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A combined angiocardiographic-echocardiographic method for estimating right ventricular wall mass is described. Biplane cineangiocardiograms are analyzed for ventricular volume in end-diastole, and wall thickness is determined from echocardiograms obtained with a high frequency transducer and strip chart recorder, The intracavitary and the external surface volumes of the ventricle are derived, and the difference multiplied by 1.050, the specific gravity of myocardium. Excellent correlation was observed between right ventricular wall mass and body surface area in normal children (r = 0.93). The mean right ventricular mass was 44.5 g/M2 as compared to 78.1 g/M2 for the left ventricle, corresponding mass/EDV values were 0.48 g/cm3 and 1.26 g/cm3, respectively. In isolated right ventricular pressure overload, the increase in right ventricular mass is chiefly due to the increase in wall thickness; in volume overload, it is due mostly to the increase in chamber volume,

A patient is reported with hypertrophic cardiomyopathy where midventricular obstruction was found in association with mitral stenosis. Partial relief of the intraventricular obstruction was obtained by extensive papillary and trabecular muscle resection in the mid-left ventricular area, in conjunction with mitral valve replacement with a porcine heterograft.

Left ventricle dimensions and wall stress were measured echocardiographically before and immediately after exercise in 14 athletes and 7 control subjects. Our findings suggest that afterload is an important determinant of cardiac performance and wall hypertrophy in athletes. In spite of major changes in heart rate and blood pressure, left ventricular wall stress remains unchanged following submaximal exercise, in trained and untrained hearts. It would appear that the changes in heart size during exercise are to a large extent limited in untrained ventricles, as smaller left ventricular dimensions are required, to "normalise" wall stress. This results in a lower stroke volume for a given stroke dimensional change. Consequently cardiac output is a function of heart rate rather than stroke volume in untrained subjects. The effect of increased muscle mass in athletes, is to permit larger left ventricular dimensions for a given afterload, thus stroke volume can be augmented. The increase h/R ratio suggests that afterload is more important than preload in the development of left ventricular hypertrophy in rowers and swimmers.

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