• Exposure to HAART Is Associated With an Increased Risk of Myocardial Infarction: The D:A:D Study (Oral 130)
  Authored by N. Friis-Møller, R. Weber, A. D'Arminio Monforte, W. El-Sadr, P. Reiss, F. Dabis, L. Morfeldt, S. De Wit, C. Pradier, G. Calvo, M. Law, O. Kirk, C. Sabin, J.D. Lundgren
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The debate over whether HIV and its therapy are associated with the development of coronary heart disease (CHD) was as prominent at this year's conference as it was at last year's conference. Once again we heard conflicting data as the studies are either retrospective, with many confounding factors, or prospective and of short duration, thus making it impossible to know how much HIV and its therapies are contributing to the development of CHD, if at all.

Dr. Friis-Møller presented the results of a prospective observational study of 23,468 subjects from 11 cohorts in three continents. Subjects were enrolled from July 1999-April 2001 with the final data collection/analysis, having been taken during August 2002, being presented here.

Although the subjects were followed prospectively starting July 1999, the investigators entered data based on how many years ago subjects were started on HAART (PI or NNRTI), which varied from none to greater than six years.

It is unclear if they truly have source documentation of all 23,468 subjects' first date of HAART or whether they derived this date from the subject's history as documented in a chart. Data on HIV disease, risk factors for myocardial infarction (MI) and incident MI was collected. The median age of this cohort is 39 years, 24 percent female, 60 percent smokers and 30 percent had elevated triglycerides (TG).

During 36,479 person years, a total of 126 subjects had a MI -- a subgroup comprised of 90 percent men with a median age 48 years. Thirty-six (25 percent) of the subjects had a fatal MI (different data than in written abstract). Not surprisingly traditional risk factors remained independent predictors of developing an MI such as age, male sex, previous history of CHD and smoking. Other important risks included diabetes and hypertension. The relative risk per year of exposure to HAART was 1.26. Interestingly, lipodystrophy was a protective risk (RR 0.6), however, this term was defined by subjective measures and needs to be further studied before any conclusions can be drawn.

The investigators concluded that HAART use was associated with a 26 percent relative increase in the rate of MI per year of exposure over the first seven years. I agree with the investigators that this cohort should be followed longitudinally over the next few years. This database has many of the same limitations that other databases have that collect information retrospectively and then follow subjects that have many confounding factors prospectively.

Hopefully, over time, as they follow this cohort, particularly the many subjects who entered the study on no HAART or initial regimens, we can begin to sort out those factors contributing to CHD from HIV and its therapies versus traditional risk factors.

The investigators are to be commended for developing such a large cohort and collecting data from various international centers. The work involved in maintaining such a database is enormous. This will be a very valuable cohort to follow and I look forward to their yearly reports. As Dr. Friis-Møller noted, the risk of MI at this point is low and the obvious benefits of HAART outweigh concerns over potential CHD. Nevertheless, it remains important to consider all aspects of health care for HIV-infected individuals, including modification of traditional CHD risk factors if possible as well as treating the complications of HAART as they arise.