Tricuspid regurgitation pathophysiology: Difference between revisions
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* [[Chordae tendineae]] | * [[Chordae tendineae]] | ||
* [[Papillary muscle]]s | * [[Papillary muscle]]s | ||
=== Pathogenesis === | |||
* The pathogenesis of the tricuspid regurgitation involves backflow of blood into the right atrium during systole. | |||
* 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 | |||
===Primary Tricuspid Regurgitation=== | ===Primary Tricuspid Regurgitation=== | ||
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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
Pathogenesis
- The pathogenesis of the tricuspid regurgitation involves backflow of blood into the right atrium during systole.
- 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
Primary Tricuspid Regurgitation
- Primary TR results from an organic abnormality in one or more parts of the tricuspid valve. [5][7][8]
- Conditions that might contribute to the primary distortion of the tricuspid valve include:
- Rheumatic heart disease
- Marantic endocarditis
- Drug-induced tricuspid regurgitation by using drugs like fenfluramine, phentermine and pergolide[9][10]
- 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
- 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][11][12][13][14]
- 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 remodeling 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). - ↑ 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.
- ↑ 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.
- ↑ 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.