New Research Adds Weight to the Evidence That the Link Between Obesity and CVD Risk Goes Beyond BMI

Ample evidence supports obesity as an independent risk factor for cardiovascular disease (CVD). Traditionally, obesity is defined by body mass index (BMI), a ratio of height and weight. More recently, data have emerged that suggest metabolic syndrome and excess adipose tissue play more of a role than BMI in determining CVD risk.

In the session “Obesity and Cardiovascular Disease (CVD): Beyond Body Weight,” researchers presented results from studies that examined these risk factors.

In the first study, Jaime Armando, PhD, and colleagues from the Cooper Institute at the University of Texas Southwestern Medical Center examined the relationship between coronary arterial disease (CAD), obesity, and metabolic syndrome. Although metabolic syndrome is a risk factor in itself, whether people who are normal weight with metabolic syndrome are at increased risk for elevated coronary atherosclerosis is unknown, Dr Armando said. The team sought to determine the degree to which BMI and metabolic syndrome were linked to CAD.

The study included more than 11,000 subjects from the Cooper Clinic Longitudinal Study with no history of CAD. For the analyses, the cohort was divided into 6 risk groups according to BMI class (normal weight, overweight, or obese) and the presence or absence of metabolic syndrome, defined by having at least 3 of 4 risk factors exclusive of obesity (blood pressure greater than 130/85 mm Hg, glucose level greater than 100 mg/dL, triglycerides greater than 150 mg/dL, and a high-density lipoprotein cholesterol level less than 40 mg/dL).

To determine risk for coronary atherosclerotic disease, researchers measured coronary artery calcium (CAC) using computerized tomography. Researchers then tested for trends across obesity levels and adjusted for age and smoking status.

Overall, 55% of the study group had a CAC score greater than zero. Results showed a trend in the CAC scores across BMI groups that was significant (P = .01). However, the presence or absence of metabolic syndrome did not alter this trend significantly. Among the cohort with metabolic syndrome, those who were normal weight were likely to have a CAC score comparable to those who were overweight or obese.

“The striking finding is that normal-weight individuals with metabolic syndrome appear as likely to have clinical signs of cardiovascular disease as overweight and obese persons with the syndrome,” she said.

In a second study, investigators used F-18 fluorodeoxyglucose positron emission tomography (FDG-PET) imaging to examine the relationship between CVD risk and adiposity (subcutaneous and visceral). Amparo Figueroa, MD, MPH, a researcher at Massachusetts General Hospital, presented the results.

“We aimed to assess CVD risk using common imaging. We hypothesized that inches of visceral adipose tissue in PET scanning would be associated with CVD risk.”

The study included 508 individuals (median age 55 years; 42% male) who were free of active cancer, CVD, or acute or chronic and who underwent FDG-PET imaging at the Massachusetts General Hospital between 2005 and 2008. CVD events (n = 44) were independently adjudicated (stroke, transient ischemic attack, acute coronary syndrome, revascularization, new-onset angina, or peripheral arterial disease).

Data showed that risk of CVD was higher among those with excess visceral adipose tissue (hazard ratio [HR], 3.36; P = .04). This risk was present regardless of whether the person was obese, Dr Figueroa told attendees. The risk was also independent of other known risk factors such as age, gender, smoking status, and cholesterol. However, the risk of CVD was not associated with BMI or subcutaneous adiposity.

The findings suggest that visceral, but not subcutaneous adiposity, is an independent predictor of CVD risk. More research is needed to confirm these findings, Dr Figueroa said.