A total of 6,517 patients met criteria for the study, with AMI occurring in 273 (4.2%). Demographic characteristics, cardiovascular risk factors, HIV-related factors, antiretroviral medication use, and encounter history are shown in . The median time from laboratory measurement to either AMI or last encounter was 55 days for CD4 (interquartile range [IQR] 161) and 55 days for HIV viral load (IQR 144). Patients with an AMI had significantly higher rates of hypertension, diabetes, chronic kidney disease, and coronary heart disease and higher rates of dyslipidemia and smoking. Among patients with AMI, a significantly increased proportion had CD4 counts less than 200/mm3 or HIV viral loads greater than 100,000 copies/ml. Patients with AMI were more likely to be African-American and had more encounters but a shorter overall duration of follow-up in the health care system. Antiretroviral medication use patterns according to AMI status are shown in the table.
In univariate regression models, CD4 count less than 200/mm3 (OR 2.00, 95% CI 1.48-2.71; P<0.0001) and viral load greater than 100,000 copies/ml (OR 2.23, 95% CI 1.37-3.65; P=0.001) were associated with an increased risk of AMI. Conversely, viral load less than 400 copies/ml (OR 0.56, 95% CI 0.38-0.82; P=0.003) was associated with a decreased risk of AMI.
In a multivariate regression model adjusting simultaneously for CD4 count, viral load, age, gender, race, hypertension, diabetes, dyslipidemia, chronic kidney disease, smoking, years since first ART use, and antiretroviral medications individually associated with AMI, CD4 count less than 200/mm3 was significantly associated with an increased risk of AMI (OR 1.74, 95% CI 1.07-2.81; P=0.02). Having a viral load greater than 100,000 was also a predictor of AMI, but this effect did not reach statistical significance (OR 1.63, 95% 0.91-2.93, P=0.10). We tested for an interaction and did not find evidence of a statistically significant interaction between CD4 count and viral load as dichotomous variables (P=0.47). Other covariates significantly associated with an increased risk of AMI included age, male gender, non-Caucasian race, and hypertension. Tenofovir, but not other individual antiretroviral medications, was associated with AMI (OR 0.48, 95% CI 0.25-0.92, P=0.03). The odds ratios and 95 percent confidence intervals for all covariates in the model are shown in .
Odds Ratio for AMI in a Multivariate Analysis
A series of models was constructed to further explore the relationships between CD4 and viral load with AMI. When both CD4 count and viral load were represented as continuous variables, a CD4 count increase of 50/mm3 was associated with a decreased risk of AMI (OR 0.93, 95% CI 0.89-0.97; P=0.002). Similarly, when CD4 nadir and peak viral load were evaluated in the same model, a CD4 nadir count increase of 50/mm3 was associated with a somewhat decreased risk of AMI, although this result did not reach statistical significance (OR 0.95, 95% CI 0.89-1.01, P=0.09). Viral load did not significantly predict AMI when included with CD4 count as a continuous variable or as peak level.
When included individually in the multivariate model without viral load, the effects of the CD4 count on AMI were similar, with CD4 count less than 200/mm3 conferring an increased risk (OR 1.53, 95% CI 1.08-2.16, P=0.02) and a CD4 count increase of 50/mm3 conferring a decreased risk (OR 0.95, 95% CI 0.92-0.98, P=0.001). An increase of CD4 nadir count did not demonstrate a significant effect. In multivariate models including viral load parameters but not CD4 count, a higher viral load was consistently and significantly associated with AMI (for viral load greater than 100,000 copies/ml, OR 2.16, 95% CI 1.26-3.69, P=0.01; for each log10 increase in viral load, OR 1.23, 95% CI 1.04-1.44, P=0.01; for each log10 increase in peak viral load, OR 1.23, 95% CI 1.04-1.44, P=0.02). Viral load less than 400 copies/ml significantly predicted a decreased risk of AMI (OR 0.60, 95% CI 0.38-0.93, P=0.02).