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An electron microscopic study of left ventricular myocardium was carried out in 15 patients who had isolated rheumatic mitral stenosis, with particular reference to the relation among ultrastructural pathological findings, the severity of mitral stenosis and left ventricular function. They were divided into 2 groups based on left ventricular performance evaluated by 2-dimensional echocardiography and angiocardiography. The severity of mitral stenosis was determined by hemodynamic data and mitral valve areas measured by 2-dimensional echocardiography. Regardless of the level of left ventricular contractile function we consistently demonstrated varying degrees of ultrastructural pathological alterations of left ventricular muscle cells, involving the myofibrils, mitochondria, nuclei and other elements of the sarcoplasm and membranes surrounding the myocardial cells in all specimens examined. The ultrastructural pathological findings did not correlate with the severity of mitral stenosis reflected in the echocardiographic and hemodynamic data. However, those patients with abnormal left ventricular function always exhibited more extensive loss of myofibrils resulting from either disproportion of the mitochondria-to-myofibril ratio or myofibrillar degeneration. The present investigation provides the morphological data at the ultrastructural level to support the widely held concept of a myocardial factor i.e., the extent of myocardial involvement by the rheumatic process as the basic pathogenetic mechanism responsible for left ventricular dysfunction in patients with isolated rheumatic mitral stenosis. Furthermore, it is suggested that pathological alterations of myocardial ultrastructure were related to the extent of myocardial involvement by the rheumatic process rather than being structural adaptations in response to the hemodynamic derangement.

japanese heart journal

Ultrastructural pathological study of left ventricular myocardium in patients with isolated rheumatic mitral stenosis with normal or abnormal left ventricular function.