Mitral Regurgitation (MR) Or Mitral Incompetence And Its Hemodynamic Changes
The mitral valve apparatus consists of six components:
- Valve cusps
- Mitral annulus
- Choradae tendinae
- Papillary muscles,
- Portion of the left ventricle where the papillary muscles are implanted, and
- Portion of the left atrium adjacent to the mitral annulus.
Defective function of one or more of these components may lead to inadequate adaptation of the mitral leaflets in systole giving rise to various degrees of mitral regurgitation. The common etiological factors of isolated mitral regurgitation are:
- Rheumatic involvement of the mitral valve,
- Myxomatous degeneration of mitral valve (mitral valve prolapsed syndrome)
- Ischemic heart disease
- Infective endocardities, and
- Dilatation of the valve ring occurring in left ventricular dilatation as is seen in hypertension, cardiomyopathy or ischemic heart disease.
Mitral valve prolapsed syndrome has been dealt with separately. Apart from mitral valve prolapsed, rheumatic lesions account for many of these cases of mitral regurgitation in Asia.
In rheumatic mitral regurgitation, the valve leaflets are thickened, fibrosed and contracted. The chordate are also shortened and fused. This process causes inadequate closure of the mitral leaflets in systole and hence MR results.
Ischemic heart disease leading to MR is commonly seen in makes after the age of 40. Transient or permanent dysfunction of the papillary muscle is more commonly involved. Occasionally, rupture of the papillary muscles may complicate myocardial infarction and this results in severe acute mitral regurgitation. Ischemia of the myocardium can result in transient dyskinesia of the portion of left ventricle where the papillary muscles are implanted and this may result in MR. Chronic ischemic heart disease with ventricular aneurysm may also be associated with MR.
Cardiomyopathy involving the left ventricle results in MR. It may be seen in all the three main types of cardiomyopathy (endomyocardial fibrosis, dilated cardiomyopathy (endomyocardial fibrosis, dilated cardiomyopathy and hypertrophic cardiomyopathy). Severity of mitral regurgitation varies widely in these cases.
Left ventricular blood regurgitates into the left atrium during systole. The blood ejected into the aorta is correspondingly reduced. The blood returning from the left atrium is larger in volume, leading to diastolic overfilling of the left ventricle. In mild cases, the cardiac function is well compensated, but in severe cases, gross left ventricular dilatation and hypertrophy develop. Ultimately left ventricular failure supervenes, resulting in pulmonary hypertension and right ventricular failure as well.
© 2014 Funom Theophilus Makama