Association between genetic risk of high SBP and hypertension control: the CoLaus|PsyColaus study

Abstract

Objective: To assess whether a genetic risk score (GRS) for high SBP is associated with poor control of hypertension.Methods: Data from the four waves of a populationbased, prospective study conducted in Lausanne, Switzerland. Control of hypertension was defined based on SBP less than 140 mmHg and DBP less than 90 mmHg. A weighted GRS was computed from 362 SNPs.Results: Overall, 1097 (51% men, mean age 61 years), 1126 (53% men, age 65 years), 1020 (52% men, age 69 years) and 809 (50% men, age 71 years) participants treated for hypertension were selected from the baseline (2003-2006), first (2009-2012), second (2014-2017) and third (2018-2021) surveys. Hypertension control rates were 50, 58, 52 and 59% for the baseline, first, second and third surveys, respectively. No association was found between GRS and hypertension control: multivariateadjusted mean AE standard error for controlled vs. uncontrolled participants: 9.30 AE 0.09 vs. 9.50 AE 0.09 (P ¼ 0.12); 9.32 AE 0.08 vs. 9.53 AE 0.10 (P ¼ 0.10); 9.17 AE 0.08 vs. 9.34 AE 0.11 (P ¼ 0.22), and 9.18 AE 0.09 vs. 9.46 AE 0.11 (P ¼ 0.07) for the baseline, first, second and third surveys, respectively. Power analysis showed that a minimum of 3410 people treated for hypertension would be necessary to detect an association between the GRS and hypertension control rates. Notably, positive associations between the GRS and SBP levels were found among participants not treated for hypertension, with Spearman correlations ranging between 0.05 and 0.09 (all P < 0.05). Conclusion:Using a GRS associated with SBP levels is not predictive of hypertension control. The use of GRS for hypertension management is not warranted in clinical practice.

No association between genetic markers and hypertension control in multiple cross-sectional studies

“…No association was found between the GRS and hypertension control in both surveys and for both thresholds. Our results are in line with a previous paper from our group where no association between a 362-SNP GRS and BP control was found 19 and with a recent Finnish study, where no clear association between a 793-SNP PRS and BP control was found 38 . A likely explanation is that the effect of those GRS is too small to be detected with the current sample size.…”

“…For instance, a genetic variant in the catechol- O -methyl transferase ( COMT ) gene was significantly associated with a lower systolic blood pressure (SBP) level among subjects treated with calcium channel blockers 16 , while SNP rs2106809 of the ACE2 gene was associated with response to ACE inhibitors in women 17 . Indeed, it has been suggested that genotyping might improve hypertension management 18 , but in a previous study we failed to find any association between a GRS made of 362 SNPs and hypertension management 19 . Still, whether GRS or specific genetic variants might influence hypertension control has been little studied.…”