Objective: To examine whether altered levels of adipokines, adipose-derived peptides associated with myocardial infarction in the general population, may contribute to subclinical coronary atherosclerosis in HIV-infected persons.
Design: Nested cohort study.
Methods: We studied HIV-infected (HIV+) and HIV-uninfected (HIV−) men in the Multicenter AIDS Cohort Study with noncontrast computed tomography (CT) to measure coronary artery calcium and regional adiposity; 75% additionally underwent coronary CT angiography to measure plaque composition and stenosis. Adiponectin and leptin levels were assessed. Multiple regression models were used to assess associations between adipokine levels and HIV disease parameters, regional adiposity, and plaque adjusted for age, race, HIV serostatus, and cardiovascular disease (CVD) risk factors.
Results: Significant findings were limited to adiponectin. HIV-positive men (n = 493) had lower adiponectin levels than HIV-negative men (n = 250) after adjusting for CVD risk factors (P <0.0001), which became nonsignificant after adjustment for abdominal visceral and thigh subcutaneous adipose tissue. Among HIV-positive men, lower adiponectin levels were associated with higher CD4+ T-cell counts (P = 0.004), longer duration of antiretroviral therapy (P = 0.006), and undetectable HIV RNA levels (P = 0.04) after adjusting for age, race, and CVD risk factors; only CD4+ cell count remained significant after further adjustment for adipose tissue. In both groups, lower adiponectin levels were associated with increased odds of coronary stenosis more than 50% (P <0.007). Lower adiponectin levels were associated with increased extent of plaque in HIV-positive and of mixed plaque in HIV-negative men.
Conclusion: Adiponectin levels were lower in HIV-infected men and related to the severity of subclinical atherosclerosis, independent of traditional CVD risk factors.
Johns Hopkins University, Baltimore, Maryland, USA.
Correspondence to Todd T. Brown, MD, PhD, Division of Endocrinology, Diabetes, and Metabolism, Johns Hopkins University, 1830 East Monument Street, Suite 333, Baltimore, MD 21287, USA. E-mail: email@example.com
Received 24 October, 2013
Revised 17 December, 2013
Accepted 17 December, 2013