Tricuspid stenosis pathophysiology: Difference between revisions

Jump to navigation Jump to search
No edit summary
Line 7: Line 7:


==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.

Revision as of 15:25, 13 February 2020

Tricuspid stenosis Microchapters

Home

Patient Information

Overview

Classification

Pathophysiology

Causes

Differentiating Tricuspid stenosis from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X-ray

Echocardiography and Ultrasound

CT scan

MRI

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Tricuspid stenosis pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Tricuspid stenosis pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Tricuspid stenosis pathophysiology

CDC on Tricuspid stenosis pathophysiology

Tricuspid stenosis pathophysiology in the news

Blogs on Tricuspid stenosis pathophysiology

Directions to Hospitals Treating Psoriasis

Risk calculators and risk factors for Tricuspid stenosis pathophysiology

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:

References

  1. 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.

Template:WH

Template:WS