Author + information
- Received July 21, 1989
- Revision received October 18, 1989
- Accepted October 26, 1989
- Published online March 1, 1990.
- Yasuro Sugishita, MD, FACC∗,
- Keiji Iida, MD,
- Kimihiko Yukisada, MD and
- Iwao Ito, MD
- ↵∗Address for reprints: Yasuro Sugishita, MD, Cardiovascular Division, Department of Internal Medicine, Institute of Clinical Medicine, The University of Tsukuba, Tsukuba, Ibaraki 305, Japan.
To study the cardiac determinants of regression of left ventricular hypertrophy in hypertension, left ventricular mass, fractional shortening and end-systolic wall stress were measured echocardiographically in 36 patients with essential hypertension and left ventricular hypertrophy. The patients were classified into two groups. Group I consisted of 15 patients with subnormal end-systolic wall stress, and Group II consisted of 21 patients with normal end-systolic wall stress. There were no significant differences between groups in systolic or diastolic blood pressure. After treatment for 4.4±1.7 years, echocardiographic studies were repeated. There were no significant differences between groups in the duration of the follow-up period and the kinds of antihypertensive drugs.
After treatment, blood pressure decreased significantly in both groups (p < 0.001 for both), with no significant difference between groups. Left ventricular mass increased significantly in Group I (from 331 ± 7 to 363 ± 24 g, mean ± SEM, p < 0.05), whereas it decreased significantly in Group II (from 318 ± 16 to 268 ± 17 g, p < 0.001). Myocardial contractility (the relation between end-systolic wall stress and fractional shortening) remained almost the same as before treatment.
In conclusion, in patients with hypertensive ventricular hypertrophy with subnormal end-systolic wall stress (inappropriate hypertrophy, probably induced by a neurohumoral factor), a decrease in blood pressure with antihypertensive treatment does not lead to regression of left ventricular hypertrophy, but rather to an increase in left ventricular mass. In patients with normal end-systolic wall stress (appropriate hypertrophy, probably induced by high arterial pressure) antihypertensive treatment decreases left ventricular mass if it has the potency to cause regression of hypertrophy.
☆ This work was supported by grants for the study of idiopathic cardiomyopathy from the Japanese Ministry of Health and Welfare, Tokyo, Japan.
- Received July 21, 1989.
- Revision received October 18, 1989.
- Accepted October 26, 1989.