OBJECTIVES We sought to test whether the differences in activity of the ren
in-angiotensin and sympathetic nervous systems at rest or during exercise c
an explain the differing cardiovascular properties and outcomes of lean and
obese hypertensive patients.
BACKGROUND Although lean hypertensive patients have fewer metabolic abnorma
lities than obese hypertensive patients, paradoxically they appear to have
a poorer cardiovascular prognosis.
METHODS To evaluate the heightened risks in lean hypertensive patients, thi
s study compared metabolic, neuroendocrine and cardiovascular characteristi
cs at rest and during a standardized treadmill protocol in obese (body mass
index [BMI] = 32.5 +/- 0.3 kg/m(2) n =55) and lean (BMI = 24.3 +/- 0.2 kg/
m(2), n = 66) hypertensive patients. Normotensive obese (n = 21) and lean (
n = 55) volunteers served as control subjects.
RESULTS Compared with the lean normotensive subjects, the lean and obese hy
pertensive patients had greater left ventricular mass index (LVMI) values,
but on multivariate analysis, LVMI correlated with plasma renin activity (p
< 0.001) and plasma norepinephrine (PNE) (p < 0.01) in the lean but not th
e obese hypertensive patients. Arterial compliance (stroke volume/pulse pre
ssure ratio) was reduced in the lean hypertensive patients, in whom it corr
elated (p = 0.033) with PNE. The PNE rose less (22%) in the obese than in t
he lean (55%) hypertensive patients in response to standing (p < 0.05). Lik
ewise, during treadmill exercise, there were lesser increases in renin (65%
vs. 145%, p < 0.01) and epinephrine (200% vs. 500%, p < 0.05) in the obese
hypertensive patients. These changes were also less in obese patients than
in lean control subjects, indicating attenuated neurohormonal responses to
stress in obesity.
CONCLUSIONS Compared with obese hypertensive patients, cardiovascular prope
rties in lean hypertensive patients are more dependent on catecholamines an
d the renin system. The different neuroendocrine responses to dynamic stimu
li in lean and obese patients also might help to explain the disparity in t
heir cardiovascular outcomes. (J Am Cell Cardiol 2001;37:169-74) (C) 2001 b
y the American College of Cardiology.