Tricuspid regurgitation 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] ; Vamsikrishna Gunnam M.B.B.S [4]
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
Pathogenesis
- The pathogenesis of the tricuspid regurgitation involves backflow of blood into the right atrium during systole.[7]
- When compared to other chambers in the heart right atrium is relatively and hemodynamically stable so there are no noticeable consequences with mild to moderate tricuspid regurgitation.
- But when the regurgitation is severe there is noticeable increase in the venous pressure and right atrial pressure which might result in right-sided heart failure.
- Symptoms of right-sided heart failure include:
- Ascites
- Liver failure
- Shortness of breath
- Fatigue
- Edema in ankles, legs, feet and/or abdomen
- Right ventricular systolic dysfunction leads to decreased cardiac output due to continuous rise in right ventricular pressure.[8]
- Impaired renal function ensues in the presence of increased central and renal venous pressure.[9]
Primary Tricuspid Regurgitation
- Primary TR results from an organic abnormality in one or more parts of the tricuspid valve. [5][10][11][12]
- Conditions that might contribute to the primary distortion of the tricuspid valve include:[13][14][15]
- Rheumatic heart disease
- Marantic endocarditis
- Drug-induced tricuspid regurgitation by using drugs like fenfluramine, phentermine and pergolide[16][17]
- Ischemic heart disease in which the damages to right ventricle and papillary muscles rupture
- By placing a permanent pacemaker
- Implantable cardioverter-defibrillator lead placement
- Endomyocardial biopsy in cardiac transplant recipients
- Congenital etiologies like ebstein's anomaly and marfan syndrome
- Carcinoid syndrome
- Iatrogenic etiologies
- Infectious etiologies which include infective endocarditis.
Secondary Tricuspid Regurgitation
- The most common cause of tricuspid regurgitation in adults is secondary / functional which can be defined as without anatomical anomalies and normal leaflet and chords structure.
- 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][18]
- The underlying pathophysiology of secondary TR involves the following changes:[1][19][20][21][22]
- 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.
- The conditions that might lead to pulmonary hypertension and right ventricular dilation include the following:
- Left heart failure
- Mitral stenosis / mitral regurgitation
- Pulmonic valve stenosis
- Pulmonary artery stenosis
- Pulmonary disease
- Shunt from left to right
- Eisenmenger syndrome
- Hyperthyroidism
- When secondary TR is present, it causes further progressive right ventricular remodeling which distorts 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). - ↑ Waller BF (1987). "Etiology of pure tricuspid regurgitation". Cardiovasc Clin. 17 (2): 53–95. PMID 3536106.
- ↑ Mullens W, Abrahams Z, Francis GS, Sokos G, Taylor DO, Starling RC; et al. (2009). "Importance of venous congestion for worsening of renal function in advanced decompensated heart failure". J Am Coll Cardiol. 53 (7): 589–596. doi:10.1016/j.jacc.2008.05.068. PMC 2856960. PMID 19215833.
- ↑ Maeder MT, Holst DP, Kaye DM (2008). "Tricuspid regurgitation contributes to renal dysfunction in patients with heart failure". J Card Fail. 14 (10): 824–30. doi:10.1016/j.cardfail.2008.07.236. PMID 19041045.
- ↑ Mutlak D, Lessick J, Reisner SA, Aronson D, Dabbah S, Agmon Y (2007). "Echocardiography-based spectrum of severe tricuspid regurgitation: the frequency of apparently idiopathic tricuspid regurgitation". J Am Soc Echocardiogr. 20 (4): 405–8. doi:10.1016/j.echo.2006.09.013. PMID 17400120.
- ↑ 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.
- ↑ Shah PM, Raney AA (2008). "Tricuspid valve disease". Curr Probl Cardiol. 33 (2): 47–84. doi:10.1016/j.cpcardiol.2007.10.004. PMID 18222317.
- ↑ Shiran A, Sagie A (2009). "Tricuspid regurgitation in mitral valve disease incidence, prognostic implications, mechanism, and management". J Am Coll Cardiol. 53 (5): 401–8. doi:10.1016/j.jacc.2008.09.048. PMID 19179197.
- ↑ Waller BF, Moriarty AT, Eble JN, Davey DM, Hawley DA, Pless JE (1986). "Etiology of pure tricuspid regurgitation based on anular circumference and leaflet area: analysis of 45 necropsy patients with clinical and morphologic evidence of pure tricuspid regurgitation". J Am Coll Cardiol. 7 (5): 1063–74. doi:10.1016/s0735-1097(86)80224-8. PMID 3958362.
- ↑ Waller BF, Moriarty AT, Eble JN, Davey DM, Hawley DA, Pless JE (1986) Etiology of pure tricuspid regurgitation based on anular circumference and leaflet area: analysis of 45 necropsy patients with clinical and morphologic evidence of pure tricuspid regurgitation. J Am Coll Cardiol 7 (5):1063-74. DOI:10.1016/s0735-1097(86)80224-8 PMID: 3958362
- ↑ Baseman DG, O'Suilleabhain PE, Reimold SC, Laskar SR, Baseman JG, Dewey RB (2004). "Pergolide use in Parkinson disease is associated with cardiac valve regurgitation". Neurology. 63 (2): 301–4. doi:10.1212/01.wnl.0000129842.49926.07. PMID 15277624.
- ↑ Pritchett AM, Morrison JF, Edwards WD, Schaff HV, Connolly HM, Espinosa RE (2002). "Valvular heart disease in patients taking pergolide". Mayo Clin Proc. 77 (12): 1280–6. doi:10.4065/77.12.1280. PMID 12479512.
- ↑ Sagie A, Schwammenthal E, Padial LR, Vazquez de Prada JA, Weyman AE, Levine RA (1994). "Determinants of functional tricuspid regurgitation in incomplete tricuspid valve closure: Doppler color flow study of 109 patients". J Am Coll Cardiol. 24 (2): 446–53. doi:10.1016/0735-1097(94)90302-6. PMID 8034882.
- ↑ 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.