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  ID Week
October 2-6, 2013
San Francisco
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Higher Intramyocardial Lipids in Antiretroviral-Treated Men Than in HIV-Negatives
  IDWeek, October 2-6, 2013, San Francisco
Mark Mascolini
Compared with matched HIV-negative controls, HIV-positive men taking antiretroviral therapy (ART) had significantly higher intramyocardial lipid deposits, according to results of a study using cardiac magnetic resonance spectroscopy (cMR Spec) [1]. The finding could help explain the higher risk of heart disease in HIV-positive than HIV-negative people.
Concern persists that combination ART contributes to abnormal body fat changes, abnormal lipids, hyperglycemia, and a heightened risk of atherosclerosis, coronary artery disease, myocardial infarction, and thromboembolism. Because the contribution of intramyocardial lipids to this clinical scenario remains poorly understood, researchers at Cedars-Sinai Medical Center in Los Angeles and other sites conducted this case-control study of antiretroviral-treated men and an age-matched group without HIV.
The asymptomatic HIV-positive study participants were all men taking ART for at least 3 years. The investigators excluded current smokers and men with coronary artery disease, diabetes, injection drug or cocaine use, an estimated glomerular filtration rate below 60 mL/min, or a prior AIDS illness. Controls tested negative for HIV and matched HIV-positive men by age (+/- 3 years), sexual orientation, and medical history. All study participants underwent cMR Spec, which measures triglyceride percentage in 3.7 cm(3) of the myocardial interventricular septum.
Among the 20 HIV-positive men who contributed data to the analysis, median time since HIV diagnosis stood at 18.5 years (range 4 to 28) and median time on ART at 14 years (range 4 to 26). Median months of treatment with protease inhibitors, nonnucleosides, and nucleosides were 78, 11.3, and 102.5. Median exposure to abacavir or didanosine, nucleosides implicated in cardiovascular risk in some research, was 2.5 months (range 0 to 212). Median exposure to high-risk protease inhibitors (amprenavir, fosamprenavir, indinavir, or lopinavir) was 48.5 months (range 0 to 102.5).
Compared with 19 HIV-negative controls, the 20 HIV-positive men were similar in median age (50 HIV- and 49.5 HIV+), median body mass index 24.4 and 24.8 kg/m(2), median high-density lipoprotein cholesterol (50 and 51 mg/dL), 10-year Framingham risk score (3% and 3%), and proportion with metabolic syndrome (31.5% and 30%). The HIV-negative group had somewhat lower median low-density lipoprotein cholesterol (83.5 versus 91 mg/dL), lower (better) median waist-to-hip ratio (0.92 versus 0.96), and a lower percentage of ever-smokers (11% versus 45%), but somewhat higher median systolic blood pressure (125 versus 110 mm Hg).
Median intramyocardial lipid content in HIV-positive men more than tripled the median in HIV-negative men (0.87% versus 0.25%, P < 0.05). Average intramyocardial lipid content in men with HIV almost doubled the average in HIV-negative controls (1.13% versus 0.65%, P < 0.05). Lipid content ranges were 0 to 4.28% in men with HIV and 0 to 3.87% in men without HIV.
The investigators observed that cardiac steatosis (fat build-up from abnormal lipid retention) has been linked to several Framingham risk factors, including diabetes, hypertension, and abnormal plasma lipids. People with cardiac steatosis have increased stroke volume and heart rate [2]. One hypothesis explaining how metabolic changes lead to cardiovascular disease, the researchers noted, involves over-storage of lipids and lipotoxic injury to heart muscle [3,4].
The researchers proposed that "this increase in cardiac lipids may contribute to or be associated with an increased risk of cardiovascular disease, including end-stage heart failure in this [HIV-positive] patient population."
1. Tellalian D, Szczepaniak L, Ramirez D, et al. Pilot study to evaluate intramyocardial lipid accumulation in HIV+ patients receiving highly active antiretroviral therapy (HAART). IDWeek 2013. October 2-6, 2013. San Francisco. Abstract 322.
2. Kenchaiah S, Evans J, Levy D, et. al. Obesity and risk of heart failure. N Engl J Med. 2002;347:305-313
3. McGavock J, Victor R, Unger R, Szcepaniak L. Adiposity of the heart, revisited. Ann Intern Med. 2006;144:517-524
4. Zhou Y, Grayburn P, Karim A, et al. Lipotoxic heart disease in obese rats: implications for human obesity. Proc Natl Acad Sci USA. 2000;97:1784-1789.