Long-term follow-up studies have indicated that obesity is a predictor of cardiovascular risk in both genders. Obesity is the culprit behind heart ailments like hypertension, heart attack, high cholesterol and coronary artery disease.

Arterial stiffening occurs as we age and is is associated with an increased risk of cardiovascular diseases like Stroke and myocardial infarction. The gold standard method to check arterial stiffness is by measuring the carotid femoral pulse wave velocity. Increased arterial stiffness is  reflected by an increased pulse wave velocity (PWV) and is generally seen to be associated with higher risk for cardiovascular morbidity and mortality.

Recently in the past few years it has been demonstrated that individuals with obesity are likely to have an increased aortic stiffness which predisposes them to risk for  cardiovascular diseases. This is independent of Blood pressure level, ethnicity, and age.

Though the pathophysiologic mechanisms that link abdominal adiposity to stiffening are not fully understood, several mechanisms have been cited.

·       Visceral adipocytes have an elevated lipolytic activity that results in increased free fatty acids release in the portal vein with an accumulation (liver, pancreas, and muscles) that contributes to insulin resistance.

·       Other mechanisms such as increases in circulating pro-inflammatory cytokines or leptin. High levels of leptin have been documented in individuals with obesity and found to be correlated with reduction in arterial distensibility.

·       In addition, leptin induces oxidative stress in endothelial cells, and this action triggers the transcription of oxidant-sensitive genes that participate in atherogenesis.

·       Leptin increases sympathetic nervous activity. It is possible that the high levels of leptin that are observed in obesity could contribute to its adverse effects on cardiovascular health.

·       Increase in circulating pro-inflammatory cytokines may contribute to the development of  cardiovascular disease in obese individuals.

·       The reduced arterial elasticity may be the consequence of hyperglycemias and/or insulin’s acting either directly or through the development of advanced glycation end products. Non-enzymatic glycosylation of the matrix proteins of arterial vessels may enhance the production of cross-links between collagen fibers, which in turn could cause arterial stiffness and systolic hypertension.

All the above reasons could be attributed to arterial stiffening in an obese individual.

In a recent study published on bio-medcentral, it was found that most measures of obesity like the Body Mass Index, Waist circumference, Waist to hip ratio or the  visceral fat are strong predictors of arterial stiffness. These can also be used to asses ones risk to arterial stiffening and cardiovascular disease risk.

References:

Nordstrand N et al.The relationship between various measures of obesity and arterial stiffness in morbidly obese patients”.BMC Cardiovascular disorders, 2011.

Safar M.E et al “Obesity, Arterial Stiffness, and Cardiovascular Risk”. American Society of Nephrology, 2006, 17: 109-111

Source-Medindia