Table 2.
Group and subgroup$ (uutcome = CVD, unless specified) | No. of studies | Fixed effects | Shore-adjusted# | Random effects# | Heterogeneity | ||||
---|---|---|---|---|---|---|---|---|---|
sRR | 95% CI | 95% CI | sRR | 95% CI | χ2 | P | I2 value (%) | ||
Recent exposure | |||||||||
All studies | 17 | 1.56 | 1.44, 1.69 | 1.40, 1.74 | 1.35 | 1.20, 1.53 | 28.5 | 0.03 | 44 |
Excluding Bedimo et al., 2011 | 16 | 1.61 | 1.48, 1.75 | NA | NA | NA | 13.6 | 0.57 | 0 |
Outcome | |||||||||
AMI | 11 | 1.68 | 1.49, 1.90 | NA | NA | NA | 9.30 | 0.50 | 0 |
Study population | |||||||||
ART-naïve | 5 | 1.91 | 1.48, 2.46 | NA | NA | NA | 0.79 | 0.94 | 0 |
Study design | |||||||||
Observational studies | 15 | 1.60 | 1.48, 1.74 | NA | NA | NA | 10.30 | 0.74 | 0 |
Data year$ | |||||||||
Pre-2008 | 8 | 1.85 | 1.63, 2.10 | NA | NA | NA | 5.63 | 0.58 | 0 |
Post-2008 | 2 | 1.53 | 1.30, 1.81 | 1.14, 2.06 | 1.62 | 1.16, 2.25 | 3.19 | 0.07 | 69 |
Comparator agent | |||||||||
Tenofovir | 2 | 2.94 | 1.19, 7.25 | 0.88, 9.76 | 3.41 | 0.91,12.76 | 1.76 | 0.18 | 43 |
Confounder adjustment | |||||||||
Potential causal mediators or traditional CVD risk factors* | 15 | 1.56 | 1.44, 1.70 | NA | NA | NA | 13.84 | 0.46 | 0 |
Substance abuse | 12 | 1.64 | 1.49, 1.82 | 1.48, 1.83 | 1.26 | 1.13, 1.41 | 12.39 | 0.33 | 11 |
Smoking status | 12 | 1.55 | 1.42, 1.68 | 1.41, 1.69 | 1.37 | 1.25, 1.51 | 12.32 | 0.34 | 11 |
Prior CVD | 12 | 1.57 | 1.43, 1.71 | 1.41, 1.73 | 1.41 | 1.26, 1.57 | 14.87 | 0.19 | 26 |
CD4 cell count and HIV viral load | 11 | 1.56 | 1.42, 1.72 | NA | NA | NA | 9.78 | 0.46 | 0 |
Cumulative exposure (per year) | |||||||||
Model not adjusted for recent exposure | 4 | 1.12 | 1.07, 1.18 | 1.05, 1.20 | 1.11 | 1.02, 1.21 | 6.71 | 0.08 | 55 |
Model adjusted for recent abacavir exposure | 5 | 1.00 | 0.94, 1.06 | 0.93, 1.08 | 1.00 | 0.92, 1.10 | 6.75 | 0.15 | 41 |
AMI, acute myocardial infarction; ART, antiretroviral therapy; Cl, confidence interval; sRR, summary relative risk.
Studies included in this group adjusted for at least three of five potential factors (hypertension, diabetes mellitus, renal dysfunction, dyslipidemia, and lipodystrophy) that may lie on the causal pathway between abacavir exposure and risk of CVD.
Shore-adjusted confidence intervals and random-effects models may be used when the χ2 statistic was greater than the degrees of freedom (number of studies minus 1).