DOES OBESITY INFLUENCE EARLY TARGET ORGAN DAMAGE IN HYPERTENSIVE PATIENTS

Citation
Re. Schmieder et Fh. Messerli, DOES OBESITY INFLUENCE EARLY TARGET ORGAN DAMAGE IN HYPERTENSIVE PATIENTS, Circulation, 87(5), 1993, pp. 1482-1488
Citations number
56
Categorie Soggetti
Cardiac & Cardiovascular System",Hematology
Journal title
ISSN journal
00097322
Volume
87
Issue
5
Year of publication
1993
Pages
1482 - 1488
Database
ISI
SICI code
0009-7322(1993)87:5<1482:DOIETO>2.0.ZU;2-Z
Abstract
Background. Various prospective studies have found that lean hypertens ive patients have greater cardiovascular morbidity and mortality than obese hypertensive subjects. It was therefore hypothesized that hypert ension is more benign when associated with obesity. In the present stu dy, we evaluated effects of obesity on early target organ damage in pa tients with essential hypertension. Methods and Results. In a total of 207 subjects, systemic and renal hemodynamics as well as left ventric ular structure and function were assessed by measuring cardiac output (indocyanine green dye dilution), renal blood How (clearance of I-131 paraimmunohippuric acid), and mean arterial pressure (invasively) and by two-dimensionally guided M-mode echocardiographic findings. Systemi c and renal vascular resistance, compliance of the large arteries eval uated by the stroke volume/pulse pressure index, and left ventricular mass served as parameters for early target organ damage. All individua ls were categorized into four groups: lean and obese normotensive as w ell as lean and obese hypertensive subjects. In obese hypertensive pat ients, total peripheral resistance was significantly lower and stroke volume/pulse pressure index was higher than in the lean hypertensive g roup, almost reaching values of normotensive control subjects. No effe ct of obesity on the renal circulation was noted, whereas in hypertens ion, renal vascular resistance was elevated. The degree of left ventri cular hypertrophy was more pronounced in the hypertensive groups than in their normotensive counterparts and progressively increased with ob esity. Nevertheless, in obese hypertensive patients, left ventricular function, as measured by fractional fiber shortening and velocity of c ircumferential fiber shortening, was maintained despite the fact that the heart had been exposed to the double burden of an increased preloa d (obesity) and afterload (hypertension). Conclusions. Obesity had a d isparate effect on target organs in hypertension. At rest, obesity see med to mitigate cardiovascular changes in the systemic vascular bed ca used by hypertension. However, no such mitigation was observed in the renal vasculature, and left ventricular hypertrophy was even exacerbat ed by the presence of obesity. Our findings in part negate the concept that obesity is able to exert a protective effect on early target org an damage in hypertensive patients and, in particular, on the heart.