Myocardial Fibrosis and Calcareous Emboli in Valvular Heart Disease

In the past decade the great advances of cardiac surgery have focused new attention on aortic and mitral valve disease.The investigation of these cases by clinical and technical means has been the subject of increased interest (Wood, 1954;Gorlin et al., 1955).Study of the pathology of the mitral and aortic valves has correspondingly increased (Brock, 1952).The observation that myo- cardial fibrosis is unduly frequent and occasionally extensive in cases of congenital and acquired aortic stenosis with little or no coronary artery disease has often been made (Friedberg, 1949;Marquis and Long, 1955).The occurrence of angina pectoris, the electrocardiographic changes on exercise and the liability to sudden death in these cases have led these authors and others to suggest that the myocardial fibrosis is due to myocardial ischmmia as a result of functional coronary in- sufficiency.In addition, in cases of mitral stenosis, the occurrence of angina pectoris and the cardiographic changes on exercise have been attributed to myocardial ischemia as a result of functional coronary insufficiency (Wood;Stuckey, 1955).In an attempt to determine how much myocardial fibrosis that is, not attributable to coronary disease or to rheumatic myocarditis, and therefore possibly due to functional coronary insufficiency, may occur in these two groups, seven cases of aortic stenosis and seven cases of mitral stenosis (with and without regurgitation) were studied post mortem by a method combining a coronary artery injection technique with careful examination of the myocardium.The necropsy findings of a large number of cases of both aortic and mitral stenosis were also reviewed.The amount of myocardial fibrosis noted in the two groups together with the finding of previously undescribed arterial lesions prompt this report of the results.METHOD At necropsy the hearts were carefully dissected, cleared of any clots, and weighed.Shortly there- after (usually within three hours), the coronary arteries were cannulated under water at 370 C. and perfused with water of the same temperature until the washings returned clear from the coronary sinus.Approximately 100 ml. of 15 per cent formol-calcium were then injected in order to fix the musculature, followed by 10 to 20 ml. of warm water (to prevent mixing of the formol-calcium and the barium gelatine).Warmed barium-gelatine, prepared according to the technique of Gross (1921), was then injected into the arteries at a pressure of 140 mm.Hg.The heart was placed in iced water until the gelatine had set, and an X-ray was taken.Following this the heart was placed in a solution of 15 per cent formol-calcium for further fixation for at least one week.Dissection of the heart was then carried out.Using the radiograph as a guide the coronary arteries were sectioned at 3-4 mm.intervals in order to extend, by gross and microscopic examination, the X-ray findings.The heart muscle was then sliced from apex to base at 5-mm.intervals and the slices examined under a magnifying lens.The position, appearance, and size of any myocardial lesion were recorded, blocks being taken from the abnormal areas for microscopic examination.In addition blocks were taken * During the tenure of a British Council Scholarship.