Diversity of patterns of hypertrophy in patients with systemic hypertension and marked left ventricular wall thickening

Document Type

Journal Article

Publication Date



The American Journal of Cardiology








In selected patients with systemic hypertension it may be difficult to ascertain whether left ventricular (LV) hypertrophy is a secondary end-organ consequence of long-term elevations in blood pressure or, alternatively, a manifestation of a coexistent primary hypertrophic cardiomyopathy. To address this issue and better characterize LV hypertrophy in systemic hypertension, 2-dimensional echocardiography was used to define the patterns of LV hypertrophy in 102 patients with sustained systemic hypertension and marked degrees of wall thickening. Patients ranged in age from 31 to 88 years (mean 61) and were predominantly female (58%); all were black. By selection, each patient had a maximal LV wall thickness of >15 mm (range 16 to 29). Distribution of hypertrophy was judged to be symmetric (i.e., concentric) in most patients (67 of 102, 66%). However, a substantial proportion (35 patients, 34%) demonstrated nonuniform, asymmetric patterns of hypertrophy in which at least 1 segment of the LV wall was at least 1.5 times the thickness of any other. In these 35 patients, the distribution of hypertrophy was similar to that characteristic of the morphologic spectrum of hypertrophic cardiomyopathy, with thickening of portions of both the ventricular septum and free wall in 16 patients, anterior and posterior ventricular septum alone in 11 patients and segmental involvement of only the anterior ventricular septum in 8. Patients with asymmetric patterns of wall thickening did not differ from the patients with symmetric hypertrophy with regard to age, sex or clinical findings. Asymmetric LV hypertrophy appears to represent an important feature of the morphologic spectrum of severe hypertensive heart disease. Moreover, the diverse patterns of hypertrophy observed in hypertensive patients with marked LV wall thickening often cannot be distinguished definitively, on a morphologic basis alone, from those characteristic of hypertrophic cardiomyopathy. © 1990.