Tricuspid regurgitation pathophysiology: Difference between revisions
Rim Halaby (talk | contribs) No edit summary |
No edit summary |
||
Line 4: | Line 4: | ||
==Overview== | ==Overview== | ||
Tricuspid regurgitation (TR) | 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.<ref name="pmid19470900">{{cite journal| author=Rogers JH, Bolling SF| title=The tricuspid valve: current perspective and evolving management of tricuspid regurgitation. | journal=Circulation | year= 2009 | volume= 119 | issue= 20 | pages= 2718-25 | pmid=19470900 | doi=10.1161/CIRCULATIONAHA.108.842773 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19470900 }} </ref> 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.<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> | ||
==Pathophysiology== | ==Pathophysiology== | ||
Line 14: | Line 14: | ||
===Primary Tricuspid Regurgitation=== | ===Primary Tricuspid Regurgitation=== | ||
Primary TR results from an organic abnormality in one or more parts of the [[tricuspid valve]]. | 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.<ref name="pmid19470900">{{cite journal| author=Rogers JH, Bolling SF| title=The tricuspid valve: current perspective and evolving management of tricuspid regurgitation. | journal=Circulation | year= 2009 | volume= 119 | issue= 20 | pages= 2718-25 | pmid=19470900 | doi=10.1161/CIRCULATIONAHA.108.842773 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19470900 }} </ref> | ||
===Secondary Tricuspid Regurgitation=== | ===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:<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> | 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:<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> | ||
* [[Left heart failure]] and/or [[pulmonary hypertension]] | * [[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 that causes 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 that causes tethering of the leaflets. | ||
* When secondary TR is present, it causes further progressive right ventricular remodelling which distort normal leaflet coaptation. | * When secondary TR is present, it causes further progressive right ventricular remodelling which distort normal leaflet coaptation. |
Revision as of 19:12, 13 December 2016
Tricuspid Regurgitation Microchapters |
Diagnosis |
---|
Treatment |
Case Studies |
Tricuspid regurgitation pathophysiology On the Web |
American Roentgen Ray Society Images of Tricuspid regurgitation pathophysiology |
Risk calculators and risk factors for Tricuspid regurgitation pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Rim Halaby, M.D. [2]
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.[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 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 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.