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.