The mechanism of the intraventricular pressure gradient in idiopathic hypertrophic subaortic stenosis.

T HE INTRAVENTRICULAR pressure gradients that are recorded in patients with idiopathic hypertrophic subaortic stenosis (IHSS) differ in many respects from those observed in patients with the various discrete forms of obstruction to left ventricular outflow. Thus, it is now generally recognized that the magnitude of the pressure gradient measured in the resting state may bear little relation to the severity of the patient's symptoms, and that in some patients, variations in the magnitude of the pressure gradient occur in the course of a single hemodynamic study, or at sequential cardiac catheterizations. The finding that in patients with IHSS approximately 80% of the stroke volume is ejected during the first half of left ventricular systole led Hernandez and co-workers' to consider the possibility that no obstruction to left ventricu-lar outflow occurs in this disease. These investigators suggested that little or no orthograde flow might emanate from the area of high pressure and that the elevated systolic pressure might exist only within trabeculations in the wall of the empty ventricle. Burchell,2 on the basis of angiocardiographic observations, also raised the possibility that in some patients with IHSS the small apical portion of the left ventricle might act as a "self-obstructing diverticulum," although like many other observers,3-6 he considered the basic obstructive lesion to lie in the left ventricular out-flow tract. Recently, Criley and associates,7 on the basis of cineangiographic and hemo-dynamic studies, have supported the theory 558 that no obstruction to left ventricular outflow exists in IHSS and have questioned the rationale of operations designed to relieve obstructions in patients with this disease. The hypothesis that muscular hypertrophy of the left ventricular outflow tract results in systolic obstruction to ejection in patients with IHSS has been developed in a number of laboratories since the initial clinical description of this entity by Brock, in 1957.8 A considerable body of clinical, angiographic, hemodynamic, and anatomic information has now accumulated, much of which appears consistent with this theory, and a detailed review of these studies has been presented recently .6 It would appear of considerable importance from both theoretical and therapeutic points of view to consider carefully the problem of whether or not obstruction to oufflow exists in IHSS, particularly since a number of recent reports have described the application of operations designed to relieve left ventricular outflow tract obstruction in patients with IHSS;9-18 many of these operative methods, as well as earlier surgical …