title: [Echocardiographic features of left ventricular hypertrophy and contractility in malignant hypertension].
abstract: To assess the hemodynamic characteristics in malignant hypertension, echocardiography was performed in 18 patients with malignant essential hypertension (MH-I, n = 9) and secondary hypertension (MH-II, n = 9). Patients with benign hypertension with or without left ventricular hypertrophy (n = 8 and 7, respectively), patients with hypertensive heart failure (n = 7) and normotensive volunteers (n = 10) were subjected to controls. Plasma noradrenaline (NA) and renin activity (PRA) were also measured prior to the antihypertensive therapy. There were no significant differences in the durations of hypertension before the malignant phase, and the mean arterial pressure between MH-I and MH-II. Although posterior wall thickness (PWTd) in MH-II was similar to that in MH-I, interventricular septal thickness (IVSTd) was less marked in MH-II. The plasma NA and PRA were markedly increased in both MH-I and MH-II. End-diastolic dimension (Dd) of the left ventricle was within normal range, but end-systolic dimension (Ds) was significantly increased in MH-I, MH-II and hypertensive heart failure. The moderate decreases in ejection fraction (EF) and mean velocity of circumferential fiber shortening (mVcf) were observed in both MH-I and MH-II. Marked decreases in EF and mVcf were also observed in patients with hypertensive heart failure. The relationship between systolic blood pressure and Dd/PWTd was shifted toward the right and upper portion of the normal relation in MH-I and MH-II. The present study demonstrated that the hemodynamic characteristics in malignant hypertension are an inappropriate left ventricular hypertrophy due to a marked increase in systolic stress; dilatation of the left ventricle in systole; and a moderate decrease in ventricular systolic function. It is suggested that a decrease in left ventricular systolic function in malignant hypertension might be due in part to a marked increase in the influence of neurohumoral factors on hemodynamics.
authors.affiliation: Department of Medicine, Wakayama Medical College.
authors.forename: Y
authors.initials: Y
authors.lastname: Nakamura
authors.forename: M
authors.initials: M
authors.lastname: Arita
authors.forename: S
authors.initials: S
authors.lastname: Fujiwara
authors.forename: Y
authors.initials: Y
authors.lastname: Tomobuchi
authors.forename: H
authors.initials: H
authors.lastname: Nakamura
authors.forename: M
authors.initials: M
authors.lastname: Shiotani
authors.forename: K
authors.initials: K
authors.lastname: Yamamoto
authors.forename: Y
authors.initials: Y
authors.lastname: Ueno
authors.forename: I
authors.initials: I
authors.lastname: Nishio
authors.forename: Y
authors.initials: Y
authors.lastname: Masuyama
mesh_terms: D000328:Adult; D006332:Cardiomegaly / Q000175:diagnosis* / Q000209:etiology / Q000503:physiopathology; D004452:Echocardiography; D006801:Humans; D006974:Hypertension, Malignant / Q000150:complications* / Q000503:physiopathology; D008875:Middle Aged; D009200:Myocardial Contraction; D009638:Norepinephrine / Q000097:blood; D012083:Renin / Q000097:blood
chemical_list: D012083:Renin; D009638:Norepinephrine