Table 4.
Proportion of dose variability uniquely explained by clinical and genetic in race combined and race-stratified analysis using dosing algorithms shown in Tables 2 and 3
| Model 1 | Model 2 | P | |
|---|---|---|---|
| Race combined | 45.7 | 48.3 | <.001 |
| Clinical | 16.1 | 17.4 | <.001 |
| Genetic | 22.1 | 23.5 | <.001 |
| Race stratified | |||
| European Americans | 51.4 | 54.0 | <.001 |
| Clinical | 14.7 | 16.4 | <.001 |
| Genetic | 34.1 | 34.6 | .009 |
| African Americans | 29.3 | 33.9 | <.001 |
| Clinical | 21.5 | 22.8 | .002 |
| Genetic | 7.0 | 10.0 | <.001 |
Model 1 included predictors implemented in the COAG study: age, BSA, smoking status, VTE (as primary indication for warfarin therapy [vs non-VTE indications such as atrial fibrillation]), amiodarone cotherapy, CYP2C9*2, CYP2C9*3, and VKORC1. BSA was calculated as [(weight in kg)0.425 × (height in cm)0.725]/139.2. CYP2C9*2, CYP2C9*3, and VKORC1 were included as additive: 0 if no variants, 1 if heterozygous, and 2 if homozygous for the variant allele. Model 2 included model 1 predictors and CKD, CYP4F2, African American–specific variants CYP2C9*5, *6, *11, and rs12777823.