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Whether cardiovascular risk scores geographically aggregate and inform on spatial development of atherosclerotic cardiovascular diseases (ASCVD) remains unknown. Our aim is to determine the spatial distribution of 10-year predicted cardiovascular risk and ASCVD, and to compare the overlap of the resulting spatial distributions. Using prospective data from the CoLaus|PsyCoLaus cohort study (2003-2021) we computed SCORE2 in participants free from ASCVD. Geographical distributions of predicted risk and events were determined using the Gi* Getis-Ord autocorrelation statistic. 6203 individuals (54% women, mean age 52.5 ± SD 10.7, ASCVD incidence rate 5.7%) were included. We identified clusters of high versus low predicted risk (4%, 6%, respectively) and ASCVD (5%, 5% respectively) at baseline. They persisted at follow-up. Overlap of SCORE2 and ASCVD clusters was marginal. Body-mass index and alcohol consumption explained most of the predicted risk distribution. For ASCVD, high clusters persisted or were reinforced after multivariate adjustment, while low incidence clusters were reduced, multifactorial determinants. Incidence rate of ASCVD was 2.5% higher (IC 95%, 1.4-3.7) in clusters of higher incidence of ASCVD. To develop up-to-date, geographically targeted prevention strategies, there is a need to study novel geographically risk factors affecting ASCVD and to update commonly used prediction models for a population approach., (© 2024. The Author(s).)

We aimed to assess whether genetic markers are associated with hypertension control using two cross-sectional surveys conducted in Lausanne, Switzerland. Management of hypertension was assessed as per ESC guidelines using the 140/90 or the 130/80 mm Hg thresholds. One genetic risk score (GRS) for hypertension (18 SNPs) and 133 individual SNPs related to response to specific antihypertensive drugs were tested. We included 1073 (first) and 1157 (second survey) participants treated for hypertension. The prevalence of controlled participants using the 140/90 threshold was 58.8% and 63.6% in the first and second follow-up, respectively. On multivariable analysis, only older age was consistently and negatively associated with hypertension control. No consistent associations were found between GRS and hypertension control (140/90 threshold) for both surveys: Odds ratio and (95% confidence interval) for the highest vs. the lowest quartile of the GRS: 1.06 (0.71-1.58) p = 0.788, and 1.11 (0.71-1.72) p = 0.657, in the first and second survey, respectively. Similar findings were obtained using the 130/80 threshold: 1.23 (0.79-1.90) p = 0.360 and 1.09 (0.69-1.73) p = 0.717, in the first and second survey, respectively. No association between individual SNPs and hypertension control was found. We conclude that control of hypertension is poor in Switzerland. No association between GRS or SNPs and hypertension control was found., (© 2023. The Author(s).)

Apolipoprotein A-IV (apoA-IV) has been observed to be associated with lipids, kidney function, adiposity- and diabetes-related parameters. To assess the causal relationship of apoA-IV with these phenotypes, we conducted bidirectional Mendelian randomization (MR) analyses using publicly available summary-level datasets from GWAS consortia on apoA-IV concentrations (n = 13,813), kidney function (estimated glomerular filtration rate (eGFR), n = 133,413), lipid traits (HDL cholesterol, LDL cholesterol, triglycerides, n = 188,577), adiposity-related traits (body-mass-index (n = 322,206), waist-hip-ratio (n = 210,088)) and fasting glucose (n = 133,010). Main analyses consisted in inverse-variance weighted and multivariable MR, whereas MR-Egger regression and weighted median estimation were used as sensitivity analyses. We found that eGFR is likely to be causal on apoA-IV concentrations (53 SNPs; causal effect estimate per 1-SD increase in eGFR = -0.39; 95% CI = [-0.54, -0.24]; p-value = 2.4e-07). Triglyceride concentrations were also causally associated with apoA-IV concentrations (40 SNPs; causal effect estimate per 1-SD increase in triglycerides = -0.06; 95% CI = [-0.08, -0.04]; p-value = 4.8e-07), independently of HDL-C and LDL-C concentrations (causal effect estimate from multivariable MR = -0.06; 95% CI = [-0.10, -0.02]; p-value = 0.0014). Evaluating the inverse direction of causality revealed a possible causal association of apoA-IV on HDL-cholesterol (2 SNPs; causal effect estimate per one percent increase in apoA-IV = -0.40; 95% CI = [-0.60, -0.21]; p-value = 5.5e-05).