NEW ORLEANS — Obese individuals with no other complicating diseases have an abnormally stiff aorta, predisposing them to heart failure and other cardiovascular diseases, Monique Robinson, M.B., said at the annual scientific sessions of the American Heart Association.
“The take-home message is this: Being just overweight or obese is not OK. I think in primary care practice, our focus has been on the comorbidities associated with obesity.
We treat you if you're diabetic. We treat you if you've got hypertension. We also need to treat our obese people who are just obese, because our results suggest that there may be an increased cardiovascular risk for these patients,” said Dr. Robinson, a cardiovascular research fellow at the University of Oxford, England.
Using MRI, she investigated the mechanical elastic functioning of the aorta in 27 obese subjects with a mean body mass index of 34 kg/m2 without diabetes, hypercholesterolemia, or hypertension, and in 12 normal-weight controls.
Mean aortic distensibility was reduced by 59% in obese subjects, compared with normal-weight subjects. Mean aortic compliance was 40% less, as well. An aortic stiffness index was also markedly increased in the obese subjects.
“What this means is, the aorta in obese subjects was less able to expand and contract to deal with high-velocity blood flow from the left main pumping chamber, as compared with the normal controls,” she explained.
Multiple linear regression analysis showed that fat mass, body mass index, leptin, and HDL cholesterol were all robust predictors of aortic elastic function in obese individuals.
Dr. Robinson and her Oxford coinvestigators are focusing on leptin, a hormone produced by fat cells, as the most likely chief mechanism by which obesity results in increased aortic stiffness.
Hyperleptinemia is a hallmark of obesity, and leptin has previously been shown to stimulate increased levels of tumor necrosis factor-alpha and other cytokines that can increase vascular tone and thereby reduce elasticity.