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Low CD4s Trump Other MI Risk Factors in 6500-Person US Analysis
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XVIII International AIDS Conference, July 18-23, 2010, Vienna
Mark Mascolini
A CD4 count under 200 predicted acute myocardial infarction (MI) independently of other cardiovascular risk factors and individual antiretrovirals in a 6500-person analysis at Massachusetts General Hospital [1]. Treatment with abacavir did not boost MI risk after the investigators considered four sets of potential confounders or after they eliminated people with chronic kidney disease. Tenofovir use or female gender halved MI risk in this analysis.
The study focused on 6517 HIV-infected people who had two or more visits at Massachusetts General Hospital between December 1998 and February 2008. The investigators defined antiretroviral use as exposure to that drug during the study period. They considered CD4 counts and viral loads measured just before acute MI or at the last visit in people without MI. Multivariate analyses considered the following variables in additive sequence: (1) demographics, (2) concurrent antiretroviral use significant in univariate analysis, (3) comorbidities (hypertension, diabetes, lipid abnormalities, chronic kidney disease), and (4) CD4 count and viral load.
In the final multivariate model, four variables independently raised the risk of acute MI, and two variables independently lowered the risk at the following odds ratios (OR) and 95% confidence intervals (CI):
Associated with higher MI risk:
-- Latest CD4 below 200: OR 1.74, 95% CI 1.07 to 2.81, P = 0.02
-- Every 10 years of age: OR 1.26, 95% CI 1.00 to 1.57,P = 0.05
-- Non-Caucasian race: OR 1.67, 95% CI 1.10 to 2.54, P = 0.02
-- Hypertension: OR 1.97, 95% CI 1.25 to 3.12, P = 0.04
Associated with lower MI risk:
-- Tenofovir use: OR 0.48, 95% CI 0.25 to 0.92, P = 0.03
-- Female gender: OR 0.47, 95% CI 0.27 to 0.81, P = 0.01
Looking at the impact of individual antiretrovirals in the final multivariate model, the investigators linked three drugs to a higher risk of acute MI:
Antiretrovirals associated with higher MI risk:
-- Indinavir: OR 1.92, 95% CI 1.04 to 3.57, P = 0.04
-- Nelfinavir: OR 1.75, 95% CI 1.02 to 3.02, P = 0.04
-- Didanosine: OR 1.74, 95% CI 0.99 to 3.30, P = 0.05
Abacavir independently upped the risk of acute MI in the first three models, which considered (1) demographics, (2) demographics plus antiretrovirals, and (3) demographics, antiretrovirals, and comorbidities. But when the researchers added latest CD4 count and viral load to create the final model, abacavir no longer independently boosted MI risk (OR 1.42, 95% CI 0.85 to 2.34, P = 0.18). And when the researchers considered only people without chronic kidney disease, abacavir was not associated with a significantly higher MI risk in any of the four models.
The Massachusetts General team believes their findings "support potential roles for immune dysfunction and possibly inflammation as etiologic [causative] in HIV-related cardiovascular disease." Treating people with antiretrovirals, they suggested, "may decrease cardiovascular disease risk, with beneficial effects of immune reconstitution outweighing proatherogenic effects of individual antiretroviral medications."
Reference
1.Triant VA, Regan S, Lee H, Sax P, Meigs JB, Grinspoon SK. Association of antiretroviral therapy, immunologic and virologic factors with myocardial infarction in a U.S. health care system. XVIII International AIDS Conference. July 18-23, 2010. Vienna. Abstract WEPE0130.
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