Association of Parental Hypertension With Arterial Stiffness in Nonhypertensive Offspring

High arterial stiffness is increasingly conceptualized as a cause of hypertension, in addition to being a consequence of long-standing high blood pressure. For instance, recent observations from the Framingham Offspring cohort suggest that increases in blood pressure and new-onset hypertension were antedated by higher arterial stiffness. A similar relation between vascular stiffness and later-life high blood pressure has been observed previously in the Atherosclerosis Risk In Communities study (ARIC). Arterial stiffness is a moderately heritable phenotype, with heritability estimates ranging between 0.2 and 0.5. Hypertension is also a heritable condition, with reported heritability estimates of similar magnitude to those of arterial stiffness measures (ie, 0.2–0.5). Of note, although both hypertension and arterial stiffness are heritable and clinically related conditions, the genetic link between these 2 phenotypes is insufficiently investigated. If high arterial stiffness is causally involved in the pathogenesis of clinical hypertension, offspring of parents with hypertension would be expected to display greater arterial stiffness than offspring of parents without hypertension even before they develop clinically manifest hypertension. We investigated this hypothesis by assessing the relations of parental hypertension with 4 offspring arterial stiffness measures (ie, mean arterial pressure [MAP], carotid–femoral pulse wave velocity, forward pressure wave amplitude, and augmentation index) in a sample of nonhypertensive, young adults (mean age: 38 years) of the Framingham Heart Study. Abstract—High arterial stiffness seems to be causally involved in the pathogenesis of hypertension. We tested the hypothesis that offspring of parents with hypertension may display higher arterial stiffness before clinically manifest hypertension, given that hypertension is a heritable condition. We compared arterial tonometry measures in a sample of 1564 nonhypertensive Framingham Heart Study third-generation cohort participants (mean age: 38 years; 55% women) whose parents were enrolled in the Framingham Offspring Study. A total of 468, 715, and 381 participants had 0 (referent), 1, and 2 parents with hypertension. Parental hypertension was associated with greater offspring mean arterial pressure (multivariable-adjusted estimate=2.9 mm Hg; 95% confidence interval, 1.9–3.9, and 4.2 mm Hg; 95% confidence interval, 2.9–5.5, for 1 and 2 parents with hypertension, respectively; P<0.001 for both) and with greater forward pressure wave amplitude (1.6 mm Hg; 95% confidence interval, 0.6–2.7, and 1.9 mm Hg; 95% confidence interval, 0.6–3.2, for 1 and 2 parents with hypertension, respectively; P=0.003 for both). Carotid–femoral pulse wave velocity and augmentation index displayed similar dose-dependent relations with parental hypertension in sex-, age-, and height-adjusted models, but associations were attenuated on further adjustment. Offspring with at least 1 parent in the upper quartile of augmentation index and carotid–femoral pulse wave velocity had significantly higher values themselves (P≤0.02). In conclusion, in this community-based sample of young, nonhypertensive adults, we observed greater arterial stiffness in offspring of parents with hypertension. These observations are consistent with higher vascular stiffness at an early stage in the pathogenesis of hypertension. (Hypertension. 2016;68:584-589. DOI: 10.1161/HYPERTENSIONAHA.116.07426.) • Online Data Supplement