Asymmetric septal hypertrophy in patients with aortic stenosis: An adaptive mechanism or a coexistence of hypertrophic cardiomyopathy

Abstract

Myocardial histologic features and left ventricular dynamics were assessed in 24 patients with severe aortic stenosis, 12 with (group 1) and 12 without (group 2) associated asymmetric septal hypertrophy. In 10 patients from group 1, echocardiography showed a septal/pos-terior wall ratio of 1.5; in the other 2, asymmetric septal hypertrophy was diagnosed by direct inspection at the time of surgery. Septal myectomy in all 12 patients in group 1 was completed at the time of aortic valve replacement. Septal histologic features were assessed from surgical specimens in 10 patients in group 1. Transseptal endomyocardial biopsy specimens of the anterolateral wall taken during preoperative cardiac catheterization were evaluated by light microscopy in 10 patients from group 1 and all patients of group 2. Left ventricular end-diastolic and peak systolic pressure, peak pressure gradient, calculated valve area and angiographic muscle mass did not differ significantly in groups 1 and 2; ejection fraction (68 versus 58%; probability [p] < 0.01) was larger and end-diastolic volume (109 versus 144 ml/m 2 ; difference not significant [NS]) was smaller in group 1 than in group 2. Muscle fiber diameter of the anterolateral wall was similar in groups 1 and 2 (26.5 versus 29.1 μ; NS), but muscle fiber diameter of the septum in group 1 was significantly smaller (24.4 μ; p < 0.01) than that of the anterolateral wall in group 2. No morphologic abnormalities typical for hypertrophic cardiomyopathy (fiber disarray) were seen in samples from the patients in either group. By 18 months postoperatively, septal wall thickness had decreased significantly from 2.0 to 1.5 cm (p < 0.01) and posterior wall thickness from 1.4 to 1.2 cm (p < 0.05) in group 1. In group 2, septal wall thickness decreased from 1.5 to 1.3 cm (NS) and posterior wall thickness from 1.4 to 1.2 cm (NS) 8 months postoperatively. Asymmetric septal hypertrophy in patients with aortic stenosis is an adaptive mechanism to the long-standing pressure overload, and hence there is no evidence of coexistence of idiopathic hypertrophic cardiomyopathy and aortic valve disease. Although the degree of valve obstruction was similar in both groups, left ventricular ejection performance was significantly lower in the group without asymmetric hypertrophy, probably because these patients had a more advanced stage of myocardial disease. After successful valve replacement, there is a significant regression of septal hypertrophy in patients with aortic stenosis and asymmetric septal hypertrophy.