- Disorder of mitral valve (MV) closure, either primary, secondary (functional), or mixed, resulting in a backflow of the left ventricular (LV) stroke volume into the left atrium (LA); uncompensated, this leads to LV and LA enlargement, elevated pulmonary pressures, atrial fibrillation (AF), heart failure (HF), and sudden cardiac death.
- Types of mitral regurgitation (MR):
- Acute versus chronic
- Primary versus secondary (functional) and mixed
- Primary: abnormalities at any level of the MV structures (annulus, leaflets, chordae tendineae, and papillary muscles)
- Secondary: No valvular abnormalities are found. The abnormal and dilated LV causes papillary muscle displacement, resulting in leaflet tethering with annular dilatation that prevents coaptation.
- Mixed: mixed abnormalities of both primary and secondary types
- System(s) affected: cardiac; pulmonary
Moderate to severe MR affects 2.5 million people in the United States (2000 data). It is the most common valvular disease and is expected to double by 2030.
- By severity on echocardiography:
- Mild MR: 19% (up to 40% if trivial jets included)
- Moderate MR: 1.9%
- Severe MR: 0.2%
- By category: degenerative (myxomatous disease, annular calcification): 60–70%, ischemic: 20%, endocarditis: 2–5%, rheumatic: 2–5%
Etiology and Pathophysiology
- Acute MR
- Leaflet perforation: infective endocarditis, trauma
- Chordae tendineae rupture: trauma, spontaneous rupture, infective endocarditis, or rheumatic fever
- Papillary muscle rupture or dysfunction: acute myocardial infarction (MI), severe myocardial ischemia, or trauma
- Chronic MR
- Primary—degenerative (mitral annular calcification, MV prolapse [MVP]), infective endocarditis, rheumatic heart disease (RHD), inflammatory diseases (lupus, eosinophilic endocardial disease), toxin induced (anorectic drugs), congenital
- Secondary (functional)
- Ischemic: coronary artery disease (CAD)/MI
- Nonischemic: cardiomyopathy from any cause, annular dilatation from chronic AF, dyssynchrony from right ventricular pacing
- Acute MR: Acute MV damage leads to sudden LA and LV volume overload. Sudden rise in LV volume load without LV remodeling results in impaired forward cardiac output and possible cardiogenic shock.
- Chronic MR: LV eccentric hypertrophy compensates for increased regurgitant volume to maintain forward cardiac output and alleviate pulmonary congestion. However, LV remodeling can result in LV dysfunction. LA compensatory dilatation for the larger regurgitant volume predisposes patients to develop AF.
- Ischemic MR: papillary muscle rupture, ischemia during acute MI, and incomplete coaptation of leaflets or restricted valve movement from chronic ischemia
Age, hypertension, RHD, endocarditis, anorectic drugs, radiation
- Risk factor modification for CAD
- Antibiotic prophylaxis for poststreptococcal RHD
- Routine dental endocarditis prophylaxis is no longer recommended.
Commonly Associated Conditions
MVP with MR common in Marfan syndrome
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