Tricuspid stenosis pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
The pathophysiology of tricuspid stenosis depends on the underlying etiology:<ref name="pmid7720297">{{cite journal| author=Waller BF, Howard J, Fess S| title=Pathology of tricuspid valve stenosis and pure tricuspid regurgitation--Part I. | journal=Clin Cardiol | year= 1995 | volume= 18 | issue= 2 | pages= 97-102 | pmid=7720297 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7720297 }} </ref> | |||
*The tricuspid disease is characterized by diffuse fibrous thickening of the leaflets and fusion of 2 or 3 commissures. | |||
*Leaflet thickening usually occurs in the absence of calcific deposits, and the anteroseptal commissure is most commonly involved. | |||
*Incompletely developed leaflets, shortened or malformed chordae, a small annulus, or an abnormal number or size of papillary muscles may result in TS. | |||
*The valves consist of an outer layer of valve endothelial cells (VECs) surrounding three layers of the extracellular matrix each with specialized function and interspersed with interstitial valve cells (VICs). | |||
*Genetic or acquired/environmental causes that disrupt the normal organization and composition of the extracellular matrix and communication between VECs and VICs alter valve mechanics and interfere with the valve leaflet function, culminating in heart failure. | |||
*The primary result of TS is right atrial pressure elevation and consequent right-sided congestion. | |||
*The pathophysiology of tricuspid stenosis depends on the underlying etiology:<ref name="pmid7720297">{{cite journal| author=Waller BF, Howard J, Fess S| title=Pathology of tricuspid valve stenosis and pure tricuspid regurgitation--Part I. | journal=Clin Cardiol | year= 1995 | volume= 18 | issue= 2 | pages= 97-102 | pmid=7720297 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7720297 }} </ref> | |||
* Rheumatic tricuspid stenosis: | * Rheumatic tricuspid stenosis: | ||
** Diffuse scarring and fibrosis of the valve leaflets from inflammation. Fusion of the commissures may or may not occur. | ** Diffuse scarring and fibrosis of the valve leaflets from inflammation. Fusion of the commissures may or may not occur. | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Fatimo Biobaku M.B.B.S [2]
Overview
Tricuspid stenosis is characterized by structural changes in the tricuspid valve. The pathophysiology of tricuspid valve depends on the underlying etiology. In rheumatic heart disease which is the most common cause of tricuspid stenosis, there is fibrous thickening of the valve leaflets and chordae tendineae with/without fusion of the commissures as a result of inflammation.[1]The obstruction to right ventricular filling due to the stenotic tricuspid valve can result in systemic venous hypertension and congestion.
Pathophysiology
- The tricuspid disease is characterized by diffuse fibrous thickening of the leaflets and fusion of 2 or 3 commissures.
- Leaflet thickening usually occurs in the absence of calcific deposits, and the anteroseptal commissure is most commonly involved.
- Incompletely developed leaflets, shortened or malformed chordae, a small annulus, or an abnormal number or size of papillary muscles may result in TS.
- The valves consist of an outer layer of valve endothelial cells (VECs) surrounding three layers of the extracellular matrix each with specialized function and interspersed with interstitial valve cells (VICs).
- Genetic or acquired/environmental causes that disrupt the normal organization and composition of the extracellular matrix and communication between VECs and VICs alter valve mechanics and interfere with the valve leaflet function, culminating in heart failure.
- The primary result of TS is right atrial pressure elevation and consequent right-sided congestion.
- The pathophysiology of tricuspid stenosis depends on the underlying etiology:[1]
- Rheumatic tricuspid stenosis:
- Diffuse scarring and fibrosis of the valve leaflets from inflammation. Fusion of the commissures may or may not occur.
- Chordae tendineae may become thickened and shortened.
- As a result of the dense collagen and elastic fibers that make up leaflet tissue, the normal leaflet layers become significantly distorted.
- Carcinoid heart disease:
- Fibrous white plaques located on the valvular and mural endocardium are characteristic presentations of carcinoid valve lesions.
- Valve leaflets become thick, rigid and smaller in area.
- Atrial and ventricular surfaces of the valve structure contain fibrous tissue proliferation.
- Congenital tricuspid stenosis:
- More common in infants
- Lesions may present in a number of different ways, either singularly or in any combination of the following:
- Incompletely developed leaflets
- Shortened or malformed chordae
- Small annuli
- Papillary muscles of abnormal size and number
- Infective endocarditis:
- Stenosis may develop as a result of large infected vegetations obstructing the opening of the tricuspid valve.
- Other conditions may mimic tricuspid stenosis by the mechanical obstruction of flow through the tricuspid valve:
- Supravalvular obstruction from congenital diaphragms
- Intracardiac or extracardiac tumors
- Thrombosis or emboli
- Large endocarditis vegetations
- Other conditions that impair right-sided filling
References
- ↑ 1.0 1.1 Waller BF, Howard J, Fess S (1995). "Pathology of tricuspid valve stenosis and pure tricuspid regurgitation--Part I." Clin Cardiol. 18 (2): 97–102. PMID 7720297.