학술논문

Obesity and left ventricular diastolic function: noninvasive study in normotensives and newly diagnosed never-treated hypertensives.
Document Type
Article
Source
International Journal of Obesity & Related Metabolic Disorders. Aug2000, Vol. 24 Issue 8, p954. 5p.
Subject
*OBESITY
*LEFT heart ventricle
*DIASTOLE (Cardiac cycle)
*HYPERTENSION
Language
ISSN
0307-0565
Abstract
OBJECTIVE: To evaluate the influence of obesity, per se or associated with hypertension, on left ventricular (LV) diastolic function. PATIENTS: Thirty-two obese newly-diagnosed never-treated hypertensives; 32 obese normotensives matched for age, sex and BMI with hypertensives; 32 lean newly diagnosed never-treated hypertensives and 32 lean normotensives, matched for age, sex and 24 h blood pressure (BP) with the obese subjects. METHODS: Twenty-four-hour ambulatory blood pressure monitoring and digitized M-mode LV echocardiograms. PARAMETERS EVALUATED: Twenty-four-hour, day-time and night-time BP and heart rate, percentage nocturnal BP fall; LV end-diastolic diameter index, septal and posterior wall thickness, LV mass index, peak shortening and lengthening rate of LV diameter, peak thinning rate of LV posterior wall. RESULTS: A main effect was found for obesity on LV diameter and LV mass and for hypertension on LV mass; LV systolic function was normal in all the subjects and similar among the four groups; LV diastolic function was significantly reduced in both obese groups with respect to lean ones. This difference persisted after correction of diastolic parameters for 24 h BP and heart rate, LV diameter and LV mass index and disappeared only after correction for body mass index. This latter was inversely related with diastolic parameters only in the obese groups. CONCLUSIONS: Obesity is associated with a preclinical impairment of LV diastolic function in both normotensives and hypertensives; the diastolic impairment is independent of haemodynamic factors, such as 24 h BP and heart rate, and bears no relation to LV geometry in normotensives and only little relation in hypertensives, having therefore to be ascribed to obesity itself. International Journal of Obesity (2000) 24, 954–958 [ABSTRACT FROM AUTHOR]