Central aortic pulsatile hemodynamics in obese premenopausal women

J Am Soc Hypertens. 2007 Sep-Oct;1(5):341-6. doi: 10.1016/j.jash.2007.06.004.

Abstract

Obesity is a known risk factor for cardiovascular disease (CVD) but the mechanism by which obesity contributes to cardiovascular risk is not well understood. Arterial stiffness is a CVD risk factor associated with obesity. We studied 16 obese body mass index (BMI > 30) and 10 lean (BMI < 25) healthy premenopausal women. We measured fasting glucose, insulin, and lipids, blood pressure, and arterial tonometry to assess arterial stiffness. Obese women had higher glucose, insulin, total cholesterol and triglyceride levels, blood pressures, cardiac output, and peak flow. Characteristic impedance was lower (146 +/- 31 [(dyne . s) . cm(-5)] vs. 187 +/- 48 [(dyne . s) . cm(-5)]; P = .01), aortic diameter was greater (2.54 +/- 0.20 cm vs. 2.29 +/- 0.21 cm; P < .01), and peripheral pulse pressure was similar in obese compared with lean women. Obesity in premenopausal women is associated with increased cardiac output and peak aortic flow. Increased aortic diameter in obese women was associated with reduced characteristic impedance, potentially preventing an increase in peripheral pulse pressure despite elevated flow, which suggests proximal aortic remodeling. When aortic remodeling and compensation for increased hemodynamic demands are limited by environmental or genetic interference, hypertension or CVD may result.