Tricuspid regurgitation pathophysiology
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
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Overview
Tricuspid regurgitation refers to the failure of the tricuspid valve to close properly during systole. As a result, with each heart beat some blood passes from the right ventricle to the right atrium, the opposite of the normal direction. The pathophysiology of tricuspid regurgitation (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.[1] Secondary TR results from hemodynamic and structural changes in the right ventricle and tricuspid valve apparatus secondary to left heart failure 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.[2]
Pathophysiology
The Tricuspid Valve Apparatus
The tricuspid valve apparatus includes the following structures:[2]
- Leaflets: septal, anterior, and posterior
- Chordae tendineae
- Papillary muscles: anterior, posterior, and a third variable
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, congenital, iatrogenic, and infectious etiologies.[1]
Secondary Tricuspid Regurgitation
Secondary TR results from hemodynamic and structural changes in the right ventricle and tricuspid valve apparatus secondary to left heart failure and/or pulmonary hypertension. The underlying pathophysiology of secondary TR involves the following changes:[2]
- Left heart failure and/or pulmonary hypertension cause a 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 that causes 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. In addition, tethering of the leaflets and inadequate leaflet coaptation also contribute to secondary TR.[2]
References
- ↑ 1.0 1.1 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.
- ↑ 2.0 2.1 2.2 2.3 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.