Tricuspid regurgitation pathophysiology: Difference between revisions

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__NOTOC__
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{{Tricuspid regurgitation}}
{{Tricuspid regurgitation}}
{{CMG}} {{AE}} {{Rim}} {{FB}}
{{CMG}} ; {{AE}} {{Rim}} ; {{FB}} ; {{VKG}}


==Overview==
==Overview==
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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]].<ref name="pmid3536106">{{cite journal| author=Waller BF| title=Etiology of pure tricuspid regurgitation. | journal=Cardiovasc Clin | year= 1987 | volume= 17 | issue= 2 | pages= 53-95 | pmid=3536106 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3536106  }}</ref>
* 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.<ref name="pmid19215833">{{cite journal| author=Mullens W, Abrahams Z, Francis GS, Sokos G, Taylor DO, Starling RC | display-authors=etal| title=Importance of venous congestion for worsening of renal function in advanced decompensated heart failure. | journal=J Am Coll Cardiol | year= 2009 | volume= 53 | issue= 7 | pages= 589-596 | pmid=19215833 | doi=10.1016/j.jacc.2008.05.068 | pmc=2856960 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19215833  }}</ref>
*Impaired [[renal function]] ensues in the presence of increased central and [[renal]] [[venous]] pressure.<ref name="pmid19041045">{{cite journal| author=Maeder MT, Holst DP, Kaye DM| title=Tricuspid regurgitation contributes to renal dysfunction in patients with heart failure. | journal=J Card Fail | year= 2008 | volume= 14 | issue= 10 | pages= 824-30 | pmid=19041045 | doi=10.1016/j.cardfail.2008.07.236 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19041045  }}</ref>


===Primary Tricuspid Regurgitation===
===Primary Tricuspid Regurgitation===


* Primary TR results from an organic abnormality in one or more parts of the [[tricuspid valve]]. <ref name="pmid19470900" /><ref name="pmid28706863">{{cite journal |vauthors=Adler DS |title=Non-functional tricuspid valve disease |journal=Ann Cardiothorac Surg |volume=6 |issue=3 |pages=204–213 |date=May 2017 |pmid=28706863 |pmc=5494423 |doi=10.21037/acs.2017.04.04 |url=}}</ref>
* Primary TR results from an organic abnormality in one or more parts of the [[tricuspid valve]]. <ref name="pmid19470900" /><ref name="pmid17400120">{{cite journal| author=Mutlak D, Lessick J, Reisner SA, Aronson D, Dabbah S, Agmon Y| title=Echocardiography-based spectrum of severe tricuspid regurgitation: the frequency of apparently idiopathic tricuspid regurgitation. | journal=J Am Soc Echocardiogr | year= 2007 | volume= 20 | issue= 4 | pages= 405-8 | pmid=17400120 | doi=10.1016/j.echo.2006.09.013 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17400120  }}</ref><ref name="pmid28706863">{{cite journal |vauthors=Adler DS |title=Non-functional tricuspid valve disease |journal=Ann Cardiothorac Surg |volume=6 |issue=3 |pages=204–213 |date=May 2017 |pmid=28706863 |pmc=5494423 |doi=10.21037/acs.2017.04.04 |url=}}</ref><ref name="pmid18222317">{{cite journal| author=Shah PM, Raney AA| title=Tricuspid valve disease. | journal=Curr Probl Cardiol | year= 2008 | volume= 33 | issue= 2 | pages= 47-84 | pmid=18222317 | doi=10.1016/j.cpcardiol.2007.10.004 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18222317  }}</ref>
* Conditions that might contribute to the primary distortion of the [[tricuspid valve]] include [[rheumatic heart disease]] and [[congenital]], [[iatrogenic]], or [[infectious]] etiologies.
* Conditions that might contribute to the primary distortion of the [[tricuspid valve]] include:<ref name="pmid19179197">{{cite journal| author=Shiran A, Sagie A| title=Tricuspid regurgitation in mitral valve disease incidence, prognostic implications, mechanism, and management. | journal=J Am Coll Cardiol | year= 2009 | volume= 53 | issue= 5 | pages= 401-8 | pmid=19179197 | doi=10.1016/j.jacc.2008.09.048 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19179197  }}</ref><ref name="pmid3958362">{{cite journal| author=Waller BF, Moriarty AT, Eble JN, Davey DM, Hawley DA, Pless JE| title=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. | journal=J Am Coll Cardiol | year= 1986 | volume= 7 | issue= 5 | pages= 1063-74 | pmid=3958362 | doi=10.1016/s0735-1097(86)80224-8 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3958362  }}</ref><ref name="pmid39583622">Waller BF, Moriarty AT, Eble JN, Davey DM, Hawley DA, Pless JE (1986) [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=3958362 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. [http://dx.doi.org/10.1016/s0735-1097(86)80224-8 DOI:10.1016/s0735-1097(86)80224-8] PMID: [https://pubmed.gov/3958362 3958362]</ref>
**[[Rheumatic heart disease]]
**[[Marantic endocarditis]]
**[[Drug-induced]] [[tricuspid regurgitation]] by using drugs like [[fenfluramine]], [[phentermine]] and [[pergolide]]<ref name="pmid15277624">{{cite journal| author=Baseman DG, O'Suilleabhain PE, Reimold SC, Laskar SR, Baseman JG, Dewey RB| title=Pergolide use in Parkinson disease is associated with cardiac valve regurgitation. | journal=Neurology | year= 2004 | volume= 63 | issue= 2 | pages= 301-4 | pmid=15277624 | doi=10.1212/01.wnl.0000129842.49926.07 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15277624  }}</ref><ref name="pmid12479512">{{cite journal| author=Pritchett AM, Morrison JF, Edwards WD, Schaff HV, Connolly HM, Espinosa RE| title=Valvular heart disease in patients taking pergolide. | journal=Mayo Clin Proc | year= 2002 | volume= 77 | issue= 12 | pages= 1280-6 | pmid=12479512 | doi=10.4065/77.12.1280 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12479512  }}</ref>
**[[Ischemic heart disease]] in which the damages to [[right ventricle]] and [[Papillary muscle|papillary muscles]] rupture
**By placing a permanent [[pacemaker]]
**[[Implantable cardioverter defibrillator|Implantable cardioverter-defibrillator]] lead placement
**[[Endomyocardial]] [[biopsy]] in cardiac transplant recipients
**[[Congenital]] etiologies like [[ebstein's anomaly]] and [[Marfan's syndrome|marfan syndrome]]
**[[Carcinoid syndrome]]
**[[Iatrogenic]] etiologies
**[[Infectious]] etiologies which include [[infective endocarditis]].


===Secondary Tricuspid Regurgitation===
===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.<ref name="pmidPMID: 27048553">{{cite journal| author=Rodés-Cabau J, Taramasso M, O'Gara PT| title=Diagnosis and treatment of tricuspid valve disease: current and future perspectives. | journal=Lancet | year= 2016 | volume= 388 | issue= 10058 | pages= 2431-2442 | pmid=PMID: 27048553 | doi=10.1016/S0140-6736(16)00740-6 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27048553  }} </ref> The underlying pathophysiology of secondary TR involves the following changes:<ref name="pmid22340261">{{cite journal| author=Taramasso M, Vanermen H, Maisano F, Guidotti A, La Canna G, Alfieri O| title=The growing clinical importance of secondary tricuspid regurgitation. | journal=J Am Coll Cardiol | year= 2012 | volume= 59 | issue= 8 | pages= 703-10 | pmid=22340261 | doi=10.1016/j.jacc.2011.09.069 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22340261  }} </ref><ref name="pmid6691254">{{cite journal |vauthors=Mikami T, Kudo T, Sakurai N, Sakamoto S, Tanabe Y, Yasuda H |title=Mechanisms for development of functional tricuspid regurgitation determined by pulsed Doppler and two-dimensional echocardiography |journal=Am. J. Cardiol. |volume=53 |issue=1 |pages=160–3 |date=January 1984 |pmid=6691254 |doi=10.1016/0002-9149(84)90702-1 |url=}}</ref><ref name="pmid26022823">{{cite journal |vauthors=Dreyfus GD, Martin RP, Chan KM, Dulguerov F, Alexandrescu C |title=Functional tricuspid regurgitation: a need to revise our understanding |journal=J. Am. Coll. Cardiol. |volume=65 |issue=21 |pages=2331–6 |date=June 2015 |pmid=26022823 |doi=10.1016/j.jacc.2015.04.011 |url=}}</ref><ref name="pmid23647591">{{cite journal |vauthors=Di Mauro M, Bezante GP, Di Baldassarre A, Clemente D, Cardinali A, Acitelli A, Salerni S, Penco M, Calafiore AM, Gallina S |title=Functional tricuspid regurgitation: an underestimated issue |journal=Int. J. Cardiol. |volume=168 |issue=2 |pages=707–15 |date=September 2013 |pmid=23647591 |doi=10.1016/j.ijcard.2013.04.043 |url=}}</ref><ref name="pmid26050849">{{cite journal |vauthors=Nemoto N, Lesser JR, Pedersen WR, Sorajja P, Spinner E, Garberich RF, Vock DM, Schwartz RS |title=Pathogenic structural heart changes in early tricuspid regurgitation |journal=J. Thorac. Cardiovasc. Surg. |volume=150 |issue=2 |pages=323–30 |date=August 2015 |pmid=26050849 |doi=10.1016/j.jtcvs.2015.05.009 |url=}}</ref>
 
* 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]].<ref name="pmidPMID: 27048553">{{cite journal| author=Rodés-Cabau J, Taramasso M, O'Gara PT| title=Diagnosis and treatment of tricuspid valve disease: current and future perspectives. | journal=Lancet | year= 2016 | volume= 388 | issue= 10058 | pages= 2431-2442 | pmid=PMID: 27048553 | doi=10.1016/S0140-6736(16)00740-6 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27048553  }} </ref><ref name="pmid8034882">{{cite journal| author=Sagie A, Schwammenthal E, Padial LR, Vazquez de Prada JA, Weyman AE, Levine RA| title=Determinants of functional tricuspid regurgitation in incomplete tricuspid valve closure: Doppler color flow study of 109 patients. | journal=J Am Coll Cardiol | year= 1994 | volume= 24 | issue= 2 | pages= 446-53 | pmid=8034882 | doi=10.1016/0735-1097(94)90302-6 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8034882  }}</ref>
* The underlying pathophysiology of secondary TR involves the following changes:<ref name="pmid22340261">{{cite journal| author=Taramasso M, Vanermen H, Maisano F, Guidotti A, La Canna G, Alfieri O| title=The growing clinical importance of secondary tricuspid regurgitation. | journal=J Am Coll Cardiol | year= 2012 | volume= 59 | issue= 8 | pages= 703-10 | pmid=22340261 | doi=10.1016/j.jacc.2011.09.069 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22340261  }} </ref><ref name="pmid6691254">{{cite journal |vauthors=Mikami T, Kudo T, Sakurai N, Sakamoto S, Tanabe Y, Yasuda H |title=Mechanisms for development of functional tricuspid regurgitation determined by pulsed Doppler and two-dimensional echocardiography |journal=Am. J. Cardiol. |volume=53 |issue=1 |pages=160–3 |date=January 1984 |pmid=6691254 |doi=10.1016/0002-9149(84)90702-1 |url=}}</ref><ref name="pmid26022823">{{cite journal |vauthors=Dreyfus GD, Martin RP, Chan KM, Dulguerov F, Alexandrescu C |title=Functional tricuspid regurgitation: a need to revise our understanding |journal=J. Am. Coll. Cardiol. |volume=65 |issue=21 |pages=2331–6 |date=June 2015 |pmid=26022823 |doi=10.1016/j.jacc.2015.04.011 |url=}}</ref><ref name="pmid23647591">{{cite journal |vauthors=Di Mauro M, Bezante GP, Di Baldassarre A, Clemente D, Cardinali A, Acitelli A, Salerni S, Penco M, Calafiore AM, Gallina S |title=Functional tricuspid regurgitation: an underestimated issue |journal=Int. J. Cardiol. |volume=168 |issue=2 |pages=707–15 |date=September 2013 |pmid=23647591 |doi=10.1016/j.ijcard.2013.04.043 |url=}}</ref><ref name="pmid26050849">{{cite journal |vauthors=Nemoto N, Lesser JR, Pedersen WR, Sorajja P, Spinner E, Garberich RF, Vock DM, Schwartz RS |title=Pathogenic structural heart changes in early tricuspid regurgitation |journal=J. Thorac. Cardiovasc. Surg. |volume=150 |issue=2 |pages=323–30 |date=August 2015 |pmid=26050849 |doi=10.1016/j.jtcvs.2015.05.009 |url=}}</ref>
   
   
* [[Left heart failure]] and/or [[pulmonary hypertension]] causes dilation of the [[right ventricle]] and subsequent tricuspid annular dilation.  
* [[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 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.
*The conditions that might lead to [[pulmonary hypertension]] and [[Right ventricle|right ventricular]] dilation include the following:
**[[Left heart failure]]
**[[Mitral stenosis]] / [[mitral regurgitation]]
**Pulmonic valve [[stenosis]]
**[[Pulmonary artery stenosis]]
**[[Pulmonary disease]]
**[[Shunt (medical)|Shunt]] from left to right
**[[Eisenmenger's syndrome|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.<ref name="pmid22340261">{{cite journal| author=Taramasso M, Vanermen H, Maisano F, Guidotti A, La Canna G, Alfieri O| title=The growing clinical importance of secondary tricuspid regurgitation. | journal=J Am Coll Cardiol | year= 2012 | volume= 59 | issue= 8 | pages= 703-10 | pmid=22340261 | doi=10.1016/j.jacc.2011.09.069 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22340261  }} </ref>
* 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.<ref name="pmid22340261">{{cite journal| author=Taramasso M, Vanermen H, Maisano F, Guidotti A, La Canna G, Alfieri O| title=The growing clinical importance of secondary tricuspid regurgitation. | journal=J Am Coll Cardiol | year= 2012 | volume= 59 | issue= 8 | pages= 703-10 | pmid=22340261 | doi=10.1016/j.jacc.2011.09.069 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22340261  }} </ref>


==References==
==References==

Latest revision as of 15:40, 3 May 2020

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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]

Pathogenesis

Primary Tricuspid Regurgitation

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]
  • 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. ↑ 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.
  2. ↑ 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.
  3. ↑ 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.
  4. ↑ 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. ↑ 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. ↑ 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).
  7. ↑ Waller BF (1987). "Etiology of pure tricuspid regurgitation". Cardiovasc Clin. 17 (2): 53–95. PMID 3536106.
  8. ↑ 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.
  9. ↑ 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.
  10. ↑ 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.
  11. ↑ 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.
  12. ↑ 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.
  13. ↑ 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.
  14. ↑ 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.
  15. ↑ 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
  16. ↑ 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.
  17. ↑ 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.
  18. ↑ 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.
  19. ↑ 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.
  20. ↑ 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.
  21. ↑ 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.
  22. ↑ 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.

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