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Judith A. Aberg, Heather Ribaudo, Cardiac Risk: Not So Simple, The Journal of Infectious Diseases, Volume 201, Issue 3, 1 February 2010, Pages 315–317, https://doi.org/10.1086/649898
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Understanding the risk of cardiovascular disease in persons with human immunodeficiency virus (HIV) infection is complex. Controversy exists as to how much risk can be attributed to host genetics, traditional risk factors, adverse effects from antiretroviral therapy, and the inflammatory state associated with HIV itself [1]. Nevertheless, the INTERHEART study [2], conducted in the general population, clearly suggests there is synergy among cardiovascular risk factors, such that the co-occurrence of 2 or more risk factors (eg, hypertension and dyslipidemia), may have greater-than-additive effects on overall cardiovascular risk. Thus, all factors potentially contributing to coronary heart disease (CHD) need to be considered when managing persons infected with HIV. The difficulties in determining risks among those with HIV infection have largely been due to the lack of matched controls, small sample size, and lack of standardized definitions, plus the unknown contribution from HIV itself. Previously, the Data Collection on Adverse Events of Anti-HIV Drugs (D:A:D) investigators reported an increased relative rate (RR) of myocardial infarction (MI) with cumulative use of protease inhibitors (RR per year of exposure, 1.16 [95% confidence interval {CI}, 1.10–1.23]) but not nonnucleoside reverse-transcriptase inhibitors (RR per year of exposure, 1.05 [95% CI, 0.98–1.13]). In a subsequent analysis focusing on nucleoside reversetranscriptase inhibitor use, an unexpected increased risk of MI was found with recent use of abacavir (RR, 1.90 [95% CI, 1.47–2.45]) and didanosine (RR, 1.49 [95% CI, 1.14–1.95]), but not with cumulative use [3]. Criticism of the study at that time was that abacavir had been preferentially prescribed to those with metabolic syndromes, lipoatrophy, dyslipidemia, renal disease, and CHD and that the study results reflected provider prescribing bias, especially given that there was an inadequate duration of time to evaluate the effects of tenofovir, a nucleotide similarly prescribed as abacavir except among those with renal disease. In a study by Worm et al [4] in this issue of the Journal, with 1 additional year of follow-up of the cohort, the D:A:D investigators were able to examine the association of tenofovir with CHD and found no such association. Of the drugs studied in their analysis, only indinavir, ritonavir-boosted lopinavir, didanosine, and abacavir were associated with an increased risk of having an MI. Although use of these agents was associated with increased cardiovascular risk, it is important to compare this risk with those resulting from other factors. For example, according to prior D:A:D results, protease inhibitor-associated risk was considerably lower than the annual increase in risk associated with advanced age (RR, 1.39; P>.001), male sex (RR, 1.91; P=.002), or current smoking (RR, 2.83; P>.001) [3].
