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Longer Antiretroviral Therapy Means Bigger Coronary Plaques
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48th ICAAC, October 25-28, 2008, Washington, DC
Mark Mascolini
Longer antiretroviral therapy made larger coronary artery plaques more likely in a case-control study of 22 people with HIV and 22 uninfected controls matched for cardiovascular risk factors [1]. Extent of coronary artery calcification appeared similar in adults with and without HIV. But in the HIV group duration of antiretroviral therapy correlated more closely with coronary artery plaque volume than did traditional heart risk factors summarized by the Framingham Risk Score. The researchers cautioned, though, that lack of correlation between plaque volume and traditional risk factors in the HIV group may reflect the small size of the analysis.
The study by Colleen Hadigan and coworkers at the National Institute of Allergy and Infectious Diseases (NIAID) involved 22 HIV-infected "cases" and 22 HIV-negative controls matched for gender, age, race, body mass index, and Framingham Risk Score for cardiovascular disease. All study participants had one or more coronary artery disease risk factors, such as current smoking, hypertension, and abnormal lipids. Everyone had a creatinine at or below 1.3 mg/dL. And everyone underwent noncontrast computed tomography (CT) for calcium score and CT angiography.
Case and control groups each included 20 men and 2 women averaging about 53 years in age. The groups were somewhat racially mismatched, with 10 African Americans in the case group (45%) and 4 (18%) in the control group (P = 0.08). About one third of cases and controls smoked, and about two thirds had hypertension. One third of cases had type 2 diabetes, compared with 9% of controls. The HIV group averaged 13.9 years of HIV infection and a CD4 count of 561; two thirds had a viral load below 50 copies. Seventeen cases (77%) were taking antiretrovirals, including 6 (27%) taking a protease inhibitor.
Coronary artery plaque volume averaged 86.9 (+/- 27.0) mm(3) in the HIV group and 56.9 (+/- 16.8) mm(3) in controls, a nonsignificant difference (P = 0.35). Calcium score was equivalent in the 2 groups--106.7 (+/- 49.4) in cases and 145.7 (+/- 68.2) in controls (P = 0.65). Average Framingham Risk Score also proved similar in cases and controls (12.8 +/- 1.3 and 10.3 +/- 1.5, P = 0.20).
Nineteen HIV-infected people (86%) had atherosclerosis, 7 with moderate and 1 with severe narrowing of 1 or more coronary arteries. On a log scale coronary calcium score correlated positively with coronary plaque volume in all study participants (r = 0.58, P < 0.001), as did age (r = 0.32, P = 0.039). Framingham Risk Score did not correlate with plaque volume or coronary calcium score.
In people taking antiretrovirals, treatment duration correlated positively with log plaque volume (r = 0.46, P = 0.037). This correlation held true after adjustment for age (P < 0.05). But plaque volume did not correlate with duration of HIV infection, exposure to protease inhibitors, HIV load, or lipids. The researchers discerned a trend toward an inverse correlation between CD4 count and plaque volume in people with HIV (r = -0.42, P = 0.06).
The NIAID investigators see a need for large, longitudinal cohort studies with hard clinical endpoints and appropriate control groups "to more fully elucidate the relationship between HIV-associated coronary artery disease risk factors, antiretroviral exposure and coronary artery disease" in people with HIV infection.
Reference
1. Hadigan C, Healey L, Muldoon N, Sanko J, Georgoff P, Gharib AM. Coronary plaque volume by CT angiography correlates with duration of antiretroviral therapy. 48th Annual International Conference on Antimicrobial Agents and Chemotherapy (ICAAC). October 25-28, 2008. Washington, DC. Abstract H-2311.
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