Abstract & Commentary
HIV Infection and Subclinical Coronary Artery Disease
By Joseph F John, Jr., MD
Dr. John reports no financial relationships.
SOURCE: Post WS, Budoff M, Kingsley L et al. Associations between HIV infection and subclinical coronary artery disease. Ann Intern Med 2014 160:458-467.
This study comes from the legacy Multicenter AIDS Cohort Study (MACS) of almost 7000 men who have sex with men, both HIV-infected and non-HIV, for 3 decades. The current study asks the question whether HIV infected men have more asymptomatic coronary artery disease than matched non-HIV infected men. A large proportion were studied using coronary angio and all subjects had the use of non-contrast cardiac CT as a total measure of coronary artery disease. There were 618 infected and 383 uninfected men. The blinded readers reported several parameters of coronary artery disease (CAD): presence, size and composition of the plaque and also the degree of luminal compromise in all coronary segments. A complex statistical analysis was used to arrive at an Agatson score of coronary involvement. The HIV infected group were a bit younger and more likely to be African American but were otherwise well matched. About one third of all men used lipid-lowering agents.
The major findings were as follows:
• The prevalence of non-calcified plaques was higher in the HIV-positive group with both non-contrast and contrast studies.
• With contrast studies, there was a coronary artery stenosis of >50% was more likely in their group but there was no difference when stenosis of >70% was compared.
• When any plaque was present, total coronary plaque and non-calcified plaque, but not calcified plaque, were more common in the HIV group.
• For variables of HAART therapy, a longer duration of HAART therapy was associated with stenosis >50%.
• Stenosis of >50% was also associated lower nadir CD4+.
• Despite these results, relatively few coronary events have occurred.
COMMENTARY
HIV infection and long term HAART therapy in the HIV-infected in the MACS cohort was associated with asymptomatic coronary disease. The authors hesitate to use the term early coronary disease but that is what we are talking about here since the presence of more advanced disease, that characterized by calcified coronary plaques, was the same in the infected and the non-infected groups. The design of the study emphasizes the need for very complex statistical analysis and some of the language describing the analysis is very difficult for most practicing physicians.
The authors are reluctant to advise the use of coronary CT in asymptomatic HIV+ patients as a screening test. In a patient-centered world, however, the patients in question may press for such a study since they may feel they would have the opportunity to reduce their risk for symptomatic cardiac events. Providers of HIV care, then, are left with this knowledge that many of their patients may have evolving coronary artery disease. Further studies will define the best course of interventions and therapies. Presently, we need to warn HIV-infected men, homosexual, bisexual or not, that they may have increasingly with time and with HAART a greater risk of CAD than their non-HIV-infected counterparts. Short of actually documenting the status of the coronary arteries with coronary CT or angiography, informed medical decision making of patient and provider will dictate the best interventions until further studies are available.
