Tricuspid regurgitation pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
Tricuspid regurgitation (TR) results in a retrograde flow of blood into the right atrium due to the incompetent tricuspid valve. The pathophysiology of TR depends on whether TR is primary or secondary. Primary TR results from an organic abnormality in one or more parts of the [[tricuspid valve]], such as the leaflets, [[chordae tendineae]], or [[papillary muscle]]s. | [[Tricuspid regurgitation]] (TR) results in a retrograde flow of blood into the [[right atrium]] due to the incompetent [[tricuspid valve]]. The [[pathophysiology]] of TR depends on whether TR is primary or secondary. Primary TR results from an organic abnormality in one or more parts of the [[tricuspid valve]], such as the leaflets, [[chordae tendineae]], or [[papillary muscle]]s. Secondary TR commonly results from [[Hemodynamics|hemodynamic]] and structural changes in the [[right ventricle]] and [[tricuspid valve]] apparatus secondary to left-sided heart [[pathology]] and/or [[pulmonary hypertension]]. [[Tricuspid]] annular dilation is the most important factor in the [[pathophysiology]] of secondary TR. In addition, tethering of the leaflets and inadequate leaflet coaptation also contribute to secondary TR. | ||
==Pathophysiology== | ==Pathophysiology== | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Rim Halaby, M.D. [2] Fatimo Biobaku M.B.B.S [3]
Overview
Tricuspid regurgitation (TR) results in a retrograde flow of blood into the right atrium due to the incompetent tricuspid valve. The pathophysiology of TR depends on whether TR is primary or secondary. Primary TR results from an organic abnormality in one or more parts of the tricuspid valve, such as the leaflets, chordae tendineae, or papillary muscles. Secondary TR commonly results from hemodynamic and structural changes in the right ventricle and tricuspid valve apparatus secondary to left-sided heart pathology and/or pulmonary hypertension. Tricuspid annular dilation is the most important factor in the pathophysiology of secondary TR. In addition, tethering of the leaflets and inadequate leaflet coaptation also contribute to secondary TR.
Pathophysiology
The Tricuspid Valve Apparatus
The tricuspid valve apparatus includes the following structures:[1][2][3][4][5][6][1]
- Leaflets: septal, anterior, and posterior
- Chordae tendineae
- Papillary muscles
Primary Tricuspid Regurgitation
Primary TR results from an organic abnormality in one or more parts of the tricuspid valve. Conditions that might contribute to the primary distortion of the tricuspid valve include rheumatic heart disease and congenital, iatrogenic, or infectious etiologies.[5][7]
Secondary Tricuspid Regurgitation
More than 80% of the cases of TR seen in clinical practice is secondary(functional) in nature and related to tricuspid annular dilatation and leaflet tethering in the setting of right ventricular remodelling caused by pressure or volume overload (or both), myocardial infarction, or trauma.[6] The underlying pathophysiology of secondary TR involves the following changes:[1][8][9][10][11]
- Left heart failure and/or pulmonary hypertension causes dilation of the right ventricle and subsequent tricuspid annular dilation.
- The tricuspid annular dilatation leads to a disruption of the coordinated function of the papillary muscle, tricuspid leaflets and the tricuspid annulus, causing tethering of the leaflets.
- When secondary TR is present, it causes further progressive right ventricular remodelling which distort normal leaflet coaptation.
In summary, tricuspid annular dilation is the most important factor in the pathophysiology of secondary TR, though tethering of the leaflets and inadequate leaflet coaptation also contribute to secondary TR.[1]
References
- ↑ 1.0 1.1 1.2 1.3 Taramasso M, Vanermen H, Maisano F, Guidotti A, La Canna G, Alfieri O (2012). "The growing clinical importance of secondary tricuspid regurgitation". J Am Coll Cardiol. 59 (8): 703–10. doi:10.1016/j.jacc.2011.09.069. PMID 22340261.
- ↑ Unger P, Clavel MA, Lindman BR, Mathieu P, Pibarot P (July 2016). "Pathophysiology and management of multivalvular disease". Nat Rev Cardiol. 13 (7): 429–40. doi:10.1038/nrcardio.2016.57. PMC 5129845. PMID 27121305.
- ↑ Tornos Mas P, Rodríguez-Palomares JF, Antunes MJ (November 2015). "Secondary tricuspid valve regurgitation: a forgotten entity". Heart. 101 (22): 1840–8. doi:10.1136/heartjnl-2014-307252. PMC 4680164. PMID 26503944.
- ↑ Anyanwu AC (2010). "Functional tricuspid regurgitation: introduction". Semin. Thorac. Cardiovasc. Surg. 22 (1): 67–8. doi:10.1053/j.semtcvs.2010.06.001. PMID 20813319.
- ↑ 5.0 5.1 Rogers JH, Bolling SF (2009). "The tricuspid valve: current perspective and evolving management of tricuspid regurgitation". Circulation. 119 (20): 2718–25. doi:10.1161/CIRCULATIONAHA.108.842773. PMID 19470900.
- ↑ 6.0 6.1 Rodés-Cabau J, Taramasso M, O'Gara PT (2016). "Diagnosis and treatment of tricuspid valve disease: current and future perspectives". Lancet. 388 (10058): 2431–2442. doi:10.1016/S0140-6736(16)00740-6. PMID 27048553 PMID: 27048553 Check
|pmid=value (help). - ↑ Adler DS (May 2017). "Non-functional tricuspid valve disease". Ann Cardiothorac Surg. 6 (3): 204–213. doi:10.21037/acs.2017.04.04. PMC 5494423. PMID 28706863.
- ↑ Mikami T, Kudo T, Sakurai N, Sakamoto S, Tanabe Y, Yasuda H (January 1984). "Mechanisms for development of functional tricuspid regurgitation determined by pulsed Doppler and two-dimensional echocardiography". Am. J. Cardiol. 53 (1): 160–3. doi:10.1016/0002-9149(84)90702-1. PMID 6691254.
- ↑ Dreyfus GD, Martin RP, Chan KM, Dulguerov F, Alexandrescu C (June 2015). "Functional tricuspid regurgitation: a need to revise our understanding". J. Am. Coll. Cardiol. 65 (21): 2331–6. doi:10.1016/j.jacc.2015.04.011. PMID 26022823.
- ↑ Di Mauro M, Bezante GP, Di Baldassarre A, Clemente D, Cardinali A, Acitelli A, Salerni S, Penco M, Calafiore AM, Gallina S (September 2013). "Functional tricuspid regurgitation: an underestimated issue". Int. J. Cardiol. 168 (2): 707–15. doi:10.1016/j.ijcard.2013.04.043. PMID 23647591.
- ↑ Nemoto N, Lesser JR, Pedersen WR, Sorajja P, Spinner E, Garberich RF, Vock DM, Schwartz RS (August 2015). "Pathogenic structural heart changes in early tricuspid regurgitation". J. Thorac. Cardiovasc. Surg. 150 (2): 323–30. doi:10.1016/j.jtcvs.2015.05.009. PMID 26050849.