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J Am Coll Cardiol, 2001; 37:169-174 © 2001 by the American College of Cardiology Foundation |
*

* State University of New York Downstate Medical Center, Brooklyn, New York, USA
Veterans Affairs Medical Center, Long Beach, California, USA
Manuscript received May 18, 2000; revised manuscript received August 3, 2000, accepted September 20, 2000.
Reprint requests and correspondence: Dr. Michael A. Weber, 350 Fifth Avenue, Suite 4002, New York, New York 10118
michaelwebermd{at}cs.com
OBJECTIVES
We sought to test whether the differences in activity of the renin-angiotensin and sympathetic nervous systems at rest or during exercise can explain the differing cardiovascular properties and outcomes of lean and obese hypertensive patients.
BACKGROUND
Although lean hypertensive patients have fewer metabolic abnormalities than obese hypertensive patients, paradoxically they appear to have a poorer cardiovascular prognosis.
METHODS
To evaluate the heightened risks in lean hypertensive patients, this study compared metabolic, neuroendocrine and cardiovascular characteristics at rest and during a standardized treadmill protocol in obese (body mass index [BMI] = 32.5 ± 0.3 kg/m2, n = 55) and lean (BMI = 24.3 ± 0.2 kg/m2, 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 hypertensive 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 the obese hypertensive patients. Arterial compliance (stroke volume/pulse pressure ratio) was reduced in the lean hypertensive patients, in whom it correlated (p = 0.033) with PNE. The PNE rose less (22%) in the obese than in the lean (55%) hypertensive patients in response to standing (p < 0.05). Likewise, 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 properties in lean hypertensive patients are more dependent on catecholamines and the renin system. The different neuroendocrine responses to dynamic stimuli in lean and obese patients also might help to explain the disparity in their cardiovascular outcomes.
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