Biventricular cineangiography in the evaluation of patients with asymmetric septal hypertrophy.

Echocardiographic studies have demonstrated that the characteristic anatomic defect in idiopathic hypertrophic subaortic stenosis (IHSS) is asymmetric septal hypertrophy (ASH). Although echocardiographic diagnosis of ASH is extremely sensitive, occasionally adequate echocardiograms cannot be obtained. Moreover, echocardiographic assessment of the extent of the underlying cardiomyopathic process, known to be distributed nonuniformly, is limited to evaluation of the upper part of the ventricular septum and the posterobasal left ventricular (LV) free wall. To determine if a specific angiographic marker of ASH can be identified even in the absence of LV outflow obstruction, and to delineate the extent and degree of cardiomyopathic involvement of the ventricular septum and LV free wall in patients with ASH, septal and LV wall configuration and thickness were measured using simultaneous biventricular cineangiography. The ventricular septum was thicker in 16 patients with ASH (avg. 15.2 ± 1.5 mm) and in six patients with concentric left ventricular hypertrophy (LVH) due to aortic valve disease (avg. 12.8 ± 1.1 mm) than in seven normal subjects (avg. 6.7 ± 0.4 mm, P < 0.001). In normal subjects and in patients with concentric LV hypertrophy, the walls of the ventricular septum were parallel. In contrast, the walls diverged in ASH so that septal width increased significantly inferiorly. Thus, the ratio of upper to lower septal width was greater than 0.8 (avg. 1.04 ± 0.06 mm) in normals and LVH patients but less than 0.77 (avg. 0.70 + 0.01 mm, P < 0.001) in ASH patients. Furthermore, upper septal width and the ratio of upper to lower septal width in ASH were significantly greater in seven patients with LV outflow obstruction than in six patients without obstruction, suggesting that the upper septum bulges into the LV outflow tract to a greater extent in obstructive ASH. In addition, the LV free wall in ASH was nonuniformly thickened, whereas in LVH the hypertrophy was uniform. We conclude that angiographic delineation of the septum and LV free wall 1) demonstrates abnormalities that distinguish ASH from normal and concentrically hypertrophied hearts, 2) demonstrates abnormalities that distinguish obstructive from nonobstructive ASH, and 3) aids in characterizing the distribution of myopathic involvement in patients with ASH.