|Other names||Tricuspid regurgitation|
|Echocardiogram showing typical findings in severe tricuspid regurgitation|
|Causes||Abnormally high blood pressure , other heart problem|
Tricuspid insufficiency (TI), more commonly called tricuspid regurgitation (TR), 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 causes of TR are divided into hereditary and acquired; and also primary and secondary. Primary TR refers to a defect solely in the tricuspid valve, such as infective endocarditis; secondary TR refers to a defect in the valve as a consequence of some other pathology, such as left ventricular failure or pulmonary hypertension.
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.
Signs and symptoms
A pansystolic heart murmur may be heard on auscultation of the chest. The murmur is usually of low frequency and best heard on the lower left sternal border. It increases with inspiration, and decreases with expiration: this is known as Carvallo's sign. However, the murmur may be inaudible due to the relatively low pressures in the right side of the heart. A third heart sound may also be present, also heard at the lower sternal border, and increasing in intensity with inspiration.
On examination of the neck, there may be giant C-V waves in the jugular pulse. With severe TR, there may be an enlarged liver detected on palpation of the right upper quadrant of the abdomen; the liver may be pulsatile on palpation and even on inspection.
The causes of TR may be classified as congenital or acquired; another classification divides the causes into primary or secondary. Congenital abnormalities are much less common than acquired. The most common acquired TR is due to right ventricular dilatation. Such dilatation is most often due left heart failure or pulmonary hypertension. Other causes of right ventricular dilatation include right ventricular infarction, inferior myocardial infarction, and cor pulmonale.[medical citation needed]
In regards to primary and secondary causes they are:
- Primary causes
- Secondary causes
In terms of the mechanism of tricuspid insufficiency it involves the expansion of the tricuspid annulus (fibrous rings of heart). Tricuspid insufficiency is linked to geometric changes of the tricuspid annulus (decreased tricuspid annular release). The leaflets shape are normal but prevented from normal working mechanism due to a distortion of spatial relationships of leaflets and chords. It is also contemplated that the process via which tricuspid regurgitation emerges, is a decrease of contraction of the myocardium around the annulus,
The diagnosis of TR may be suspected if the typical murmur of TR is heard. Severe TR may be suspected if right ventricular enlargement is seen on chest x-ray, and other causes of this enlargement are ruled out.
Generally, medical rather than surgical treatment of TR is recommended if the cause is right ventricular dilatation or left-sided heart failure.
Tricuspid valve replacement using either a mechanical prosthesis or a bioprosthesis may be indicated. (Mechanical prostheses may cause thrombo‐embolic phenomena, bioprostheses may have a degeneration problem). Some evidence suggests that there are no significant differences between a mechanical or biological tricuspid valve in a recipient.
Surgery vs. no surgery for TR has been statistically assessed by looking back on consecutive series of hospital cases, mainly of secondary causes. In these cases, one finds that surgery predicts outliving non-surgery cases initially matched in health ~60% of the time (HR = .74).
The prognosis of TR is less favorable for males than females. Survival rates are proportional to TR severity; but even mild TR reduces survival compared to those with no TR. If the TR is due to left heart failure or pulmonary hypertension, prognosis is usually dictated by these conditions, not the TR.[medical citation needed]
- MedlinePlus Encyclopedia Tricuspid regurgitation
- Tricuspid Regurgitation~clinical at eMedicine
- "Tricuspid Valve Disease & Tricuspid regurgitation (TR) | Patient". Patient. Retrieved 2015-12-14.
- Berg, Dale; Worzala, Katherine (2006-01-01). Atlas of Adult Physical Diagnosis. Lippincott Williams & Wilkins. p. 90. ISBN 9780781741903.
- Rehman, Habib Ur (2013). "Giant C-V Waves of Tricuspid Regurgitation". New England Journal of Medicine. 369 (20): e27. doi:10.1056/NEJMicm1103312. PMID 24224640.
- Said, Sameh M; Dearani, Joseph A; Burkhart, Harold M; Connolly, Heidi M; Eidem, Ben; Stensrud, Paul E; Schaff, Hartzell V (2014). "Management of tricuspid regurgitation in congenital heart disease: Is survival better with valve repair?". The Journal of Thoracic and Cardiovascular Surgery. 147 (1): 412–419. doi:10.1016/j.jtcvs.2013.08.034. PMID 24084288.
- Rogers, J. H; Bolling, S. F (2009). "The Tricuspid Valve: Current Perspective and Evolving Management of Tricuspid Regurgitation". Circulation. 119 (20): 2718–2725. doi:10.1161/CIRCULATIONAHA.108.842773. PMID 19470900.
- Hung, Judy (2010). "The Pathogenesis of Functional Tricuspid Regurgitation". Seminars in Thoracic and Cardiovascular Surgery. 22 (1): 76–78. doi:10.1053/j.semtcvs.2010.05.004. PMID 20813321.
- Antunes, M. J; Barlow, J. B (2005). "Management of tricuspid valve regurgitation". Heart. 93 (2): 271–276. doi:10.1136/hrt.2006.095281. PMC 1861404. PMID 17228081.
- Shah PM, Raney AA; Tricuspid valve disease. Curr Probl Cardiol. 2008 Feb33(2):47-84
- Tricuspid Regurgitation~treatment at eMedicine
- "BestBets: Should the tricuspid valve be replaced with a mechanical or biological valve?". www.bestbets.org. Retrieved 2015-12-14.
- Kelly, Brian J.; Ho Luxford, Jamahal Maeng; Butler, Carolyn Goldberg; Huang, Chuan-Chin; Wilusz, Kerry; Ejiofor, Julius I.; Rawn, James D.; Fox, John A.; Shernan, Stanton K.; Muehlschlegel, Jochen Daniel (2018). "Severity of tricuspid regurgitation is associated with long-term mortality". The Journal of Thoracic and Cardiovascular Surgery. 155 (3): 1032–1038.e2. doi:10.1016/j.jtcvs.2017.09.141. ISSN 1097-685X. PMC 5819734. PMID 29246545. – via ScienceDirect (Subscription may be required or content may be available in libraries.)
- Nath, Jayant; Foster, Elyse; Heidenreich, Paul A (2004). "Impact of tricuspid regurgitation on long-term survival". Journal of the American College of Cardiology. 43 (3): 405–409. doi:10.1016/j.jacc.2003.09.036. PMID 15013122.
- Haddad, F; Doyle, R; Murphy, D. J; Hunt, S. A (2008). "Right Ventricular Function in Cardiovascular Disease, Part II: Pathophysiology, Clinical Importance, and Management of Right Ventricular Failure". Circulation. 117 (13): 1717–1731. doi:10.1161/CIRCULATIONAHA.107.653584. PMID 18378625.
- Desai, Ravi R; Vargas Abello, Lina Maria; Klein, Allan L; Marwick, Thomas H; Krasuski, Richard A; Ye, Ying; Nowicki, Edward R; Rajeswaran, Jeevanantham; Blackstone, Eugene H; Pettersson, Gösta B (2013). "Tricuspid regurgitation and right ventricular function after mitral valve surgery with or without concomitant tricuspid valve procedure". The Journal of Thoracic and Cardiovascular Surgery. 146 (5): 1126–1132.e10. doi:10.1016/j.jtcvs.2012.08.061. PMC 4215162. PMID 23010580.
- Badano, Luigi P; Muraru, Denisa; Enriquez-Sarano, Maurice (2013). "Assessment of functional tricuspid regurgitation". European Heart Journal. 34 (25): 1875–1885. doi:10.1093/eurheartj/ehs474. PMID 23303656.
- al.], Hugh D. Allen ... [et; Shaddy, Robert E.; Feltes, Timothy F. (2013). Moss and Adams heart disease in infants, children, and adolescents : including the fetus and young adult (8th ed.). Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. ISBN 9781451118933.