Abstract
Introduction: African ancestry (AA) is associated with higher BP prevalence, however the association of AA with response to intensive BP therapy, kidney function changes, and CV outcomes has not previously been explored. Methods: The study included participants from the SPRINT trial with available AA proportion. AA proportion was estimated using 106 biallelic genotype markers. Participants were stratified into tertiles from lowest (T1) to highest (T3) AA percentage. Time-dependent changes in SBP and eGFR were assessed by linear mixed-effect modeling after adjustment for potential confounders. Multivariable Cox models were constructed to evaluate the association of AA with risk of composite CV events (non-fatal MI, CV death, and HF event). Results: Among 2479 participants (median AA 78% [IQR: 73-87%], age 62 y, 46% female), baseline BP was similar across tertiles. At baseline, the prevalence of average Framingham CV risk (T1 vs. T2 vs. T3: mean 18.2% vs. 17.3% vs. 16.7%, p=0.01) and eGFR decreased (78 vs. 77 vs. 74, p=0.003) across increasing tertiles of AA. In contrast, the burden of DM (1.4% vs. 1.2% vs. 2.7%, p=0.05) and LV hypertrophy by EKG increased across increasing AA tertiles (11.1% vs. 12.0% vs. 15.7%, p=0.02). On follow up, the decline in BP over time was consistent across AA tertiles (mean reduction in SBP: 10 vs. 7 vs. 11 mm Hg, p=0.19) with no treatment interaction by genetic ancestry (p-int=0.60, Fig. A ). However, there was a greater decline in kidney function over time from T3 vs. T1 (mean eGFR decline = 3.8, 3.3, and 5.0 in T1-3) ( Fig. B ). The risk of adverse CV event was not different across AA tertiles [adjusted HR (95% CI): T3 vs. T1 = 0.93 (0.61-1.44); T2 vs T1 = 0.69 (0.42-1.11)]. Conclusions: Genetic AA was not significantly associated with baseline BP level or response to therapy in the SPRINT trial. Higher genetic African ancestry was associated with favorable CV risk profiles with no difference in adverse CV event risk, but greater decline in renal function over time.
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