressing OT PVCs.
  • #23 Mechanisms and Risk Factors for Premature Ventricular Contraction Induced Cardiomyopathy
    https://www.imrpress.com/journal/RCM/24/12/10.31083/j.rcm2412353/htm
    Frequent premature ventricular contractions (PVCs) can cause a reversible form of cardiomyopathy in patients without structural heart disease. […] The exact pathophysiological mechanism of PVICM has not yet been fully clarified. […] Based on animal models, abnormal calcium handling and cardiac remodeling may be the crucial mechanism underlying the development of cardiomyopathy. […] The underlying mechanism of PVICM remains controversial. […] Previous studies have consistently suggested that probable mechanisms involved in PVICM include abnormal calcium handling, dyssynchronous ventricular contraction, autonomic dysregulation and myocardial remodeling. […] PVCs lead to prolonged action potential time of ventricular cardiomyocytes and a decrease in the density of the transient outward K currents (Ito), inward rectifier K currents (IK1) and L-type Ca currents (ICaL), accompanied by decreased expression of the associated ion channel subunits.
  • #24 Mechanisms and Risk Factors for Premature Ventricular Contraction Induced Cardiomyopathy
    https://www.imrpress.com/journal/RCM/24/12/10.31083/j.rcm2412353/htm
    Changes in ion channels may lead to abnormal repolarization of cardiomyocytes, increasing the risk of malignant arrhythmias. […] In the swine model of PVICM, decreased sarcoplasmic reticulum (SR) calcium ATPase (SERCA2a) and increased ryanodine receptor type 2 (RyR2), sodium-calcium exchanger (NCX1), calcium/calmodulin-dependent protein kinase II alpha (CaMKII-α) and phospholamban (PLN) expression were observed. […] The up-regulation of the inhibitory protein PLN aggravates the E-C coupling disorder of cardiomyocytes. […] Dyssynchronous ventricular contractions have long been considered to be the primary mechanism for the development of PVICM. […] The 24-hour electrocardiogram analysis of heart rate variability in patients with idiopathic PVCs found that autonomic activities were involved in the occurrence of PVCs.
  • #25 Mechanisms and Risk Factors for Premature Ventricular Contraction Induced Cardiomyopathy
    https://www.imrpress.com/journal/RCM/24/12/10.31083/j.rcm2412353/htm
    Changes in ion channels may lead to abnormal repolarization of cardiomyocytes, increasing the risk of malignant arrhythmias. […] In the swine model of PVICM, decreased sarcoplasmic reticulum (SR) calcium ATPase (SERCA2a) and increased ryanodine receptor type 2 (RyR2), sodium-calcium exchanger (NCX1), calcium/calmodulin-dependent protein kinase II alpha (CaMKII-α) and phospholamban (PLN) expression were observed. […] The up-regulation of the inhibitory protein PLN aggravates the E-C coupling disorder of cardiomyocytes. […] Dyssynchronous ventricular contractions have long been considered to be the primary mechanism for the development of PVICM. […] The 24-hour electrocardiogram analysis of heart rate variability in patients with idiopathic PVCs found that autonomic activities were involved in the occurrence of PVCs.
  • #26 Mechanisms and Risk Factors for Premature Ventricular Contraction Induced Cardiomyopathy
    https://www.imrpress.com/journal/RCM/24/12/10.31083/j.rcm2412353/htm
    Frequent premature ventricular contractions (PVCs) can cause a reversible form of cardiomyopathy in patients without structural heart disease. […] The exact pathophysiological mechanism of PVICM has not yet been fully clarified. […] Based on animal models, abnormal calcium handling and cardiac remodeling may be the crucial mechanism underlying the development of cardiomyopathy. […] The underlying mechanism of PVICM remains controversial. […] Previous studies have consistently suggested that probable mechanisms involved in PVICM include abnormal calcium handling, dyssynchronous ventricular contraction, autonomic dysregulation and myocardial remodeling. […] PVCs lead to prolonged action potential time of ventricular cardiomyocytes and a decrease in the density of the transient outward K currents (Ito), inward rectifier K currents (IK1) and L-type Ca currents (ICaL), accompanied by decreased expression of the associated ion channel subunits.
  • #27 The Association of High Burden Premature Ventricular Contractions with Esophageal/Upper GI Diseases
    https://www.mdpi.com/2673-3846/5/4/38
    Triggered mechanisms include behavioral (sympathetic stress) or from underlying diseases, induced by increased intracellular calcium in the plateau phase of the action potential during prolonged repolarization. […] PVCs related to automaticity are present with parasystole, occurring at the same cycle length. […] The autonomic nervous system has been hypothesized to play a significant role in pathogenesis, maintenance, and interference in ventricular arrhythmias. […] The vagus nerve contributes to the formation of the esophageal plexus, innervating the smooth muscle of the esophagus, and notably gives off cardiac branches, regulating heart rate through the parasympathetic nervous system. […] Our study presents a series of six subjects with esophageal disease who had an otherwise idiopathic PVC burden, that notably appeared to originate from the base of the RVOT by 12-lead EKG criteria in all subjects.
  • #28 Mechanisms and Risk Factors for Premature Ventricular Contraction Induced Cardiomyopathy
    https://www.imrpress.com/journal/RCM/24/12/10.31083/j.rcm2412353/htm
    Changes in ion channels may lead to abnormal repolarization of cardiomyocytes, increasing the risk of malignant arrhythmias. […] In the swine model of PVICM, decreased sarcoplasmic reticulum (SR) calcium ATPase (SERCA2a) and increased ryanodine receptor type 2 (RyR2), sodium-calcium exchanger (NCX1), calcium/calmodulin-dependent protein kinase II alpha (CaMKII-α) and phospholamban (PLN) expression were observed. […] The up-regulation of the inhibitory protein PLN aggravates the E-C coupling disorder of cardiomyocytes. […] Dyssynchronous ventricular contractions have long been considered to be the primary mechanism for the development of PVICM. […] The 24-hour electrocardiogram analysis of heart rate variability in patients with idiopathic PVCs found that autonomic activities were involved in the occurrence of PVCs.
  • #29 Asymptomatic ventricular extrasystoles
    https://www.escardio.org/Councils/Council-for-Cardiology-Practice-(CCP)/Cardiopractice/asymptomatic-ventricular-extrasystoles
    The mechanism behind the link between stress/anxiety and ventricular ectopy is an increased activity of the sympathetic nervous system (SNE). […] PVC patients, including those who are free of symptoms, face the risk of developing complications such as cardiomyopathy, heart failure, and malignant ventricular arrhythmias. […] As previously mentioned, the most significant predictor of adverse events in patients with PVCs is the presence of underlying heart disease, whether structural or electrical. […] The impact of PVC burden has been investigated in various studies, revealing a potential linear correlation between the number of PVCs per day and clinical outcomes. […] Imaging findings also contribute to risk assessment, with the most robust indicator being the presence of fibrosis at CMR.
  • #30 A challenging dilemma: Can we predict which premature ventricular contractions may cause cardiomyopathy? | Revista Portuguesa de Cardiologia
    https://revportcardiol.org/pt-a-challenging-dilemma-can-we-articulo-S0870255123003803
    Premature ventricular contractions (PVCs) are the most frequent ventricular arrhythmia and are commonly associated with heart failure, ventricular arrhythmias and sudden cardiac death. […] The development of a cardiomyopathy has also been documented with frequent ventricular ectopic beats. The prevalence of left ventricular (LV) dysfunction is about 10-29% in different series of patients with frequent PVCs. […] A common clinical problem is determining whether the PVCs are the primary cause of the patient’s cardiomyopathy, or whether the PVCs are only a sign of an underlying cardiomyopathy, misdiagnosed due to relative mild forms of the disease, without clinical evidence. […] The mechanism of compromised left ventricular function is not fully understood. Some authors have reported dyssynchrony as the main cause, while others have suggested irregular rhythm, AV-uncoupling and mechanical bradycardia.
  • #31 The Association of High Burden Premature Ventricular Contractions with Esophageal/Upper GI Diseases
    https://www.mdpi.com/2673-3846/5/4/38
    Triggered mechanisms include behavioral (sympathetic stress) or from underlying diseases, induced by increased intracellular calcium in the plateau phase of the action potential during prolonged repolarization. […] PVCs related to automaticity are present with parasystole, occurring at the same cycle length. […] The autonomic nervous system has been hypothesized to play a significant role in pathogenesis, maintenance, and interference in ventricular arrhythmias. […] The vagus nerve contributes to the formation of the esophageal plexus, innervating the smooth muscle of the esophagus, and notably gives off cardiac branches, regulating heart rate through the parasympathetic nervous system. […] Our study presents a series of six subjects with esophageal disease who had an otherwise idiopathic PVC burden, that notably appeared to originate from the base of the RVOT by 12-lead EKG criteria in all subjects.
  • #32 Premature Ventricular Contraction-Induced Cardiomyopathy: Contemporary Evidence from Risk Stratification, Pathophysiology, and Management
    https://www.mdpi.com/2077-0383/13/9/2635
    The impaired LVEF in PIC could be a result from functional impairment involving calcium handling. […] LV dyssynchrony is an acute effect of PVC that could contribute to the development of cardiomyopathy. […] These results indicated the potential role of LV dyssynchrony in contributing to the development of PVC-induced cardiomyopathy.
  • #33 Premature Ventricle Contractions in Heart Failure: A Closer Examination – The Cardiology Advisor
    https://www.thecardiologyadvisor.com/features/premature-ventricle-contractions-in-heart-failure-a-closer-examination/
    Premature ventricular contractions (PVCs) are early depolarizations of the myocardium, originating in the ventricle. Once regarded as benign, PVCs even in the absence of structural heart disease are now regarded as more insidious, potentially causing or contributing to cardiomyopathy and heart failure. […] In PVCs, ventricular myocytes spontaneously depolarize to create an extra systole that creates mechanical dyssynchrony with the cardiac cycle. Affected cells are triggered by cyclic adenosine monophosphate-mediated and calcium-dependent delays in after-depolarizations. […] Frequent PVCs can cause cardiomyopathy through complex transient alterations in intracellular calcium and membrane ionic currents, heart rate dynamics, hemodynamic parameters, and myocardial and peripheral vascular autonomic stimulation and inhibition.
  • #34 A challenging dilemma: Can we predict which premature ventricular contractions may cause cardiomyopathy? | Revista Portuguesa de Cardiologia
    https://revportcardiol.org/pt-a-challenging-dilemma-can-we-articulo-S0870255123003803
    Premature ventricular contractions (PVCs) are the most frequent ventricular arrhythmia and are commonly associated with heart failure, ventricular arrhythmias and sudden cardiac death. […] The development of a cardiomyopathy has also been documented with frequent ventricular ectopic beats. The prevalence of left ventricular (LV) dysfunction is about 10-29% in different series of patients with frequent PVCs. […] A common clinical problem is determining whether the PVCs are the primary cause of the patient’s cardiomyopathy, or whether the PVCs are only a sign of an underlying cardiomyopathy, misdiagnosed due to relative mild forms of the disease, without clinical evidence. […] The mechanism of compromised left ventricular function is not fully understood. Some authors have reported dyssynchrony as the main cause, while others have suggested irregular rhythm, AV-uncoupling and mechanical bradycardia.
  • #35 Premature ventricular complexes (PVC)-induced cardiomyopathy: A review and meta-analysis of pathophysiology, diagnosis and clinical management
    https://oatext.com/premature-ventricular-complexes-pvc-induced-cardiomyopathy-a-review-and-meta-analysis-of-pathophysiology-diagnosis-and-clinical-management.php
    Tachycardia-induced mechanism is the most commonly hypothesized mechanism, to the extent some researcher considered PICM as a form of tachycardia-induced CM (TIC), which by itself is an established clinical entity. […] Electromechanical dyssynchrony is another potential mechanism associated with the development of PICM. […] PVC QRS duration is one of the most independent predictor for the development of PICM. […] The primary treatment target of PICM is the suppression of PVCs. […] The mainstay therapy of PICM is PVC suppression through either pharmacotherapy or RFA.
  • #36 Premature ventricular contraction pathophysiology – wikidoc
    https://www.wikidoc.org/index.php/Premature_ventricular_contraction_pathophysiology
    There are a number of different molecular explanations for PVCs. One explanation is most basically due to an increased amount of cyclic AMP(cAMP) in the ventricular cardiac myocytes leading to increased flow of calcium ions into the cell. […] Existing damage to the myocardium can also provoke PVCs. The myocardial scarring that occurs in myocardial infarction and also in the surgical repair of congenital heart disease can disrupt the conduction system of the heart and may also irritate surrounding viable ventricular myocytes, make them more likely to depolarize spontaneously. Inflammation of the myocardium (as occurs in myocarditis) and systemic inflammation cause surges of cytokines, which can affect the electrical properties of myocytes and may be ultimately responsible for causing irritability of myocytes.
  • #37
    https://link.springer.com/article/10.1007/s10840-017-0309-8
    The arrhythmogenic substrate for PVCs in patients with prior myocardial infarction (post-MI group) is well-described as being scar-related re-entry with a fixed CI (in cases of monomorphic PVC/VT). […] The majority of the patients in the NIDCM group exhibited similar CI variability as the patients of the post-MI and idiopathic VA groups, which suggests that (despite a rather heterogeneous etiological background) the main mechanisms for arrhythmogenesis might essentially be similar to the ones of the previous groups, namely: scar-related micro/macro re-entry or focal-triggered activity with fixed CIs. […] The patients of the familial dilated cardiomyopathy group (PLN/LMNA mutation group) exhibited high CI variability, which indicates that a mechanism different from re-entry or triggered activity might be responsible for PVC generation in this group. This mechanism may be abnormal automaticity, parasystole, or another more complex mechanism.
  • #38
    https://scispace.com/authors/yue-chen-3tf9ew1x64
    Higher High-Sensitivity C Reactive Protein is Associated with Future Premature Ventricular Contraction: a Community Based Prospective Cohort Study. […] Elevated serum hs-CRP was an independent predictor of PVC in Chinese population, especially in men, and elevated serum h’s- CRP was associated with future PVC in participants without history of myocardial infarction or stroke.
  • #39 Premature ventricular contraction pathophysiology – wikidoc
    https://www.wikidoc.org/index.php/Premature_ventricular_contraction_pathophysiology
    There are a number of different molecular explanations for PVCs. One explanation is most basically due to an increased amount of cyclic AMP(cAMP) in the ventricular cardiac myocytes leading to increased flow of calcium ions into the cell. […] Existing damage to the myocardium can also provoke PVCs. The myocardial scarring that occurs in myocardial infarction and also in the surgical repair of congenital heart disease can disrupt the conduction system of the heart and may also irritate surrounding viable ventricular myocytes, make them more likely to depolarize spontaneously. Inflammation of the myocardium (as occurs in myocarditis) and systemic inflammation cause surges of cytokines, which can affect the electrical properties of myocytes and may be ultimately responsible for causing irritability of myocytes.
  • #40 Premature Ventricular Contractions | Cedars-Sinai
    https://www.cedars-sinai.org/health-library/diseases-and-conditions/p/premature-ventricular-contractions.html
    Many heart conditions increase the risk for PVCs. These include high blood pressure, heart attack, coronary heart disease, dilated cardiomyopathy, hypertrophic cardiomyopathy, congenital heart disease, and heart failure. […] PVCs are a kind of abnormal heart rhythm. The signal to start your heartbeat starts somewhere in the ventricles instead of in the SA node. […] Medicines and catheter ablation are options if you have PVCs that cause symptoms or occur often.
  • #41 Asymptomatic ventricular extrasystoles
    https://www.escardio.org/Councils/Council-for-Cardiology-Practice-(CCP)/Cardiopractice/asymptomatic-ventricular-extrasystoles
    Premature ventricular contractions (PVCs) are common in clinical practice and may affect both patients with and without previous cardiovascular diseases. […] PVCs can occur in many different conditions, both cardiac and extra-cardiac, they share three pathophysiological mechanisms: re-entry, triggered activity and enhanced electrical automaticity. […] In patients with structural heart disease, re-entry is the most common mechanism. This is due to the presence of tissue with different electrophysiological features than the healthy myocardium (most commonly fibrotic areas), allowing a depolarisation wave to slow down enough to reach an area of the myocardium that is no longer refractory, thus leading to one or several extra beats. […] Considering that PVCs are more prevalent in the presence of structural heart disease, whether diagnosed or undetected, their finding should prompt the physician to pursue an appropriate diagnostic approach to identify or rule out any underlying conditions.
  • #42 Premature ventricular contractions (PVCs) – Symptoms & causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/premature-ventricular-contractions/symptoms-causes/syc-20376757
    Premature ventricular contractions (PVCs) are extra heartbeats that begin in one of the heart’s two lower pumping chambers (ventricles). These extra beats disrupt the regular heart rhythm, sometimes causing a sensation of a fluttering or a skipped beat in the chest. […] The cause of premature ventricular contractions isn’t always clear. Certain things including heart diseases or changes in the body can make cells in the lower heart chambers electrically unstable. Heart disease or scarring may cause the heart’s signals to be misrouted. […] PVCs are irregular contractions that start in the ventricles instead of the atria. The contractions usually beat sooner than the next expected heartbeat. […] Premature ventricular contractions may be caused by: Certain medications, including decongestants and antihistamines; Alcohol or drug misuse; Stimulants such as caffeine or tobacco; Increased levels of adrenaline in the body due to exercise or anxiety; Injury to the heart muscle due to disease. […] Having frequent premature ventricular contractions (PVCs) or certain patterns of them might increase the risk of developing irregular heart rhythms (arrhythmias) or weakening of the heart muscle (cardiomyopathy).
  • #43 When to worry about premature ventricular contractions (PVCs)
    https://www.healthline.com/health/arrhythmia/when-to-worry-about-pvc
    According to a 2017 report, having more than 10,000 and up to 20,000 PVCs a day can decrease your hearts function. Doctors refer to this as PVC-induced cardiomyopathy. Its reversible in most patients if the PVCs are treated. […] Some studies say that having more than 1,000 PVCs a day can weaken your left ventricle over several years. This can increase your risk of developing dilated cardiomyopathy, sometimes called an enlarged heart. […] If your doctor has already diagnosed heart disease, PVCs can increase your mortality risk or risk for early death. […] Most doctors dont know exactly what causes PVCs. But some factors can increase your risk of having PVCs, including: anxiety, too much caffeine, irregular electrolyte levels, especially low potassium, low magnesium, or high calcium, lack of sleep, using excess amounts of alcohol, tobacco, or illegal drugs. […] Some medical conditions increase your likelihood of having PVCs. These include: anemia, bundle branch block, cardiomyopathy, hypertension (high blood pressure), hyperthyroidism, mitral valve prolapse, myocardial infarction (heart attack).
  • #44 Premature Ventricular Contractions (PVCs)
    https://my.clevelandclinic.org/health/diseases/17381-premature-ventricular-contractions
    Premature ventricular contractions (PVCs) are a type of irregular heartbeat. They occur when the electrical signal that starts your heartbeat comes from one of your bottom two heart chambers (ventricles). The signal typically starts in the top right chamber (atrium). […] PVCs are not always a problem. But if they repeatedly happen for months or years, they can cause a type of cardiomyopathy, or heart muscle weakening. PVCs usually go away with medication or other minimally invasive treatments. […] In PVCs, that first signal starts in one of your ventricles. As a result, the signal travels differently through your heart and causes an irregular heartbeat. Sometimes, a PVC may feel like your heart skipped a beat. […] Several conditions or factors can trigger a premature ventricular contraction, including electrolyte imbalances, such as low potassium or magnesium, heart attack (myocardial infarction), heart failure, high adrenaline, such as from anxiety or stress, and reduced blood flow to your heart, such as in coronary artery disease. […] PVCs can increase your risk of sudden cardiac death if you have underlying structural heart disease or if they arise from specific areas in your heart. However, in most people, PVCs are benign and don’t lead to sudden cardiac death.
  • #45 Premature ventricular contractions (PVCs) – Symptoms & causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/premature-ventricular-contractions/symptoms-causes/syc-20376757
    Premature ventricular contractions (PVCs) are extra heartbeats that begin in one of the heart’s two lower pumping chambers (ventricles). These extra beats disrupt the regular heart rhythm, sometimes causing a sensation of a fluttering or a skipped beat in the chest. […] The cause of premature ventricular contractions isn’t always clear. Certain things including heart diseases or changes in the body can make cells in the lower heart chambers electrically unstable. Heart disease or scarring may cause the heart’s signals to be misrouted. […] PVCs are irregular contractions that start in the ventricles instead of the atria. The contractions usually beat sooner than the next expected heartbeat. […] Premature ventricular contractions may be caused by: Certain medications, including decongestants and antihistamines; Alcohol or drug misuse; Stimulants such as caffeine or tobacco; Increased levels of adrenaline in the body due to exercise or anxiety; Injury to the heart muscle due to disease. […] Having frequent premature ventricular contractions (PVCs) or certain patterns of them might increase the risk of developing irregular heart rhythms (arrhythmias) or weakening of the heart muscle (cardiomyopathy).
  • #46 Association of Premature Ventricular Contraction (PVC) with hematological parameters: a data mining approach | Scientific Reports
    https://www.nature.com/articles/s41598-025-86557-z
    Premature ventricular contraction (PVC) is characterized by early repolarization of the myocardium originating from Purkinje fibers. PVC may occur in individuals who are otherwise healthy. However, it may be associated with some pathological conditions. […] Previous studies have shown that PVC may be related to heart diseases. However, PVC may be triggered by non-cardiac causes, such as excessive alcohol consumption, hyperthyroidism, and sarcoidosis. The results of previous studies about the clinical importance of PVCs have been controversial; nevertheless, the clinical benefits of PVC suppression are necessary in patients with cardiac diseases. PVC is seen among 14% of the general population and can lead to symptoms such as palpitations, chest pain, heart failure, and syncope. […] It has been shown previously that PVC may be associated with cardiac dysfunction, and it has been reported that frequent PVC could be a result of congestive heart failure. Also, previous studies have brought up that PVC could potentially be associated with a higher risk of sudden cardiac death. Hence, it is essential to identify factors that may correlate with PVC.
  • #47 Premature ventricular contractions (PVCs) – Symptoms & causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/premature-ventricular-contractions/symptoms-causes/syc-20376757
    Premature ventricular contractions (PVCs) are extra heartbeats that begin in one of the heart’s two lower pumping chambers (ventricles). These extra beats disrupt the regular heart rhythm, sometimes causing a sensation of a fluttering or a skipped beat in the chest. […] The cause of premature ventricular contractions isn’t always clear. Certain things including heart diseases or changes in the body can make cells in the lower heart chambers electrically unstable. Heart disease or scarring may cause the heart’s signals to be misrouted. […] PVCs are irregular contractions that start in the ventricles instead of the atria. The contractions usually beat sooner than the next expected heartbeat. […] Premature ventricular contractions may be caused by: Certain medications, including decongestants and antihistamines; Alcohol or drug misuse; Stimulants such as caffeine or tobacco; Increased levels of adrenaline in the body due to exercise or anxiety; Injury to the heart muscle due to disease. […] Having frequent premature ventricular contractions (PVCs) or certain patterns of them might increase the risk of developing irregular heart rhythms (arrhythmias) or weakening of the heart muscle (cardiomyopathy).
  • #48 Premature Ventricular Contractions (PVCs) Induced by Administration of Cilostazol after Myocardial Infarction | Russian Open Medical Journal
    https://www.romj.org/2013-0105
    Cilostazol is a phosphodiesterase III inhibitor, which was approved by FDA (food and drug administration) for intermittent claudication in 1999. […] In our case, the PVCs are obviously related to cilostazol and probably the safety of cilostazol in patients having a history of myocardial infarction or malignant arrhythmias should be reevaluated. […] Cilostazol was also reported to reduce ST segment elevation, thus acting to diminish the action potential notch and suppress the substrate and trigger for ventricular tachycardia/fibrillation (VT/VF), which made it a candidate for brugada syndrome treatment. […] It was reported that cilostazol increased the incidence of ventricular arrhythmias and the mean number of episodes in infarcted animals. […] Since he didn’t have any histories of arrhythmias and after discontinuation of cilostazol, the PVCs decreased significantly, the arrhythmia is highly associated with cilostazol. […] Even though, we still should be careful to apply cilostazol in patients having a history of myocardial infarction or malignant arrhythmias.
  • #49 When to worry about premature ventricular contractions (PVCs)
    https://www.healthline.com/health/arrhythmia/when-to-worry-about-pvc
    According to a 2017 report, having more than 10,000 and up to 20,000 PVCs a day can decrease your hearts function. Doctors refer to this as PVC-induced cardiomyopathy. Its reversible in most patients if the PVCs are treated. […] Some studies say that having more than 1,000 PVCs a day can weaken your left ventricle over several years. This can increase your risk of developing dilated cardiomyopathy, sometimes called an enlarged heart. […] If your doctor has already diagnosed heart disease, PVCs can increase your mortality risk or risk for early death. […] Most doctors dont know exactly what causes PVCs. But some factors can increase your risk of having PVCs, including: anxiety, too much caffeine, irregular electrolyte levels, especially low potassium, low magnesium, or high calcium, lack of sleep, using excess amounts of alcohol, tobacco, or illegal drugs. […] Some medical conditions increase your likelihood of having PVCs. These include: anemia, bundle branch block, cardiomyopathy, hypertension (high blood pressure), hyperthyroidism, mitral valve prolapse, myocardial infarction (heart attack).
  • #50 Premature Ventricular Contractions (PVC): Symptoms, Cause, Treatment
    https://www.webmd.com/heart-disease/premature-ventricular-contractions-facts
    If your heart feels out of rhythm or flutters, especially when you’re anxious or stressed, it could be caused by premature ventricular contractions (PVCs). […] PVCs happen when the electrical signal to start your next heartbeat comes from a lower chamber of your heart, called a ventricle, instead of from the usual upper chamber. […] PVCs are extra heartbeats that start with an electrical signal in one of the ventricles. […] If you have PVCs, your heartbeat pattern goes like this: normal heartbeat, extra beat (PVC), slight pause, and then a stronger-than-normal beat. That last beat has an extra kick because your heart fills with more blood during the pause. […] Experts aren’t sure what causes most PVCs. But certain triggers and health conditions may make PVCs more likely. […] Most of the time, there’s no known cause. However, many people notice they have more when they feel anxious or stressed or use caffeine.
  • #51 Mechanisms and Risk Factors for Premature Ventricular Contraction Induced Cardiomyopathy
    https://www.imrpress.com/journal/RCM/24/12/10.31083/j.rcm2412353
    Frequent premature ventricular contractions (PVCs) can cause a reversible form of cardiomyopathy in patients without structural heart disease. […] Because of the challenging nature of PVC-induced cardiomyopathy (PVICM), the mechanisms and risk factors for PVICM are still unclear. […] Based on animal models, abnormal calcium handling and cardiac remodeling may be the crucial mechanism underlying the development of cardiomyopathy. […] Understanding these mechanisms and risk factors is important for the diagnosis and management of this condition, which can lead to heart failure if left untreated.
  • #52 Mechanisms and Risk Factors for Premature Ventricular Contraction Induced Cardiomyopathy
    https://www.imrpress.com/journal/RCM/24/12/10.31083/j.rcm2412353
    Frequent premature ventricular contractions (PVCs) can cause a reversible form of cardiomyopathy in patients without structural heart disease. […] Because of the challenging nature of PVC-induced cardiomyopathy (PVICM), the mechanisms and risk factors for PVICM are still unclear. […] Based on animal models, abnormal calcium handling and cardiac remodeling may be the crucial mechanism underlying the development of cardiomyopathy. […] Understanding these mechanisms and risk factors is important for the diagnosis and management of this condition, which can lead to heart failure if left untreated.
  • #53 A challenging dilemma: Can we predict which premature ventricular contractions may cause cardiomyopathy? | Revista Portuguesa de Cardiologia
    https://revportcardiol.org/pt-a-challenging-dilemma-can-we-articulo-S0870255123003803
    The PVC burden to induce cardiomyopathy has been cited as more than 5-10% of all the daily heart beats during an unknown interval of time. […] However, not all patients with frequent PVCs will develop cardiomyopathy. Indeed, some patients with a high PVC burden never seem to develop any LV dysfunction, so attempts have been made to a search for risk factors and hypothesis to predict the occurrence of this type of cardiomyopathy. […] PVC-induced cardiomyopathy is a potentially reversible condition in which left ventricular dysfunction can improve and even normalize with pharmacological suppression or ablation techniques. […] This article highlights the utility of echo parameters in the analysis of PVCs and their association with the development of cardiomyopathy. […] Left ventricular strain has become popular in a lot of situations as a precocious parameter of LV dysfunction. Even in cases of preserved LVEF, recent studies have shown significant decreased LV-GLS in patients with frequent PVCs. […] Beyond the interest of this topic, further and greater studies are needed to support these findings.
  • #54 A challenging dilemma: Can we predict which premature ventricular contractions may cause cardiomyopathy? | Revista Portuguesa de Cardiologia
    https://revportcardiol.org/pt-a-challenging-dilemma-can-we-articulo-S0870255123003803
    The PVC burden to induce cardiomyopathy has been cited as more than 5-10% of all the daily heart beats during an unknown interval of time. […] However, not all patients with frequent PVCs will develop cardiomyopathy. Indeed, some patients with a high PVC burden never seem to develop any LV dysfunction, so attempts have been made to a search for risk factors and hypothesis to predict the occurrence of this type of cardiomyopathy. […] PVC-induced cardiomyopathy is a potentially reversible condition in which left ventricular dysfunction can improve and even normalize with pharmacological suppression or ablation techniques. […] This article highlights the utility of echo parameters in the analysis of PVCs and their association with the development of cardiomyopathy. […] Left ventricular strain has become popular in a lot of situations as a precocious parameter of LV dysfunction. Even in cases of preserved LVEF, recent studies have shown significant decreased LV-GLS in patients with frequent PVCs. […] Beyond the interest of this topic, further and greater studies are needed to support these findings.
  • #55 A challenging dilemma: Can we predict which premature ventricular contractions may cause cardiomyopathy? | Revista Portuguesa de Cardiologia
    https://revportcardiol.org/pt-a-challenging-dilemma-can-we-articulo-S0870255123003803
    The PVC burden to induce cardiomyopathy has been cited as more than 5-10% of all the daily heart beats during an unknown interval of time. […] However, not all patients with frequent PVCs will develop cardiomyopathy. Indeed, some patients with a high PVC burden never seem to develop any LV dysfunction, so attempts have been made to a search for risk factors and hypothesis to predict the occurrence of this type of cardiomyopathy. […] PVC-induced cardiomyopathy is a potentially reversible condition in which left ventricular dysfunction can improve and even normalize with pharmacological suppression or ablation techniques. […] This article highlights the utility of echo parameters in the analysis of PVCs and their association with the development of cardiomyopathy. […] Left ventricular strain has become popular in a lot of situations as a precocious parameter of LV dysfunction. Even in cases of preserved LVEF, recent studies have shown significant decreased LV-GLS in patients with frequent PVCs. […] Beyond the interest of this topic, further and greater studies are needed to support these findings.
  • #56 Pathophysiological Mechanisms of Premature Ventricular Complexes
    https://pmc.ncbi.nlm.nih.gov/articles/PMC7247859/
    Premature ventricular complexes (PVCs) are the most common ventricular arrhythmia. Despite the high prevalence, the cause of PVCs remains elusive in most patients. A better understanding of the underlying pathophysiological mechanism may help to steer future research. This review aims to provide an overview of the potential pathophysiological mechanisms of PVCs and their differentiation. […] Highly frequent PVCs, however, can have detrimental effects on the left ventricular function over time and may cause or worsen heart failure. A reduction in their burden may, therefore, be beneficial. […] Indeed, observational studies have shown that a reduction of PVCs by the use of pharmacological agents such as -blockers, amiodarone or flecainide or by catheter ablation can improve the left ventricular function.
  • #57 Premature Ventricular Complex – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK547713/
    The primary mechanisms thought to result in PVCs include triggered activity, automaticity, and reentry. Identification of the pathophysiological is essential as this informs the management approach. […] Triggered activity arises during the early depolarization phase due to exceeding the cell membrane activation threshold. The PVCs associated with bradycardia are often caused by this mechanism, along with other factors like electrolyte abnormalities, ischemia, and digoxin toxicity. […] Automaticity involves PVCs originating from abnormal cardiomyocyte activity, often showing parasystole. The enhanced automaticity characteristically results from an ectopic ventricular focus that fires spontaneously. […] Though usually linked to sustained arrhythmias, reentry can also cause PVCs. It requires 2 distinct pathways with unidirectional block, often involving scars, fibrosis, or abnormal conduction in specific regions. This mechanism is seen in phenomena like bundle-branch or fascicular PVCs.
  • #58 Premature ventricular contractions: Reassure or refer? | Cleveland Clinic Journal of Medicine
    https://www.ccjm.org/content/83/7/524
    In our practice we explain to patients that there are two primary indications for treating idiopathic PVCs: (1) to relieve symptoms or (2) in asymptomatic patients with presumed arrhythmia-induced cardiomyopathy, to try to reverse the cardiomyopathy by eliminating the PVCs. […] Even if they have no symptoms or only minimal symptoms, patients with a high PVC burden require follow-up because of the association between frequent PVCs and arrhythmia-induced cardiomyopathy. […] Eliminating the high burden of PVCs in patients with left ventricular dysfunction may significantly improve left ventricular systolic function. […] Treatment of the PVCs may be indicated in patients with systolic heart failure receiving cardiac resynchronization therapy, ie, a biventricular pacemaker. […] Beta-blockers and nondihydropyridine calcium channel blockers have both been used to treat symptomatic PVCs.
  • #59 Effect of carvedilol on premature ventricular complexes originating from the ventricular outflow tract | International Journal of Arrhythmia | Full Text
    https://arrhythmia.biomedcentral.com/articles/10.1186/s42444-020-00015-7
    Carvedilol is one of the most effective beta-blockers in reducing ventricular tachyarrhythmias and mortality in patients with heart failure. One of the possible antiarrhythmic mechanisms of carvedilol is the suppression of store overload-induced Ca2+ release, especially for the triggered activity. […] Premature ventricular complex (PVC) originating from the ventricular outflow tract (OT) is the most common form of idiopathic PVC, and its main mechanism is related to triggered activity. […] The mechanism underlying the favorable antiarrhythmic effect of carvedilol remains unclear. […] Recently, inhibition of store overload-induced calcium release (SOICR) has been suggested as an antiarrhythmic effect of carvedilol. […] The OT PVCs associated with disruptive symptoms and frequent OT PVCs can lead to cardiomyopathy. Therefore, the OT PVC often requires treatment.
  • #60 Flecainide in Idiopathic Premature Ventricular Contractions and Related Cardiomyopathy
    https://ctv.veeva.com/study/flecainide-in-idiopathic-premature-ventricular-contractions-and-related-cardiomyopathy
    Frequent PVCs-defined as a burden 5% on two separate 24-hour Holter recordings-are increasingly recognized as a cause of reversible systolic dysfunction in patients without structural heart disease. […] Despite being considered benign in structurally normal hearts, a persistently high PVC burden-particularly above 10%-is increasingly recognized as a cause of reversible left ventricular dysfunction and a potential trigger for cardiomyopathy. […] This condition is frequently underdiagnosed and may lead to unnecessary treatments or delayed intervention. […] Flecainide, a Class IC antiarrhythmic agent with sodium channel-blocking properties, is administered as monotherapy. […] Preliminary results indicate significant PVC burden reduction and symptomatic improvement, supporting the potential utility of flecainide as an effective non-invasive therapeutic option in appropriately selected patients.
  • #61 Monomorphic premature ventricular contractions in patients without cardiac structural changes: clinical and prognostic significance and evaluation of therapy effectiveness (clinical and experimental study) | Olesin | Russian Journal of Cardiology
    https://russjcardiol.elpub.ru/jour/article/view/5663?locale=en_US
    To determine the individualized choice of therapy for monomorphic premature ventricular contractions (PVCs) in patients without structural cardiac changes by assessing the predictors of arrhythmogenic cardiomyopathy (ACM) and the clinical and prognostic significance of its course. […] Experimental study. Animals were used to model PVCs by the mechanism of early post-depolarization (EPD) (aconitine), re-entry (peroxide or H2O2 arrhythmia). […] When modeling ventricular arrhythmias using the EPD mechanism, early (R/T) monotopic PVCs were recorded, and re-entry early and late monomorphic PVCs. […] In patients without structural cardiac changes, early (R/T) monotopic PVC highly correlated with ventricular ectopy induced by the EPD mechanism (aconitine) (r=0,92). […] In patients without structural cardiac changes, early and late monomorphic PVCs highly correlated with experimental ventricular ectopy caused by the re-entry mechanism (H2O2 arrhythmia). […] In patients with early monotopic ventricular ectopia, without detection of ACM predictors, the most effective were class I antiarrhythmic drugs. […] In other patients with early and late monomorphic ventricular ectopia and detected ACM predictors, class III agents were found to be effective.
  • #62 Premature Ventricle Contractions in Heart Failure: A Closer Examination – The Cardiology Advisor
    https://www.thecardiologyadvisor.com/features/premature-ventricle-contractions-in-heart-failure-a-closer-examination/
    The number or frequency of PVCs may help determine the utility of ablation. A higher percentage of PVCs makes ablation more amenable. If the burden is low, or the PVCs do not happen consistently, we may have challenges finding where they originate during an ablation. […] According to Dr Cantillon, catheter ablation is safe and effective and may be curative in many cases. However, the point at which ablation should be recommended is still under debate.
  • #63 Premature ventricular contractions originating from the left ventricular septum: Results of Radiofrequency Catheter Ablation in twenty patients | BMC Cardiovascular Disorders | Full Text
    https://bmccardiovascdisord.biomedcentral.com/articles/10.1186/1471-2261-11-27
    RFCA has been established as an effective and curative therapy for severely symptomatic PVC from the outflow tract in structurally normal hearts. […] This study aimed to investigate electrophysiologic characteristics and effects of Radiofrequency catheter ablation (RFCA) for patients with symptomatic premature ventricular contraction (PVC) originating from the left ventricular septum without including fascicular PVCs. […] The QRS morphology of PVCs originating from the left ventricular septum is similar to that seen in fascicular tachycardia. […] The distinguishing characteristic of the PVCs is that Purkinje potentials were not present at the site of successful ablation, suggesting a myocardial as opposed to fascicular substrate. […] Although the ECG characteristics of the PVCs arising from the left ventricular septum are similar to that seen in fascicular tachycardia, the electrophysiologic characteristics are different between the two types of PVCs.
  • #64 Frequent ventricular extrasystoles: significance, prognosis and treatment
    https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-9/Frequent-ventricular-extrasystoles-significance-prognosis-and-treatment
    In some cases, PVCs may be the first manifestation of underlying structural heart disease. […] For more than 20 years now, it has been accepted that the presence of PVCs in the absence of structural heart disease entails a favorable benign prognosis, even when they arise frequently. […] Nevertheless, in some cases very frequent PVCs can produce ventricular dilation and dysfunction (tachycardiomyopathy), the latter being an indication for treatment (ablation or antiarrhythmic drugs), even in the absence of symptoms. […] The prognostic significance of PVCs in ischemic heart disease is less benign. […] Indeed, in patients who have suffered a myocardial infarction, the presence of PVCs has been associated with an increase of up to three times the risk of sudden death. […] PVCs originating from the RVOT have been associated with malignant ventricular arrhythmias.
  • #65 Frequent ventricular extrasystoles: significance, prognosis and treatment
    https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-9/Frequent-ventricular-extrasystoles-significance-prognosis-and-treatment
    In some cases, PVCs may be the first manifestation of underlying structural heart disease. […] For more than 20 years now, it has been accepted that the presence of PVCs in the absence of structural heart disease entails a favorable benign prognosis, even when they arise frequently. […] Nevertheless, in some cases very frequent PVCs can produce ventricular dilation and dysfunction (tachycardiomyopathy), the latter being an indication for treatment (ablation or antiarrhythmic drugs), even in the absence of symptoms. […] The prognostic significance of PVCs in ischemic heart disease is less benign. […] Indeed, in patients who have suffered a myocardial infarction, the presence of PVCs has been associated with an increase of up to three times the risk of sudden death. […] PVCs originating from the RVOT have been associated with malignant ventricular arrhythmias.
  • #66 Frequent ventricular extrasystoles: significance, prognosis and treatment
    https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-9/Frequent-ventricular-extrasystoles-significance-prognosis-and-treatment
    In some cases, PVCs may be the first manifestation of underlying structural heart disease. […] For more than 20 years now, it has been accepted that the presence of PVCs in the absence of structural heart disease entails a favorable benign prognosis, even when they arise frequently. […] Nevertheless, in some cases very frequent PVCs can produce ventricular dilation and dysfunction (tachycardiomyopathy), the latter being an indication for treatment (ablation or antiarrhythmic drugs), even in the absence of symptoms. […] The prognostic significance of PVCs in ischemic heart disease is less benign. […] Indeed, in patients who have suffered a myocardial infarction, the presence of PVCs has been associated with an increase of up to three times the risk of sudden death. […] PVCs originating from the RVOT have been associated with malignant ventricular arrhythmias.
  • #67 Frequent ventricular extrasystoles: significance, prognosis and treatment
    https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-9/Frequent-ventricular-extrasystoles-significance-prognosis-and-treatment
    The ability of frequent PVCs originating from a focal source in triggering idiopathic ventricular fibrillation (VF) in seemingly normal hearts was first reported by Haissaguerre et al. […] Catheter ablation was shown to be effective in acutely eliminating VEBs and reducing the incidence of further VF recurrence. […] Progressive PVCs are induced with exercise or stress which can cause syncope or sudden death with polymorphic VT or VF. […] Risk of sudden cardiac death from malignant ventricular arrhythmia should be considered in patients with heart disease who have frequent PVCs. […] PVCs have also been shown to trigger malignant ventricular arrhythmias in certain patients with idiopathic ventricular fibrillation and other syndromes.
  • #68 Frequent ventricular extrasystoles: significance, prognosis and treatment
    https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-9/Frequent-ventricular-extrasystoles-significance-prognosis-and-treatment
    The ability of frequent PVCs originating from a focal source in triggering idiopathic ventricular fibrillation (VF) in seemingly normal hearts was first reported by Haissaguerre et al. […] Catheter ablation was shown to be effective in acutely eliminating VEBs and reducing the incidence of further VF recurrence. […] Progressive PVCs are induced with exercise or stress which can cause syncope or sudden death with polymorphic VT or VF. […] Risk of sudden cardiac death from malignant ventricular arrhythmia should be considered in patients with heart disease who have frequent PVCs. […] PVCs have also been shown to trigger malignant ventricular arrhythmias in certain patients with idiopathic ventricular fibrillation and other syndromes.
  • #69 Pathophysiological Mechanisms of Premature Ventricular Complexes
    https://pmc.ncbi.nlm.nih.gov/articles/PMC7247859/
    The triggered activity by delayed afterdepolarizations usually occurs in bursts of reactivations. […] Sudden stretch of the myocardium has an electrophysiological effect on the myocardium dependent on the timing during the cardiac cycle. […] Mechanical strain has been implied to predispose patients to ventricular arrhythmias in various cardiac conditions including myocardial ischemia, arrhythmogenic right ventricular cardiomyopathy and cardiac arrest in patients with mitral valve prolapse. […] The demonstration of continuous activation can be challenging. […] The mechanism at work, later termed reflection, was analyzed in more detail by local suppression of excitability of unbranched Purkinje fibers by regional encasement in hyperkalemic agar or superfusion with an isotonic sucrose solution.
  • #70 Pathophysiological Mechanisms of Premature Ventricular Complexes
    https://pmc.ncbi.nlm.nih.gov/articles/PMC7247859/
    The triggered activity by delayed afterdepolarizations usually occurs in bursts of reactivations. […] Sudden stretch of the myocardium has an electrophysiological effect on the myocardium dependent on the timing during the cardiac cycle. […] Mechanical strain has been implied to predispose patients to ventricular arrhythmias in various cardiac conditions including myocardial ischemia, arrhythmogenic right ventricular cardiomyopathy and cardiac arrest in patients with mitral valve prolapse. […] The demonstration of continuous activation can be challenging. […] The mechanism at work, later termed reflection, was analyzed in more detail by local suppression of excitability of unbranched Purkinje fibers by regional encasement in hyperkalemic agar or superfusion with an isotonic sucrose solution.
  • #71 The Association of High Burden Premature Ventricular Contractions with Esophageal/Upper GI Diseases
    https://www.mdpi.com/2673-3846/5/4/38
    Six patients in our clinical program who were diagnosed with high burden (>10%) premature ventricular contractions (PVCs) and concomitant significant upper GI disease with no other significant cardiac history demonstrated a significant reduction in the burden of PVCs following surgical or procedural interventions of the upper GI tract (68.34% reduction, p = 0.024). […] Furthermore, in all cases, the origin of the PVCs was from the base of the right ventricular outflow tract (RVOT). […] This is the first report in the literature that we are aware of that makes the unique association that we propose a dual mechanism of action of the upper GI and vagally mediated PVCs and through direct, anatomical extrinsic triggering of the right ventricular outflow tract (RVOT) of the heart. […] The mechanism of PVCs is multifactorial, and is related to extrinsically triggered activity, automaticity, and reentry.
  • #72 The Association of High Burden Premature Ventricular Contractions with Esophageal/Upper GI Diseases
    https://www.mdpi.com/2673-3846/5/4/38
    Six patients in our clinical program who were diagnosed with high burden (>10%) premature ventricular contractions (PVCs) and concomitant significant upper GI disease with no other significant cardiac history demonstrated a significant reduction in the burden of PVCs following surgical or procedural interventions of the upper GI tract (68.34% reduction, p = 0.024). […] Furthermore, in all cases, the origin of the PVCs was from the base of the right ventricular outflow tract (RVOT). […] This is the first report in the literature that we are aware of that makes the unique association that we propose a dual mechanism of action of the upper GI and vagally mediated PVCs and through direct, anatomical extrinsic triggering of the right ventricular outflow tract (RVOT) of the heart. […] The mechanism of PVCs is multifactorial, and is related to extrinsically triggered activity, automaticity, and reentry.
  • #73 Premature ventricular contraction is associated with increased risk of atrial fibrillation: a nationwide population-based study | Scientific Reports
    https://www.nature.com/articles/s41598-021-81229-0
    Premature ventricular contraction (PVC) and atrial fibrillation (AF) are common arrhythmias affecting 12% of the general population. […] The association between PVC and AF is not fully understood. In theory, retrograde ventriculo-atrial conduction can occur with PVC, which can act like atrial ectopic beats. Therefore, there is a possibility that PVC can increase the risk of AF through retrograde ventriculo-atrial conduction. […] The underlying mechanism linking PVC and increased risk of new-onset AF is not clear. Retrograde ventriculo-atrial conduction can occur with PVC. These retrograde atrial activations can act like atrial ectopies originating from pulmonary veins. […] Our study raises the hypothesis that PVC can increase the risk of new-onset AF and ischemic stroke.
  • #74 Association of Premature Ventricular Contraction (PVC) with hematological parameters: a data mining approach | Scientific Reports
    https://www.nature.com/articles/s41598-025-86557-z
    Based on the final DT the most important hematology factors associated with PVC were WBC, PLT, RDW, PDW, and HCT for males and RBC, PLT, RDW, MCV, and MXD for females. […] One of the hematological factors that was associated with the presence of PVC was RDW. However, there is no evident direct relationship between RDW and PVC, but according to previous studies some medical conditions might cause the co-occurrence of higher RDW and PVC. It has been shown that PVC could be associated with heart diseases such as coronary artery disease, structural heart disease, myocarditis, and arrhythmias. In addition, it has been shown that RDW could be associated with an increased risk of different heart diseases. […] One of the other hematological factors found to be associated with PVC was platelet count (PLT). Higher PLT may be associated with medical conditions that potentially contribute to PVC. It has been found that myocardial inflammation can lead to PVC. In addition, this is evident that PLT is elevated during inflammation. Moreover, beyond these findings, previous studies have demonstrated a direct relationship between PLT elevation and CVDs, which are the main risk factors for frequent PVC.
  • #75 Association of Premature Ventricular Contraction (PVC) with hematological parameters: a data mining approach | Scientific Reports
    https://www.nature.com/articles/s41598-025-86557-z
    Based on the final DT the most important hematology factors associated with PVC were WBC, PLT, RDW, PDW, and HCT for males and RBC, PLT, RDW, MCV, and MXD for females. […] One of the hematological factors that was associated with the presence of PVC was RDW. However, there is no evident direct relationship between RDW and PVC, but according to previous studies some medical conditions might cause the co-occurrence of higher RDW and PVC. It has been shown that PVC could be associated with heart diseases such as coronary artery disease, structural heart disease, myocarditis, and arrhythmias. In addition, it has been shown that RDW could be associated with an increased risk of different heart diseases. […] One of the other hematological factors found to be associated with PVC was platelet count (PLT). Higher PLT may be associated with medical conditions that potentially contribute to PVC. It has been found that myocardial inflammation can lead to PVC. In addition, this is evident that PLT is elevated during inflammation. Moreover, beyond these findings, previous studies have demonstrated a direct relationship between PLT elevation and CVDs, which are the main risk factors for frequent PVC.
  • #76
    https://scispace.com/authors/yue-chen-3tf9ew1x64
    Higher High-Sensitivity C Reactive Protein is Associated with Future Premature Ventricular Contraction: a Community Based Prospective Cohort Study. […] Elevated serum hs-CRP was an independent predictor of PVC in Chinese population, especially in men, and elevated serum h’s- CRP was associated with future PVC in participants without history of myocardial infarction or stroke.