Familial clustering of hypertensive target organ damage in the community

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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 context 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 left ventricular hypertrophy, increased relative wall thickness, albuminuria and conventional risk factors.


Prevalence of any TOD (left ventricular hypertrophy or albuminuria) in participants with zero and at least one parents with any TOD was 7 and 13%, respectively (P < 0.001 for difference). Having at least one parent with TOD was associated with greater odds of TOD in offspring than individuals without parental TOD [multivariable-adjusted odds ratio (OR), 1.65; 95% confidence interval (95% 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), parental increased relative wall thickness conferred increased odds of increased relative wall thickness in the offspring (OR, 1.54; 95% CI 1.16–2.04) and parental albuminuria was related to offspring albuminuria (OR, 1.49; 95% CI 1.03–2.16). These associations remained significant upon adjustment for other risk factors, including blood pressure, and in analyses of subgroups defined according to parental or offspring hypertension status.


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.

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