Abstract P402: Familial Clustering of Hypertensive Target Organ Damage in the Community

Abstract

Prior studies suggest that hypertensive target organ damage (TOD) is a heritable trait. However, the risk that parental TOD confers on propensity for TOD in their offspring, and how hypertensive TOD clusters in the background of parental versus offspring hypertension status remain unclear. We studied 3238 Framingham Heart Study participants (mean age 39±8 years, 53% women) with available parental data on TOD. Parents and offspring underwent measurements for echocardiographic left ventricular hypertrophy, microalbuminuria, and conventional risk factors. Prevalence of any TOD (left ventricular hypertrophy or microalbuminuria) in participants with 0 and ≥1 parents with any TOD was 7% (131 of 1860) and 13% (173 of 1378), respectively ( P <0.001 for difference). As illustrated in the Figure , having ≥1 parent with TOD was associated with greater odds of TOD in offspring compared to individuals without parental TOD (multivariable-adjusted odds ratio [OR], 1.65; 95% confidence interval [CI], 1.27-2.14). Similarly, parental left ventricular hypertrophy was associated with offspring left ventricular hypertrophy (OR, 2.73; 95% CI 1.92-3.89) and parental albuminuria was related to offspring albuminuria (OR, 1.49; 95% CI 1.03-2.16). These associations remained robust upon additional adjustment for risk factors and in analyses of subgroups defined according to parental or offspring hypertension status ( Figure ). Overall our data suggest that familial clustering of TOD in the community is independent of blood pressure. Additional studies are warranted to confirm our observations.