Table 3.
Total events and event rates by genotype and treatment group, genotype-by-treatment interaction results
| Outcome | FGB -455 Genotype | Total number of events | Event rate per 1000 person-years | Genotype-specific treatment effect HR (95% CI), p-value | Genotype-by-treatment interactions (pharmacogenetic effects) RHR (95% CI), p-value | ||||||
|---|---|---|---|---|---|---|---|---|---|---|---|
| LIS | AML | CHL | LIS | AML | CHL | LIS vs. AML | LIS vs. CHL | LIS vs. AML, GA+AA vs. GG | LIS vs. CHL, GA+AA vs. GG | ||
| CHD | GG | 501 | 523 | 877 | 18.5 | 19.4 | 19.0 | 0.95 (0.84–1.08), p=0.45 | 0.97 (0.87–1.09), p=0.65 | 1.09 (0.86–1.37), p=0.49 | 0.98 (0.80–1.20), p=0.84 |
| GA+AA | 204 | 201 | 354 | 19.8 | 19.1 | 20.8 | 1.04 (0.85–1.26), p=0.72 | 0.95 (0.80–1.13), p=0.60 | |||
| Stroke | GG | 304 | 221 | 445 | 11.1 | 8.1 | 9.5 | 1.38 (1.16–1.64), p<0.001 | 1.17 (1.01–1.35), p=0.04 | 0.70 (0.51–0.96), p=0.03 | 0.95 (0.71–1.26), p=0.72 |
| GA+AA | 105 | 111 | 157 | 10.1 | 10.5 | 9.1 | 0.96 (0.73–1.25), p=0.76 | 1.11 (0.87–1.42), p=0.41 | |||
| Heart failure | GG | 426 | 473 | 567 | 15.8 | 17.6 | 12.1 | 0.90 (0.79–1.02), p=0.11 | 1.30 (1.15–1.47), p<0.001 | 0.89 (0.68–1.15), p=0.37 | 0.79 (0.61–1.01), p=0.06 |
| GA+AA | 137 | 174 | 223 | 13.2 | 16.6 | 13.0 | 0.80 (0.64–0.99), p=0.05 | 1.02 (0.83–1.26), p=0.84 | |||
| All-cause mortality | GG | 889 | 790 | 1436 | 30.7 | 27.5 | 29.1 | 1.12 (1.02–1.23), p=0.02 | 1.05 (0.97–1.14), p=0.23 | 0.82 (0.68–0.99), p=0.04 | 0.83 (0.71–0.99), p=0.03 |
| GA+AA | 283 | 307 | 527 | 25.6 | 27.6 | 29.1 | 0.92 (0.78–1.08), p=0.33 | 0.88 (0.76–1.02), p=0.08 | |||
| End stage renal disease | GG | 95 | 83 | 128 | 3.4 | 3.0 | 2.7 | 1.15 (0.86–1.54), p=0.36 | 1.27 (0.97–1.65), p=0.08 | 0.53 (0.27–1.04), p=0.07 | 0.50 (0.27–0.93), p=0.03 |
| GA+AA | 17 | 28 | 44 | 1.6 | 2.6 | 2.5 | 0.61 (0.34–1.12), p=0.11 | 0.64 (0.36–1.12), p=0.12 | |||
CHL= chlorthalidone, AML = amlodipine, LIS = lisinopril, CHD = coronary heart disease