title: Mechanism of development of asymmetric septal hypertrophy in patients with essential systemic hypertension.
abstract: In order to understand the mechanism of development of asymmetric septal hypertrophy (ASH) in hypertension, 290 patients with essential hypertension (HT) were examined echocardiographically. Out of them 84 cases of advanced left ventricular hypertrophy (LVH) [37 cases of symmetric hypertrophy (HT-SH group) and 47 cases of ASH (HT-ASH group)] were compared in their clinical and echocardiographic findings with hypertrophic cardiomyopathy (HCM). In the 290 HT cases, the highest systolic pressure in each patient's history was found to correlate with left ventricular (LV) posterior wall thickness (PWT), but not with the septal wall thickness (IVST). There were no differences in LV thickness (IVST + PWT) among patients in the HT-ASH, HT-SH and HCM groups. While the HCM group patients showed no significant differences in IVST and PWT from those in the HT-ASH group, they did have greater IVST and smaller PWT than HT-SH group patients. The rapid filling rate (RFR) was also not much different in the HCM and HT-ASH groups, but was significantly lower in the HCM group than in the HT-SH group. Furthermore, HT-ASH group patients has a milder degree of hypertension and a higher incidence of familial occurrence of HCM than did those in the HT-SH group. After treatment for HT, the HT-SH group showed a significant decrease in wall thickness during long-term observation, while the HT-ASH and HCM groups, failed to exhibit such changes. Moreover, the degree of myocardial disarrangement in the HT-ASH group did not differ significantly from that in the HCM group. These results suggested that LVH in HT is related not only to pressure load but also to genetic factors similar to that in HCM.
authors.affiliation: First Department of Internal Medicine, Kobe University School of Medicine, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Yokota
authors.forename: S S
authors.initials: SS
authors.lastname: Teng
authors.forename: R
authors.initials: R
authors.lastname: Emoto
authors.forename: T
authors.initials: T
authors.lastname: Miki
authors.forename: A
authors.initials: A
authors.lastname: Takarada
authors.forename: T
authors.initials: T
authors.lastname: Seo
authors.forename: H
authors.initials: H
authors.lastname: Sano
authors.forename: H
authors.initials: H
authors.lastname: Fukuzaki
mesh_terms: D000328:Adult; D001706:Biopsy; D001794:Blood Pressure; D006332:Cardiomegaly / Q000209:etiology / Q000503:physiopathology; D002312:Cardiomyopathy, Hypertrophic / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D004452:Echocardiography; D004719:Endomyocardial Fibrosis / Q000473:pathology; D005260:Female; D006346:Heart Septum / Q000473:pathology; D006352:Heart Ventricles / Q000473:pathology; D006801:Humans; D006973:Hypertension / Q000150:complications* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged