Subaortic stenosis revisited: the importance of the dynamic pressure gradient.
Brachfeld and Gorlin's revised concept of subaortic stenosis derived from their recognition that the large magnitudes of the pressure gradients were incompatible with the relatively mild anatomic lesions found at surgery in 3 of their patients, and the rapidity of their arterial pulse upstroke. They proposed that a gradient caused by a superimposed systolic stenosis was responsible for the large pressure gradients and the overestimation of the severity of the discrete subaortic stenosis (DSAS). A fourth patient had no anatomic cause for the pressure gradient, and findings compatible with hypertrophic cardiomyopathy (HCM). All 4 patients had septal hypertrophy which they felt was instrumental in the brisk pulse contour and dynamic gradients across the outflow tract. In the ensuing decades, imaging techniques have been developed which permit detailed studies of ventricular ejection patterns in dynamic gradients associated with HCM and DSAS. These studies have been interpreted variously. The prevailing view is that there is a dynamic obstruction that increases progressively in severity during systole, as proposed by Brachfeld and Gorlin. An opposing view is that dynamic gradients can occur in the absence of any hindrance to ejection, and that these gradients instead result from rapid and complete emptying of the ventricle. Regardless of their cause, dynamic gradients are often superimposed upon gradients caused by DSAS and valvar aortic stenosis, leading to exaggerated estimates of severity. These dynamic gradients are uncovered when the anatomic cause of stenosis is removed, and seemingly increase the postoperative morbidity. A greater understanding of the significance of dynamic gradients and the mechanism(s) responsible for them should lead to more rational management of DSAS and HCM in the future.
Criley
J M
JM
Saint John's Cardiovascular Research Center, Harbor-UCLA Medical Center 90502.
Siegel
R J
RJ
D001024:Aortic Valve Stenosis / Q000175:diagnosis / Q000266:history / Q000503:physiopathology*; D002312:Cardiomyopathy, Hypertrophic / Q000175:diagnosis / Q000266:history / Q000503:physiopathology*; D005260:Female; D049673:History, 20th Century; D006801:Humans; D008875:Middle Aged