For comparison, we conducted the same analysis for zidovudine, stavudine, didanosine and lamivudine. As a supplementary analysis we used the propensity-score matching method [12]. Using logistic regression, we calculated each patient’s predicted probability of being treated with abacavir based on the patient’s covariate pattern. Covariates included in this model were

age at the start of HAART (grouped in quartiles: <32, 33–38, 39–46 and >46 years), gender, year of HIV diagnosis (before vs. after 1 January 1995), year of HAART initiation (before vs. after 1 January 1998), CD4 count at start of HAART (≤200 vs.>200 cells/μL), viral load at start of HAART (>100 000 vs. ≤100 000 copies/mL), Caucasian race (yes/no), route of infection (injecting drug use vs. other), heart diseases other than the study outcome, and the presence of comorbidities at HAART initiation (diabetes, alcoholism, chronic obstructive lung disease, hypertension, liver disease and kidney Sunitinib cost disease). Model fit was assessed using goodness-of-fit statistics (Pearson χ2, P=0.4; Hosmer and Lemeshow test, P=0.07). We found 1761 abacavir users and 1191 nonusers. We were able to match 1126 abacavir users to appropriate nonusers (94.5% of possible pairs), thereby eliminating differences in the propensity score between the users and nonusers. For most covariates the standardized

difference in percentage between abacavir users and nonusers was selleck kinase inhibitor reduced after matching. After matching there were no statistically significant differences between users and nonusers

for route of infection, age and viral load at start of HAART. Finally, we repeated the Cox regression analyses for the seven models in Table 2. We analysed data using sas software, version 9.1.3 (SAS Institute, Cary, NC, USA). The study was approved by the Danish Data Protection Vasopressin Receptor Agency. The study cohort consisted of 2952 HIV-infected patients, of whom 2257 were men (Table 1). Twenty-two patients with an MI prior to HAART initiation were excluded. Nearly 60% of patients exposed to HAART initiated abacavir during the study period of 19 124 PYR and almost one-third of the observation time was obtained from individuals after first exposure to abacavir. 97.4% of the patients had complete follow-up. We observed 67 MIs in the study period, of which 36 occurred after initiation of abacavir. The overall hospitalization rate for MI was 3.5/1000 PYR (95% CI 2.8–4.5). Prior to initiation of abacavir the incidence rate was 2.4/1000 PYR (95% CI 1.7–3.4) and after initiation of abacavir it was 5.7/1000 PYR (95% CI 4.1–7.9). In the unadjusted analysis, the relative risk of hospitalization with MI after initiation of abacavir was 2.22 (95% CI 1.31–3.76) (Table 2). The relative risk adjusted for potential confounders was 2.00 (95% CI 1.10–3.64) and the relative risk adjusted for confounding using propensity scores was also 2.00 (95% CI 1.07–3.76) (Table 2).