A Hemodynamic Technic for the Detection of Hypertrophic Subaortic Stenosis

IT IS NOW well appreciated that following a successful valvulotomy for valvular pulmonic stenosis, muscular hypertrophy in the right ventricular outflow tract may persist and be responsible for a significant resistance to right ventricular ejection.'-3 Similar muscular obstruction to the left ventricular outflow has also been noted in patients following surgical relief of discrete valvular or subvalvular stenosis. Obstruction to left ventricular ejection resulting from contraction of hypertrophied muscle in the left ventricular outflow tract, without antecedent aortic valvular or subvalvular stenosis, has recently been recognized as a distinct disease entity.4'0 Although a variety of names have been attached to this malformation, "idiopathic hypertrophic subaortic stenosis" has appeared to us to be most appropriate and the clinical, hemodynamic, and angiographic features in 14 patients studied at the National Heart Institute have been detailed elsewhere.'0 In contrast to the usual forms of obstruction to left ventricular ejection in which the orifice size is fixed, in hypertrophic subaortic stenosis the obstruction in the outflow tract relaxes during diastole and narrows during ventricular systole.10 This obstruction to left ventricular outflow results from myocardial contraction and it might be anticipated that alterations in the force of contraction could modify the effective orifice size of the left ventricular outflow tract. Accordingly, it was reasoned that the more forceful ventricular contraction which accompanies the compensatory beat following a premature contraction might narrow the orifice, reduce the stroke volume and, therefore, the systemic arterial pulse pressure. In contrast, in patients with