Niewydolność zastawki trójdzielnej
Patofizjologia i mechanizm
Niewydolność zastawki trójdzielnej (NT) to stan charakteryzujący się wstecznym przepływem krwi z prawej komory do prawego przedsionka podczas skurczu, prowadzącym do przeciążenia objętościowego prawej komory i prawostronnej niewydolności serca. NT dzieli się na pierwotną (organiczną, 10-20% przypadków) związaną z bezpośrednim uszkodzeniem aparatu zastawkowego (np. anomalia Ebsteina, infekcyjne zapalenie wsierdzia) oraz wtórną (czynnościową, 80-90% przypadków), wynikającą z nieprawidłowej funkcji zastawki na tle zmian geometrycznych prawego serca. Wtórna NT obejmuje postać związaną z nadciśnieniem płucnym (PH-FTR) i idiopatyczną/izolowaną (Id-FTR), z charakterystycznym poszerzeniem pierścienia zastawki i naciąganiem płatków. Patofizjologia wtórnej NT obejmuje poszerzenie pierścienia zastawki (zwiększenie odległości przednio-tylnej o około 80%), naciąganie płatków oraz zaburzenie koaptacji, co prowadzi do progresji niedomykalności i remodelingu prawej komory.
- Patofizjologia niewydolności zastawki trójdzielnej
- Klasyfikacja etiologiczna
- Patogeneza i mechanizm pierwotnej NT
- Patogeneza i mechanizm wtórnej NT
- Mechanizmy prowadzące do wtórnej NT
- Klasyfikacja funkcjonalna NT
- Czynniki wpływające na stopień NT
- Błędne koło niedomykalności trójdzielnej
- Konsekwencje hemodynamiczne i patofizjologiczne
- Szczególne postaci NT
- Patofizjologia NT – najważniejsze aspekty
Patofizjologia niewydolności zastawki trójdzielnej
Niewydolność zastawki trójdzielnej (NT) to stan charakteryzujący się wstecznym przepływem krwi z prawej komory do prawego przedsionka podczas skurczu, spowodowany nieszczelnym zamknięciem zastawki trójdzielnej. Mechanizm ten prowadzi do przeciążenia objętościowego prawej komory serca, co ostatecznie może skutkować prawostronną niewydolnością serca z obrzękami obwodowymi, wodobrzuszem i przekrwieniem wątroby.12
Klasyfikacja etiologiczna
Niewydolność zastawki trójdzielnej można sklasyfikować na dwa główne typy, w zależności od mechanizmu powstania:123
- Pierwotna niewydolność zastawki trójdzielnej (organiczna) – występuje u 10-20% pacjentów z NT i jest spowodowana bezpośrednim uszkodzeniem strukturalnym aparatu zastawki (płatków, strun ścięgnistych lub mięśni brodawkowatych). Przyczyny obejmują wady wrodzone (np. anomalia Ebsteina), infekcyjne zapalenie wsierdzia, chorobę reumatyczną, urazy, guzy, zmiany zwyrodnieniowe, uszkodzenia związane z elektrodami urządzeń wszczepialnych oraz zmiany indukowane lekami.123
- Wtórna niewydolność zastawki trójdzielnej (czynnościowa) – stanowi 80-90% przypadków NT i jest związana z prawidłową morfologią płatków zastawki, a nieprawidłowym funkcjonowaniem całego aparatu zastawkowego wskutek zmian geometrycznych w obrębie prawej komory i/lub prawego przedsionka.123
Patogeneza i mechanizm pierwotnej NT
W pierwotnej NT główny mechanizm patofizjologiczny związany jest z bezpośrednim uszkodzeniem strukturalnym elementów zastawki:12
- Perforacja lub ograniczenie ruchomości płatków zastawki
- Zrośnięcie komisur zastawki
- Naciąganie (tethering) lub zerwanie strun ścięgnistych
- Zmiany zwyrodnieniowe aparatu zastawkowego
- Anomalie wrodzone (np. anomalia Ebsteina – najczęstsza wrodzona postać NT)1
W anomalii Ebsteina dochodzi do nieprawidłowego rozwoju zastawki trójdzielnej, która jest położona niżej niż zwykle w prawej komorze serca, co prowadzi do niedomykalności.1
Patogeneza i mechanizm wtórnej NT
Wtórna niewydolność zastawki trójdzielnej jest skutkiem złożonych procesów patofizjologicznych prowadzących do zmian geometrycznych w prawym sercu. Można wyróżnić dwa główne typy wtórnej NT:123
- NT związana z nadciśnieniem płucnym (PH-FTR, pulmonary hypertension-functional tricuspid regurgitation):
- Długotrwałe nadciśnienie płucne powoduje niekorzystną przebudowę prawej komory, głównie jej ściany przednio-bocznej na poziomie środkowym komory
- Przemieszczenie mięśni brodawkowatych (szczególnie przedniego w kierunku doogonowym)
- Naciąganie (tethering) płatków zastawki
- Umiarkowane poszerzenie pierścienia zastawki
- Skutkiem jest deformacja zastawki z dominującym mechanizmem naciągania płatków12
- Idiopatyczna/izolowana NT (Id-FTR, idiopathic functional tricuspid regurgitation):
- Występuje bez nadciśnienia płucnego lub innych jawnych nieprawidłowości sercowych
- Często związana z migotaniem przedsionków
- Charakteryzuje się znacznym poszerzeniem prawego przedsionka i pierścienia trójdzielnego
- Prowadzi do złej koaptacji płatków zastawki
- Następuje bez wyraźnej przebudowy prawej komory123
Mechanizmy prowadzące do wtórnej NT
Rozwój wtórnej niewydolności zastawki trójdzielnej można podzielić na trzy fazy:12
- Faza początkowa: Rozstrzeń prawej komory (początkowo często wtórna do choroby lewego serca) prowadzi do poszerzenia pierścienia zastawki trójdzielnej.
- Faza progresji: Postępujące poszerzenie prawej komory i pierścienia zastawki skutkuje niewystarczającą koaptacją płatków zastawki, co prowadzi do istotnej hemodynamicznie niedomykalności.
- Faza zaawansowana: Ciągłe zniekształcenie geometrii prawej komory, szczególnie jej przedniej ściany, w połączeniu z naciąganiem płatków zastawki, pogłębia stopień niedomykalności trójdzielnej.
Kluczowe elementy mechanizmu wtórnej NT obejmują:123
- Poszerzenie pierścienia zastawki trójdzielnej – w warunkach prawidłowych pierścień ma kształt siodełkowaty, ale wraz z rozwojem NT staje się większy, bardziej płaski i okrągły. Rozszerzenie pierścienia nie jest symetryczne – odległość przednio-tylna zwiększa się o około 80%, podczas gdy odległość przyśrodkowo-boczna zwiększa się tylko o około 34%.
- Naciąganie płatków zastawki – spowodowane przemieszczeniem mięśni brodawkowatych w wyniku przebudowy prawej komory.
- Zaburzenie koaptacji płatków – zmniejszenie powierzchni przylegania płatków podczas skurczu zwiększa prawdopodobieństwo powstania niedomykalności. Fizjologiczna koaptacja zachodzi między ciałami każdego płatka (body-to-body), ale w przypadku poszerzenia pierścienia i/lub naciągania płatków, koaptacja może zachodzić na brzegach płatków, symetrycznie (edge-to-edge) lub asymetrycznie (edge-to-body), co zmniejsza margines bezpieczeństwa.
- Utrata dynamiki pierścienia – zmniejszone kurczenie się miokardium wokół pierścienia zastawki trójdzielnej.
Klasyfikacja funkcjonalna NT
Według klasyfikacji funkcjonalnej Carpentiera, opartej na ruchomości płatków, wtórną niedomykalność trójdzielną można podzielić na:12
- Typ I Carpentiera – prawidłowa ruchomość płatków z dominującym poszerzeniem pierścienia trójdzielnego, charakterystyczna dla przedsionkowej postaci wtórnej NT (związanej z migotaniem przedsionków).
- Typ IIIb Carpentiera – naciąganie płatków z ograniczoną ruchomością skurczową, typowe dla komorowej postaci wtórnej NT (związanej z nadciśnieniem płucnym i przebudową prawej komory).
Czynniki wpływające na stopień NT
Niedomykalność zastawki trójdzielnej jest dynamicznym procesem, na który wpływają różne czynniki fizjologiczne:123
- Obciążenie wstępne prawej komory (preload) – zwiększone napełnianie prawej komory może nasilać niedomykalność trójdzielną.
- Obciążenie następcze prawej komory (afterload) – zwiększone opory w krążeniu płucnym wpływają na stopień niedomykalności.
- Funkcja skurczowa prawej komory – osłabiona kurczliwość prawej komory może nasilać niedomykalność.
- Wdech – podczas wdechu dochodzi do nasilenia niedomykalności trójdzielnej. Podczas wdechu prawa komora poszerza się, co dodatkowo powiększa pierścień zastawki trójdzielnej i zwiększa efektywną powierzchnię ujścia fali zwrotnej.
- Ogólny stan objętościowy – wahania w objętości krwi krążącej mogą wpływać na stopień niedomykalności.
Błędne koło niedomykalności trójdzielnej
Niewydolność zastawki trójdzielnej tworzy samonapędzający się mechanizm, nazywany często „błędnym kołem niedomykalności”:123
- Niedomykalność trójdzielna → przeciążenie objętościowe prawej komory → poszerzenie prawej komory → poszerzenie pierścienia zastawki i/lub naciąganie płatków → zwiększenie stopnia niedomykalności → dalsza przebudowa prawej komory → postępująca niewydolność prawej komory
Ten samopodtrzymujący się mechanizm tłumaczy, dlaczego nieleczona NT może postępować nawet po skorygowaniu pierwotnej przyczyny, która ją wywołała.1
Konsekwencje hemodynamiczne i patofizjologiczne
Konsekwencje hemodynamiczne niewydolności zastawki trójdzielnej zależą od jej nasilenia:12
W przypadkach łagodnej do umiarkowanej NT nie obserwuje się istotnych następstw hemodynamicznych z powodu stosunkowo podatnego prawego przedsionka, który jest w stanie pomieścić dodatkową objętość krwi bez znaczącego wzrostu ciśnienia.1
- Przeciążenia objętościowego prawej komory
- Zwiększenia ciśnienia i objętości w prawym przedsionku
- Zwiększenia centralnego ciśnienia żylnego
- Zmniejszenia rzutu serca
- Rozwoju objawów prawostronnej niewydolności serca:
- Obrzęki obwodowe
- Wodobrzusze
- Przekrwienie wątroby
- Duszność wysiłkowa
- Progresywnej dysfunkcji prawej komory prowadzącej do niewydolności prawokomorowej
- Rozwoju migotania przedsionków
Niezależnie od pierwotnej przyczyny, ciężka NT wiąże się ze złym rokowaniem długoterminowym z powodu postępującej dysfunkcji prawej komory i zastoju w układzie żylnym.12
Szczególne postaci NT
NT związana z urządzeniami wewnątrzsercowymi: Elektrody stymulatorów i defibrylatorów mogą zakłócać funkcję zastawki trójdzielnej i prowadzić do różnego stopnia niedomykalności, która może postępować z czasem.123
NT po operacjach zastawek lewego serca: Rozwój istotnej NT po operacji zastawki mitralnej lub aortalnej nie jest rzadkością i wiąże się z niekorzystnym rokowaniem. Ważną koncepcją, która powinna zostać powszechnie zaakceptowana, jest to, że gdy pierścień trójdzielny ulegnie poszerzeniu (stanie się płaski i okrągły), nie zmienia się po leczeniu pierwotnej przyczyny przeciążenia ciśnieniowego lub objętościowego, co sugeruje, że poszerzenie pierścienia może być nieodwracalne.1
Patofizjologia NT – najważniejsze aspekty
Niewydolność zastawki trójdzielnej to złożony proces patofizjologiczny, który może mieć różnorodne przyczyny, ale prowadzi do wspólnego efektu końcowego – wstecznego przepływu krwi z prawej komory do prawego przedsionka podczas skurczu. Kluczowe elementy patogenezy i mechanizmu NT obejmują:123
- Rozróżnienie między pierwotną (organiczną) a wtórną (czynnościową) niedomykalnością zastawki trójdzielnej
- Dominujący udział wtórnej NT (80-90% przypadków), która jest wynikiem zmian geometrycznych w prawym sercu, a nie pierwotnego uszkodzenia zastawki
- Rola poszerzenia pierścienia zastawki i naciągania płatków w patogenezie wtórnej NT
- Znaczenie nadciśnienia płucnego, migotania przedsionków i niewydolności lewego serca jako głównych czynników przyczyniających się do rozwoju wtórnej NT
- Błędne koło patofizjologiczne, w którym NT prowadzi do dalszej przebudowy prawej komory, co nasila niedomykalność
- Dynamiczny charakter NT, na który wpływają czynniki takie jak obciążenie wstępne i następcze prawej komory, jej funkcja skurczowa oraz faza oddechowa
Zrozumienie złożonej patofizjologii NT jest kluczowe dla właściwej diagnostyki i leczenia tej choroby, która przez długi czas była nazywana „zapomnianą zastawką” w kardiologii.12
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Materiały źródłowe
- #1 Tricuspid Regurgitation – StatPearls – NCBI Bookshelfhttps://www.ncbi.nlm.nih.gov/books/NBK526121/
Tricuspid regurgitation is a condition characterized by the backward flow of blood from the right ventricle into the right atrium during systole due to an incompetent tricuspid valve. This regurgitation often results from structural abnormalities of the valve apparatus, including issues with the valve leaflets, annulus, or papillary muscles. Contributing factors may include valve degeneration, annular dilation, or damage from conditions such as pulmonary hypertension or infective endocarditis. The condition can lead to symptoms such as right-sided heart failure, including edema and ascites, and requires careful evaluation to determine its severity and impact on cardiac function. […] Primary structural abnormalities of the tricuspid valvular apparatus or secondary abnormalities due to myocardial dysfunction or dilatation are responsible for the structural incompetence of the tricuspid valve. The backflow of blood from the right ventricle into the right atrium during systole defines tricuspid regulation. In mild to moderate cases of tricuspid regurgitation, no significant hemodynamic consequences are noted due to the comparatively compliant nature of the right atrium. However, in severe cases, right ventricular volume overload develops, which eventually results in right-sided congestive heart failure presenting with peripheral edema, ascites, and hepatic congestion.
- #1 Tricuspid Regurgitation: Background, Anatomy, Pathophysiologyhttps://emedicine.medscape.com/article/158484-overview
Tricuspid regurgitation may result from structural alterations of any or all of the components of the tricuspid valve apparatus. The lesion may be classified as primary when it is caused by an intrinsic abnormality of the valve apparatus or as secondary when it is caused by right ventricular (RV) dilatation or other conditions (eg, left ventricular [LV] dysfunction). […] The pathophysiology of tricuspid regurgitation focuses on the structural incompetence of the valve. The incompetence can result from primary structural abnormalities of the leaflets and chordae or, more often, be secondary to myocardial dysfunction and dilatation. […] Tricuspid valve insufficiency due to leaflet abnormalities may be secondary to endocarditis or rheumatic heart disease. […] When due to the latter, it generally occurs in combination with tricuspid stenosis.
- #1 Tricuspid Regurgitationhttps://www.my-connext.com/valvular-diseases/tricuspid/overview
Approximately 10-20% of cases are due to primary TR, which is diagnosed in the presence of abnormal tricuspid valve morphology. The causes of primary TR include congenital abnormalities, infection (i.e. endocarditis), rheumatic disease, chest cavity trauma, tumors, and intravenous drug use. Structural damage to the tricuspid valve during cardiac device implantation is another common cause of primary TR. […] Secondary TR is the most common form, occurring in 80-90% of cases, and is diagnosed in the presence of normal tricuspid valve morphology. The causes of secondary TR include changes in the right ventricle or distortion of the tricuspid valve leaflets, annulus or chords. The condition typically occurs secondary to LSHD and/or Right Ventricular (RV) remodelling, Pulmonary Hypertension (HT), tricuspid annular dilation, AF or RV dysfunction. This can make it difficult to isolate the risk factors that contribute to secondary TR independently of comorbid or underlying cardiac disease(s).
- #1 Etiology, epidemiology, pathophysiology and management of tricuspid regurgitation: an overviewhttps://www.imrpress.com/journal/RCM/22/4/10.31083/j.rcm2204122/htm
The mechanisms leading to FTR differ between patients with PH-FTR and the subgroup of patients with FTR in the absence of PH, or other associated cardiac abnormalities that are named as âisolatedâ, âidiopathicâ, or âatrial fibrillation-associated FTRâ (Id-FTR). Primary RV dysfunction is quite rare, but pathophysiological alterations leading to eventual FTR are similar to those present in case of PH-FTR, since the ventricular factor is the primum movens of the disease. […] The mechanisms leading to TR are different and heterogeneous for each disease in the case of primary TR. Examples of resulting structural damage are leaflet perforation or restriction, commissural fusion, and chordal tethering or rupture. Primary TR results in pure volume overload of the right heart and therefore is usually associated with annular dilation.
- #1 Tricuspid Regurgitation: Background, Anatomy, Pathophysiologyhttps://emedicine.medscape.com/article/158484-overview
Ebstein anomaly is the most common congenital form of tricuspid regurgitation. […] Inspiration increases the severity of tricuspid regurgitation. Inspiration induces widening of the RV, which enlarges the tricuspid valve annulus and thus increases the effective regurgitant orifice area. […] Chronically, tricuspid regurgitation leads to RV volume overload, which results in right-sided congestive heart failure (CHF). This manifests as hepatic congestion, peripheral edema, and ascites.
- #1 Tricuspid valve regurgitation – Symptoms and causes – Mayo Clinichttps://www.mayoclinic.org/diseases-conditions/tricuspid-valve-regurgitation/symptoms-causes/syc-20350168
In tricuspid valve regurgitation, the valve between the two right heart chambers doesn’t close properly. The upper right chamber is called the right atrium. The lower right chamber is called the right ventricle. As a result, blood flows backward. […] Tricuspid valve regurgitation is a type of heart valve disease. The valve between the two right heart chambers doesn’t close as it should. Blood flows backward through the valve into the upper right chamber. If you have tricuspid valve regurgitation, less blood flows to the lungs. The heart has to work harder to pump blood. […] In tricuspid valve regurgitation, the tricuspid valve doesn’t close tightly. So, blood leaks backward into the upper right heart chamber. […] Causes of tricuspid valve regurgitation include: A heart problem you’re born with, also called a congenital heart defect. Some congenital heart defects affect the shape of the tricuspid valve and how it works. Tricuspid valve regurgitation in children is usually caused by a rare heart problem present at birth called Ebstein anomaly. In this condition, the tricuspid valve does not form correctly. It also is lower than usual in the lower right heart chamber.
- #1 Etiology, epidemiology, pathophysiology and management of tricuspid regurgitation: an overviewhttps://www.imrpress.com/journal/RCM/22/4/10.31083/j.rcm2204122/htm
FTR is essentially due to right atrium and/or right ventricle dilation with variable degrees of TA dilation and leaflet tethering, according to the underlying cause. FTR is thereby not a valvular disease; it is an abnormality which results from a disease process that primarily affects the atrium or ventricle and subsequently alters the TA size and the mode of TV leaflet coaptation. […] The mechanisms leading to TR are different and heterogeneous for each disease in the case of primary TR. Examples of resulting structural damage are leaflet perforation or restriction, commissural fusion, and chordal tethering or rupture. Primary TR results in pure volume overload of the right heart and therefore is usually associated with annular dilation. […] The most common type of FTR is the one associated with PH. Long-standing PH causes RV maladaptive remodeling mainly at the expense of the antero-lateral wall at the mid-ventricular level. This leads to papillary muscles displacement (bringing the anterior papillary muscle into a more caudal position) and subsequently TV leaflet tethering. Thus PH-FTR is essentially due to valve deformation with leaflet tethering and only modest annular enlargement.
- #1 Tricuspid Regurgitation: No Longer the âForgottenâ Valve – European Medical Journalhttps://www.emjreviews.com/cardiology/article/tricuspid-regurgitation-no-longer-the-forgotten-valve/
Valve regurgitation remains the principal pathology of the TV and it is more often secondary rather than caused by a primary valve lesion. Annular dilatation and increased tricuspid leaflet tethering in relation to high right ventricular (RV) pressure and/or volume overload cause secondary TR. Left-sided heart disease, atrial fibrillation, or pulmonary hypertension are frequently involved in the pathogenesis of TR. […] Shortly, the pathophysiology of functional TR can be divided into three phases. Initially, left-side heart disease, may determine impairment of RV, with progressive dilatation, which can lead to tricuspid annulus (TA) enlargement. In the second phase, the progressive dilation of the RV and TA can result in a poor leaflet coaptation leading to significant TR. Finally, in the third phase continuous distortion of RV geometry especially on the anterior wall associated with tethering of the leaflets will get worse the degree of TR. […] Unfortunately, TR has a silent evolution and patients are often referred in the latest phase, when they present with RV dysfunction and an important gap coaptation.
- #1 The pathogenesis of functional tricuspid regurgitation – PubMedhttps://pubmed.ncbi.nlm.nih.gov/20813321/
Functional tricuspid regurgitation (TR) is a common etiology of TR. Functional TR results from geometrical distortion of the normal spatial relationships of the tricuspid leaflets, annulus, chords, papillary muscles, and right ventricular (RV) walls. […] Functional TR results most commonly from left-sided heart disease, including mitral valve abnormalities and cardiomyopathy and RV dysfunction secondary to pulmonary disease (Cor pulmonale). The tricuspid annulus, which has a normal bimodal or saddle shape, becomes larger, flatter, and more circular with the development of functional TR. RV dilation can lead to papillary muscle displacement and tethering of the tricuspid leaflets, resulting in incomplete coaptation and development of functional TR.
- #1 Tricuspid Regurgitation – StatPearls – NCBI Bookshelfhttps://www.ncbi.nlm.nih.gov/books/NBK526121/
The tricuspid annulus is dynamic and changes with the change in loading conditions; factors affecting the degree of tricuspid regurgitation include right ventricular preload, afterload, and right ventricular systolic function. During inspiration, the severity of tricuspid regurgitation increases. The right ventricle widens during inspiration, further enlarging the tricuspid valve annulus and increasing the effective regurgitant orifice area. […] Carpentiers functional classification, based on leaflet mobility, can describe secondary TR effectively. Carpentier type I corresponds to normal leaflet motion with predominant tricuspid annulus dilation, which is common in atrial secondary TR. Carpentier type IIIb involves leaflet tethering with restricted systolic motion, typically seen in ventricular secondary TR. While the Carpentier classification was initially designed to guide mitral valve surgical repair or replacement, its application for TR is less established but practical for case discussion and presentation. However, the Carpentier classification may be used to discuss and present cases.
- #1 Tricuspid regurgitation: what is the real clinical impact and how often should it be treated? | EuroInterventionhttps://eurointervention.pcronline.com/article/tricuspid-regurgitation-what-is-the-real-clinical-impact-and-how-often-should-it-be-treated
Tricuspid regurgitation (TR) is characterised by a pathological amount of blood regurgitating from the right ventricle (RV) into the right atrium (RA) during systole, eventually leading to excess mortality and cardiac morbidity. […] Moderate-to-severe TR is pathological and is caused by annular dilatation and/or leaflet abnormalities. […] Recent epidemiological data indicate that FTR accounts for 90% of all-comers with severe TR, and in total 65% of FTR occurs in the context of pulmonary hypertension. The pressure overload due to pulmonary hypertension that may or may not be associated with left-sided heart disease causes RV remodelling and tricuspid annular flattening and dilatation, eventually generating FTR. […] TR begets TR by creating a vicious cycle of progressive RV dilatation, annular dilatation and leaflet tethering that results in increased TR severity and RV dilatation, eventually leading to RV dysfunction and failure.
- #1 Tricuspid regurgitation: what is the real clinical impact and how often should it be treated? | EuroInterventionhttps://eurointervention.pcronline.com/article/tricuspid-regurgitation-what-is-the-real-clinical-impact-and-how-often-should-it-be-treated
The development of significant TR after left-sided valve surgery is not uncommon and is associated with an unfavourable outcome. […] The presence of FTR predicted RV dilatation, RV dysfunction and unfavourable outcome. […] An important concept that needs to become widely accepted is that, when the annulus becomes dilated (planar and circular), it does not change after treatment of the primary cause of pressure or volume overload, thus implying that annular dilatation might be irreversible.
- #1 Tricuspid valve regurgitation – Symptoms and causes – Mayo Clinichttps://www.mayoclinic.org/diseases-conditions/tricuspid-valve-regurgitation/symptoms-causes/syc-20350168
Tricuspid valve regurgitation might happen if wires from a pacemaker or defibrillator cross the tricuspid valve. […] In severe tricuspid valve regurgitation, the heart has to work harder to pump enough blood to the body. The extra effort causes the lower right heart chamber to get bigger. Untreated, the heart muscle becomes weak. This can cause heart failure.
- #1 Tricuspid Regurgitation – Tricuspid Valve Disease – Valvular Heart Disease – Cardiovascular Diseases – Diseases – McMaster Textbook of Internal Medicinehttps://empendium.com/mcmtextbook/chapter/B31.II.2.10.2.
Tricuspid regurgitation (TR) is a reversal of blood flow from the right ventricle to the right atrium due to an incomplete closure of tricuspid valve leaflets. Patients with isolated TR (without tricuspid stenosis) usually have functional TR related to pulmonary hypertension (secondary or primary) or coexisting mitral valve disease, particularly stenosis. […] […] Functional TR (most frequent in patients with acquired valvular disease): Dilation of the tricuspid annulus of an anatomically normal valve secondary to the altered right ventricular geometry most commonly caused by pulmonary hypertension, mitral valve disease, right ventricular myocardial infarction, or congenital heart disease (eg, right ventricular outflow obstruction). […] […] TR associated with intracardiac devices: Pacemaker and defibrillator leads can interfere with function of the tricuspid valve and lead to varying degrees of regurgitation, which may be progressive. […] […] Regardless of the underlying condition, severe TR is associated with a poor long-term prognosis due to the progressive right ventricular dysfunction and systemic venous congestion.
- #1 Etiology, epidemiology, pathophysiology and management of tricuspid regurgitation: an overviewhttps://www.imrpress.com/journal/RCM/22/4/10.31083/j.rcm2204122/htm
Significant tricuspid regurgitation (TR) is a common finding, affecting about one in twenty-five subjects among the elderly and presenting more frequently in women than in men. […] FTR is a multifactorial disorder, resulting from maladaptive right ventricular remodeling secondary to pulmonary hypertension or from atrial fibrillation leading to dilation of the right atrium, tricuspid annulus and base of the right ventricle, with pathological TV coaptation. Thus two main types of FTR can be identified: pulmonary hypertension-FTR and idiopathic-FTR, depending on which factor, ventricular or atrial respectively, is the primum movens of the disease. […] FTR develops due to structural alterations in right atrial and/or ventricular myocardial geometry, leading to TA dilation and/or leaflet tethering, both associated with impaired leaflet coaptation. This is by far the most common cause of TR in adults, as shown by echocardiographic studies in which over than 90% patients with severe TR had a functional etiology.
- #1 Tricuspid valve regurgitation: no longer the âforgotten valveâhttps://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-16/Tricuspid-valve-regurgitation-no-longer-the-forgotten-valve
Tricuspid regurgitation (TR) is a highly prevalent valvular heart disease. […] Secondary or functional TR (caused by dilatation of the tricuspid annulus and remodelling of the right ventricle and right atrium) is the predominant cause, and isolated TR, associated with atrial fibrillation, is an emerging entity. […] In secondary TR, the underlying mechanism is characterised by RV dilation and dysfunction, leading to leaflet tethering, tricuspid annulus dilation and leaflet malcoaptation. […] This is most often caused by significant left-sided valvular and myocardial disease, which leads to increased left-sided pressures, pulmonary hypertension, increased RV afterload and remodelling of the RV. […] In isolated TR, the underlying mechanism is pronounced right atrial and tricuspid annular dilation, leading to leaflet malcoaptation, in the absence of any pronounced RV remodelling. […] The advent of advanced imaging techniques has provided novel insights into the important role of right heart remodelling in the pathophysiology of TR which may lead to improved risk stratification and more timely intervention in the near future.
- #2 Tricuspid Regurgitation: Background, Anatomy, Pathophysiologyhttps://emedicine.medscape.com/article/158484-overview
Tricuspid regurgitation may result from structural alterations of any or all of the components of the tricuspid valve apparatus. The lesion may be classified as primary when it is caused by an intrinsic abnormality of the valve apparatus or as secondary when it is caused by right ventricular (RV) dilatation or other conditions (eg, left ventricular [LV] dysfunction). […] The pathophysiology of tricuspid regurgitation focuses on the structural incompetence of the valve. The incompetence can result from primary structural abnormalities of the leaflets and chordae or, more often, be secondary to myocardial dysfunction and dilatation. […] Tricuspid valve insufficiency due to leaflet abnormalities may be secondary to endocarditis or rheumatic heart disease. […] When due to the latter, it generally occurs in combination with tricuspid stenosis.
- #2 Tricuspid valve regurgitation: no longer the âforgotten valveâhttps://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-16/Tricuspid-valve-regurgitation-no-longer-the-forgotten-valve
Tricuspid regurgitation (TR) is a highly prevalent valvular heart disease. […] Secondary or functional TR (caused by dilatation of the tricuspid annulus and remodelling of the right ventricle and right atrium) is the predominant cause, and isolated TR, associated with atrial fibrillation, is an emerging entity. […] In secondary TR, the underlying mechanism is characterised by RV dilation and dysfunction, leading to leaflet tethering, tricuspid annulus dilation and leaflet malcoaptation. […] This is most often caused by significant left-sided valvular and myocardial disease, which leads to increased left-sided pressures, pulmonary hypertension, increased RV afterload and remodelling of the RV. […] In isolated TR, the underlying mechanism is pronounced right atrial and tricuspid annular dilation, leading to leaflet malcoaptation, in the absence of any pronounced RV remodelling. […] The advent of advanced imaging techniques has provided novel insights into the important role of right heart remodelling in the pathophysiology of TR which may lead to improved risk stratification and more timely intervention in the near future.
- #2 From Neglected to Noticed: A Contemporary Understanding of Tricuspid Regurgitation Pathophysiology – Cardiac Interventions Todayhttps://citoday.com/articles/2021-july-aug/from-neglected-to-noticed-a-contemporary-understanding-of-tricuspid-regurgitation-pathophysiology
With the increasing awareness of the adverse impact of tricuspid regurgitation (TR) on outcomes, the need to understand the pathophysiology of this disease has grown. […] Understanding the anatomy and physiology of these components is important for the diagnosis and optimal planning of repair procedures. […] We show that functional TR is multifactorial, resulting from pulmonary hypertension, atrial fibrillation (AFib), and RV and RA remodeling. […] TR can be divided into primary and secondary causes. […] Primary TR can be caused by congenital or acquired disease processes that affect the leaflets, chordal structures, or both. […] Common causes for primary TR include rheumatic disease, endocarditis, carcinoid, radiation, drug-induced TR, flail leaflets, or congenital diseases. […] Secondary TR is much more common and can be categorized either by the etiology (disease process) or mechanism (morphologic abnormality of the tricuspid apparatus).
- #2 Etiology, epidemiology, pathophysiology and management of tricuspid regurgitation: an overviewhttps://www.imrpress.com/journal/RCM/22/4/10.31083/j.rcm2204122/htm
Significant tricuspid regurgitation (TR) is a common finding, affecting about one in twenty-five subjects among the elderly and presenting more frequently in women than in men. […] FTR is a multifactorial disorder, resulting from maladaptive right ventricular remodeling secondary to pulmonary hypertension or from atrial fibrillation leading to dilation of the right atrium, tricuspid annulus and base of the right ventricle, with pathological TV coaptation. Thus two main types of FTR can be identified: pulmonary hypertension-FTR and idiopathic-FTR, depending on which factor, ventricular or atrial respectively, is the primum movens of the disease. […] FTR develops due to structural alterations in right atrial and/or ventricular myocardial geometry, leading to TA dilation and/or leaflet tethering, both associated with impaired leaflet coaptation. This is by far the most common cause of TR in adults, as shown by echocardiographic studies in which over than 90% patients with severe TR had a functional etiology.
- #2 The tricuspid valve in review: anatomy, pathophysiology and echocardiographic assessment with focus on functional tricuspid regurgitation – Yucel – Journal of Thoracic Diseasehttps://jtd.amegroups.org/article/view/38028/html
A new entity, idiopathic FTR, has been described, where significant TR is identified without an overt cause (LV dysfunction, pacemaker lead impingement, primary TR) or any other significant concomitant valve disease. […] The role of ventricular-valvular interaction was also apparent, where PH-related FTR and RV remodeling led to a larger, longer, and more elliptical ventricle with more valve tenting and a larger effective orifice area. Conversely, the basal RV was larger and exhibited conical deformation in patients with idiopathic FTR.
- #2 Tricuspid Regurgitationhttps://www.my-connext.com/valvular-diseases/tricuspid/overview
Patients with primary TR aetiology may experience worsening of TR due to progressive cardiac remodelling and annular dilation, subsequently causing secondary TR. […] Secondary TR arising from RV remodelling can be classified in three progressive stages: Initial Right Ventricular (RV) dilatation results in Tricuspid Annulus (TA) dilatation; Progressive RV and TA dilatation results in lack of leaflet coaptation; Progressive RV distortion results in tethering of the leaflets and pulmonary hypertension.
- #2 Functional tricuspid regurgitation: Feasibility of transcatheter interventions | Cleveland Clinic Journal of Medicinehttps://www.ccjm.org/content/87/5_suppl_1/4
Functional tricuspid regurgitation (TR) develops secondary to annular dilation and leaflet tethering as a result of right ventricular remodeling. […] RV or annular dilation and tethering of the leaflets are the 2 main pathophysiologic mechanisms for the development of functional TR. While this is mostly secondary to left-sided disease, it may also be associated with isolated RV disease or pulmonary hypertension. The TR that develops through these mechanisms leads to further RV dilation and dysfunction and more tricuspid annular dilation and tethering, thereby progressively worsening the existing TR. This vicious cycle perpetuates TR and forms an integral part of the pathophysiology of severe TR. […] Anatomically, in patients with functional TR, the annulus is larger, flatter, and more circular thereby altering the saddle shape of a normal valve. The dilation of the tricuspid annulus in functional TR is not symmetric. It has been shown that the anteroposterior distance increases by approximately 80%, whereas the mediolateral distance increases by only 34%. This is because of a greater dilation along the free-wall aspect of the annulus.
- #2 From Neglected to Noticed: A Contemporary Understanding of Tricuspid Regurgitation Pathophysiology – Cardiac Interventions Todayhttps://citoday.com/articles/2021-july-aug/from-neglected-to-noticed-a-contemporary-understanding-of-tricuspid-regurgitation-pathophysiology
The common TV morphologic abnormalities associated with secondary TR due to ventricular functional TR include (1) RV dilatation resulting in a more spherical ventricle, with or without dysfunction; (2) tethering of the tricuspid leaflets in the setting of papillary muscles displacement; and (3) mild dilation of the TA, with or without RA dilatation. […] Because the severity of TR fluctuates significantly with loading conditions, the morphology of the TV is crucial for assessing both the TR severity and outcomes with surgical or percutaneous repair. […] We showed that TR is affected by a complex dynamic change of the annulus, leaflets, chords, papillary muscles, and atrial and ventricular interaction. […] In patients with type I TR, it is linked mostly to conical deformation of the RV, RA dilatation, and extreme annular dilatation without tethering. […] In patients with type IIIb TR, the major contributors are spherical deformation of the RV, papillary displacement, and leaflet tethering.
- #2 Tricuspid Regurgitation: Background, Anatomy, Pathophysiologyhttps://emedicine.medscape.com/article/158484-overview
Ebstein anomaly is the most common congenital form of tricuspid regurgitation. […] Inspiration increases the severity of tricuspid regurgitation. Inspiration induces widening of the RV, which enlarges the tricuspid valve annulus and thus increases the effective regurgitant orifice area. […] Chronically, tricuspid regurgitation leads to RV volume overload, which results in right-sided congestive heart failure (CHF). This manifests as hepatic congestion, peripheral edema, and ascites.
- #2 Tricuspid regurgitation: what is the real clinical impact and how often should it be treated? | EuroInterventionhttps://eurointervention.pcronline.com/article/tricuspid-regurgitation-what-is-the-real-clinical-impact-and-how-often-should-it-be-treated
The pathophysiology and clinical manifestations of TR are characterised by the consequences of increased RA-RV pressure and volume and decrease in cardiac output. […] The presence of right heart failure symptoms and/or exertional dyspnoea in patients without left-sided heart disease should always raise the suspicion of severe TR. […] Although there are studies attempting to evaluate the natural history and prognostic impact of FTR, their findings have sometimes been contradictory, with large variations in outcomes and debate as to whether TR severity, RV function, the underlying FTR aetiology or a combination are the predictors of poor outcome. […] The most cited article demonstrating the negative prognostic impact of FTR showed that, in a retrospective evaluation of 5,223 patients, mortality increased with increasing severity of TR.
- #2 Tricuspid Regurgitation – Tricuspid Valve Disease – Valvular Heart Disease – Cardiovascular Diseases – Diseases – McMaster Textbook of Internal Medicinehttps://empendium.com/mcmtextbook/chapter/B31.II.2.10.2.
Tricuspid regurgitation (TR) is a reversal of blood flow from the right ventricle to the right atrium due to an incomplete closure of tricuspid valve leaflets. Patients with isolated TR (without tricuspid stenosis) usually have functional TR related to pulmonary hypertension (secondary or primary) or coexisting mitral valve disease, particularly stenosis. […] […] Functional TR (most frequent in patients with acquired valvular disease): Dilation of the tricuspid annulus of an anatomically normal valve secondary to the altered right ventricular geometry most commonly caused by pulmonary hypertension, mitral valve disease, right ventricular myocardial infarction, or congenital heart disease (eg, right ventricular outflow obstruction). […] […] TR associated with intracardiac devices: Pacemaker and defibrillator leads can interfere with function of the tricuspid valve and lead to varying degrees of regurgitation, which may be progressive. […] […] Regardless of the underlying condition, severe TR is associated with a poor long-term prognosis due to the progressive right ventricular dysfunction and systemic venous congestion.
- #2 Tricuspid Regurgitation – Cardiovascular Disorders – Merck Manual Professional Editionhttps://www.merckmanuals.com/professional/cardiovascular-disorders/valvular-disorders/tricuspid-regurgitation
Tricuspid regurgitation (TR) is insufficiency of the tricuspid valve causing blood flow from the right ventricle to the right atrium during systole. The most common cause is dilation of the right ventricle. […] Secondary tricuspid regurgitation is due to leaflet tethering, which is the result of reduced leaflet coaptation caused by annular dilation (typical of right atrial dilation caused by chronic atrial fibrillation) and/or papillary muscle displacement (most commonly as a result of left heart disease causing pulmonary hypertension and leading to RV dilation or geometric distortion). […] Long-standing severe TR may lead to RV dysfunction-induced heart failure and atrial fibrillation. […] Severe tricuspid regurgitation ultimately has a poor prognosis, even if it is initially well-tolerated for years. Less severe TR also affects prognosis, though no study has conclusively shown that early intervention reduces mortality.
- #2 Tricuspid valve regurgitation – Symptoms and causes – Mayo Clinichttps://www.mayoclinic.org/diseases-conditions/tricuspid-valve-regurgitation/symptoms-causes/syc-20350168
Tricuspid valve regurgitation might happen if wires from a pacemaker or defibrillator cross the tricuspid valve. […] In severe tricuspid valve regurgitation, the heart has to work harder to pump enough blood to the body. The extra effort causes the lower right heart chamber to get bigger. Untreated, the heart muscle becomes weak. This can cause heart failure.
- #2 Tricuspid Regurgitation: No Longer the âForgottenâ Valve – European Medical Journalhttps://www.emjreviews.com/cardiology/article/tricuspid-regurgitation-no-longer-the-forgotten-valve/
Valve regurgitation remains the principal pathology of the TV and it is more often secondary rather than caused by a primary valve lesion. Annular dilatation and increased tricuspid leaflet tethering in relation to high right ventricular (RV) pressure and/or volume overload cause secondary TR. Left-sided heart disease, atrial fibrillation, or pulmonary hypertension are frequently involved in the pathogenesis of TR. […] Shortly, the pathophysiology of functional TR can be divided into three phases. Initially, left-side heart disease, may determine impairment of RV, with progressive dilatation, which can lead to tricuspid annulus (TA) enlargement. In the second phase, the progressive dilation of the RV and TA can result in a poor leaflet coaptation leading to significant TR. Finally, in the third phase continuous distortion of RV geometry especially on the anterior wall associated with tethering of the leaflets will get worse the degree of TR. […] Unfortunately, TR has a silent evolution and patients are often referred in the latest phase, when they present with RV dysfunction and an important gap coaptation.
- #3 Tricuspid Regurgitationhttps://www.my-connext.com/valvular-diseases/tricuspid/overview
Tricuspid Regurgitation (TR) is a complex disease that has multiple causes, and is associated with high rates of morbidity and mortality. TR is highly prevalent, and among valve diseases, is one of the most undertreated. If left untreated, TR initiates a cascade of events that can lead to right-sided Heart Failure (HF) and death. […] TR occurs when the tricuspid valve does not close sufficiently during ventricular contraction (systole), and consequently allows blood to flow backwards through the tricuspid valve from the right ventricle into the RA. TR places substantial strain on the heart, as the heart must work harder to pump blood into the right ventricle, against the backflow of blood regurgitating through the tricuspid valve. […] TR can be classified as primary (e.g. degenerative) or secondary (functional), depending on the underlying cause of the condition, and some patients may present with a mixed aetiology, although this is uncommon. TR is commonly associated with HF, Atrial Fibrillation (AF), pulmonary hypertension, drug use, and cardiac device implantation (e.g. pacemaker leads).
- #3 Tricuspid regurgitation – Wikipediahttps://en.wikipedia.org/wiki/Tricuspid_regurgitation
Tricuspid regurgitation (TR), also called tricuspid insufficiency, is a type of valvular heart disease in which the tricuspid valve of the heart, located between the right atrium and right ventricle, does not close completely when the right ventricle contracts (systole). TR allows the blood to flow backwards from the right ventricle to the right atrium, which increases the volume and pressure of the blood both in the right atrium and the right ventricle, which may increase central venous volume and pressure if the backward flow is sufficiently severe. […] The mechanism of TR is either a dilatation of the base (annulus) of the valve due to right ventricular dilatation, which results in the three leaflets being too far apart to reach one another; or an abnormality of one or more of the three leaflets.
- #3 From Neglected to Noticed: A Contemporary Understanding of Tricuspid Regurgitation Pathophysiology – Cardiac Interventions Todayhttps://citoday.com/articles/2021-july-aug/from-neglected-to-noticed-a-contemporary-understanding-of-tricuspid-regurgitation-pathophysiology
With the increasing awareness of the adverse impact of tricuspid regurgitation (TR) on outcomes, the need to understand the pathophysiology of this disease has grown. […] Understanding the anatomy and physiology of these components is important for the diagnosis and optimal planning of repair procedures. […] We show that functional TR is multifactorial, resulting from pulmonary hypertension, atrial fibrillation (AFib), and RV and RA remodeling. […] TR can be divided into primary and secondary causes. […] Primary TR can be caused by congenital or acquired disease processes that affect the leaflets, chordal structures, or both. […] Common causes for primary TR include rheumatic disease, endocarditis, carcinoid, radiation, drug-induced TR, flail leaflets, or congenital diseases. […] Secondary TR is much more common and can be categorized either by the etiology (disease process) or mechanism (morphologic abnormality of the tricuspid apparatus).
- #3 Functional tricuspid regurgitation: Feasibility of transcatheter interventions | Cleveland Clinic Journal of Medicinehttps://www.ccjm.org/content/87/5_suppl_1/4
Functional tricuspid regurgitation (TR) develops secondary to annular dilation and leaflet tethering as a result of right ventricular remodeling. […] RV or annular dilation and tethering of the leaflets are the 2 main pathophysiologic mechanisms for the development of functional TR. While this is mostly secondary to left-sided disease, it may also be associated with isolated RV disease or pulmonary hypertension. The TR that develops through these mechanisms leads to further RV dilation and dysfunction and more tricuspid annular dilation and tethering, thereby progressively worsening the existing TR. This vicious cycle perpetuates TR and forms an integral part of the pathophysiology of severe TR. […] Anatomically, in patients with functional TR, the annulus is larger, flatter, and more circular thereby altering the saddle shape of a normal valve. The dilation of the tricuspid annulus in functional TR is not symmetric. It has been shown that the anteroposterior distance increases by approximately 80%, whereas the mediolateral distance increases by only 34%. This is because of a greater dilation along the free-wall aspect of the annulus.
- #3 Tricuspid valve regurgitation: no longer the âforgotten valveâhttps://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-16/Tricuspid-valve-regurgitation-no-longer-the-forgotten-valve
Tricuspid regurgitation (TR) is a highly prevalent valvular heart disease. […] Secondary or functional TR (caused by dilatation of the tricuspid annulus and remodelling of the right ventricle and right atrium) is the predominant cause, and isolated TR, associated with atrial fibrillation, is an emerging entity. […] In secondary TR, the underlying mechanism is characterised by RV dilation and dysfunction, leading to leaflet tethering, tricuspid annulus dilation and leaflet malcoaptation. […] This is most often caused by significant left-sided valvular and myocardial disease, which leads to increased left-sided pressures, pulmonary hypertension, increased RV afterload and remodelling of the RV. […] In isolated TR, the underlying mechanism is pronounced right atrial and tricuspid annular dilation, leading to leaflet malcoaptation, in the absence of any pronounced RV remodelling. […] The advent of advanced imaging techniques has provided novel insights into the important role of right heart remodelling in the pathophysiology of TR which may lead to improved risk stratification and more timely intervention in the near future.
- #3 Etiology, epidemiology, pathophysiology and management of tricuspid regurgitation: an overviewhttps://www.imrpress.com/journal/RCM/22/4/10.31083/j.rcm2204122/htm
FTR is essentially due to right atrium and/or right ventricle dilation with variable degrees of TA dilation and leaflet tethering, according to the underlying cause. FTR is thereby not a valvular disease; it is an abnormality which results from a disease process that primarily affects the atrium or ventricle and subsequently alters the TA size and the mode of TV leaflet coaptation. […] The mechanisms leading to TR are different and heterogeneous for each disease in the case of primary TR. Examples of resulting structural damage are leaflet perforation or restriction, commissural fusion, and chordal tethering or rupture. Primary TR results in pure volume overload of the right heart and therefore is usually associated with annular dilation. […] The most common type of FTR is the one associated with PH. Long-standing PH causes RV maladaptive remodeling mainly at the expense of the antero-lateral wall at the mid-ventricular level. This leads to papillary muscles displacement (bringing the anterior papillary muscle into a more caudal position) and subsequently TV leaflet tethering. Thus PH-FTR is essentially due to valve deformation with leaflet tethering and only modest annular enlargement.
- #3 Tricuspid Regurgitation Therapy | ECR Journalhttps://www.ecrjournal.com/articles/tricuspid-regurgitation-disease-state-and-advances-percutaneous-therapy?language_content_entity=en
Severe tricuspid regurgitation (TR), which affects 1.6 million people in the US, leads to progressive right ventricular (RV) dilation and failure if left untreated. […] In this review, we discuss the pathophysiological and epidemiological aspects of TR, and provide a critical overview of the current and future directions of therapy focusing on novel percutaneous approaches. […] Together, the bicuspid-like valvular behaviour and the accessory chordal attachments of leaflets form the critical structural basis for the susceptibility of TV to annular dilation and malcoaptation, leading to TR. […] The tricuspid annulus is very elastic and can change markedly by RV preload, afterload, and systolic function. For this reason, the overall volume status and RV function tend to have significant influence on the degree of TR.
- #3 Tricuspid regurgitation: what is the real clinical impact and how often should it be treated? | EuroInterventionhttps://eurointervention.pcronline.com/article/tricuspid-regurgitation-what-is-the-real-clinical-impact-and-how-often-should-it-be-treated
The pathophysiology and clinical manifestations of TR are characterised by the consequences of increased RA-RV pressure and volume and decrease in cardiac output. […] The presence of right heart failure symptoms and/or exertional dyspnoea in patients without left-sided heart disease should always raise the suspicion of severe TR. […] Although there are studies attempting to evaluate the natural history and prognostic impact of FTR, their findings have sometimes been contradictory, with large variations in outcomes and debate as to whether TR severity, RV function, the underlying FTR aetiology or a combination are the predictors of poor outcome. […] The most cited article demonstrating the negative prognostic impact of FTR showed that, in a retrospective evaluation of 5,223 patients, mortality increased with increasing severity of TR.
- #3 Tricuspid Regurgitationhttps://www.my-connext.com/valvular-diseases/tricuspid/overview
Approximately 10-20% of cases are due to primary TR, which is diagnosed in the presence of abnormal tricuspid valve morphology. The causes of primary TR include congenital abnormalities, infection (i.e. endocarditis), rheumatic disease, chest cavity trauma, tumors, and intravenous drug use. Structural damage to the tricuspid valve during cardiac device implantation is another common cause of primary TR. […] Secondary TR is the most common form, occurring in 80-90% of cases, and is diagnosed in the presence of normal tricuspid valve morphology. The causes of secondary TR include changes in the right ventricle or distortion of the tricuspid valve leaflets, annulus or chords. The condition typically occurs secondary to LSHD and/or Right Ventricular (RV) remodelling, Pulmonary Hypertension (HT), tricuspid annular dilation, AF or RV dysfunction. This can make it difficult to isolate the risk factors that contribute to secondary TR independently of comorbid or underlying cardiac disease(s).
- #3 Tricuspid regurgitation â Part 1: evaluation and risk stratificationhttps://www.escardio.org/Councils/Council-for-Cardiology-Practice-(CCP)/Cardiopractice/tricuspid-regurgitation-part-1-evaluation-and-risk-stratification
Tricuspid regurgitation (TR) is classified according to its underlying pathomechanism into primary and secondary TR (STR). Primary TR (PTR) is rare, presenting in fewer than 10% of cases and is associated with abnormal leaflet morphology. Usually, PTR is observed in congenital or rheumatic heart disease or can be the consequence of infective endocarditis. Infrequently repeated myocardial biopsies after (orthotropic) heart transplant can lead to PTR. […] STR is the more prevalent pathomechanism and is due to changes in the atrial and/or ventricular geometry, leading to tethering of the leaflets or dilatation of the annulus and is usually caused by left heart disease or pulmonary hypertension. Atrial STR is newly recognised as a separate aetiology, due to long-standing atrial fibrillation (and age) with atrial remodelling. With more cardiac electronic devices being implanted, cardiac implantable electronic devices (CIED)-related TR has increased and represent a distinct entity necessitating interdisciplinary approach and management.