Mitral valve disease.

Abstract

Recent experimental work demonstrates that the cellular contractile dysfunction that occurs after a brief period of mitral regurgitation is potentially reversible, that left ventricular dysfunction may also occur due to interruption of chordal-ventricular continuity, and that muscle dysfunction can be detected independent of loading conditions with measurements of ventricular stress and strain. Experimental work has also shown that hypertrophy after experimental mitral regurgitation may be inadequate for the degree of hemodynamic overload, and that there is lysis of myofibrils. This is consistent with clinical observations that ventricular dilatation and left ventricular hypertrophy may be modest despite long-standing, severe mitral regurgitation. At the moment, end-systolic diameter remains the best predictor of outcome after mitral valve replacement; preservation of chordae has been shown to have an impact on outcome in some but not all studies. Measures of heart rate variability may also have predictive value in mitral regurgitation. The so-called myocardial factor in rheumatic mitral disease appears to be unimportant; excessive vasoconstriction is more responsible for the modest left ventricular dysfunction in mitral stenosis. There is some new information regarding beta-blocking therapy, vasodilator therapy, and antithrombotic therapy.