DALLAS – It’s not obesity per se that affects cardiovascular risk, it’s where that excess body fat is stored, according to the results of a novel adipose tissue–imaging study.
Excess visceral adipose tissue is independently associated with increased risk of developing cardiovascular disease. In contrast, increased lower body subcutaneous adipose tissue – that is, fat around the hips and a big butt – actually seems to protect against cardiovascular disease, Dr. Ian J. Neeland reported at the American Heart Association scientific sessions.
He presented an analysis of 972 obese participants in the Dallas Heart Study with a mean age of 44 years at enrollment and no baseline cardiovascular disease. All underwent dual-energy x-ray absorptiometry and MRI assessment of their body fat distribution, focusing on the visceral, abdominal subcutaneous, and lower body subcutaneous adipose tissue depots. Participants were then followed prospectively for a median 8.1 years, during which 91 cardiovascular events occurred in 68 subjects.
The impetus for the adipose tissue imaging study was the researchers’ recognition that obesity is a heterogeneous disorder.
"Currently, we know that obesity is associated with incident cardiovascular disease at a general population level. However, body mass index alone is really an inadequate marker of risk among the obese. Many individuals with even high BMIs do not develop cardiovascular disease. Marked abdominal obesity is a stronger predictor of cardiovascular disease but still lacks the necessary specificity. So there’s really a clinical need for tools to differentiate obese individuals who will develop cardiovascular disease from those who will be free of cardiovascular disease for their lifetime," explained Dr. Neeland, a fellow in cardiovascular medicine at the University of Texas Southwestern Medical Center, Dallas.
In a multivariate analysis adjusted for age, sex, race, and the conventional cardiovascular risk factors, each 1–standard deviation increase in visceral adipose tissue was independently associated with a 24% increase in the risk of developing cardiovascular disease during follow-up. Dividing the study population into quartiles on the basis of their extent of visceral adipose tissue, the cumulative incidence of cardiovascular disease rose in stepwise fashion, with subjects in the lowest quartile having the least cardiovascular events and those in the top quartile having the most.
Having more lower body subcutaneous fat had the opposite effect. For every 1–standard deviation increase in the amount of fat at that location, the cardiovascular event risk dropped by 27%.
Participants’ amount of abdominal subcutaneous fat didn’t affect their cardiovascular event risk one way or another. Nor did BMI, waist circumference, waist-hip ratio, or the amount of liver fat on MRI show any significant association with cardiovascular disease risk.
"These results really underscore the biologic importance of body fat distribution with regard to cardiovascular disease risk in obesity and suggest a possible prognostic role for imaging-based assessment of body fat distribution in high-risk obese patients," according to Dr. Neeland.
One intriguing clinical implication of this study is that preventing accumulation of visceral adipose tissue may have benefit in terms of cardiovascular disease prevention even in the absence of meaningful weight loss. It’s possible that new drugs could be developed that lower cardiovascular risk in obese patients by changing their body fat distribution profile rather than lopping off pounds.
In the Dallas study, increased visceral abdominal tissue was consistently associated with a higher risk of cardiovascular disease across subgroups based upon age, race, sex, and BMI.
"Interestingly, those with increased visceral abdominal fat who were less than 40 years of age had greater risk for cardiovascular disease than [did] those over 40. This could suggest that visceral abdominal tissue has a greater impact on the young, in whom other cardiovascular risk factors have not yet accumulated over time," Dr. Neeland observed.
The cardiovascular event endpoint in the study was a composite of cardiovascular death, acute MI, stroke, heart failure, atrial fibrillation, or event-driven coronary or peripheral artery revascularization.
The Dallas Heart Study is funded by the Donald W. Reynolds Foundation. Dr. Neeland reported having no financial conflicts.