Related Experiment Videos
Association of Parental Hypertension With Arterial Stiffness in Nonhypertensive Offspring: The Framingham Heart Study
Charlotte Andersson1, Rene Quiroz2, Danielle Enserro2
1From Boston University's and the National Heart, Lung, and Blood Institute's Framingham Heart Study, Framingham, MA (C.A., M.G.L., D.L., E.J.B., R.S.V.); Section of Cardiology, Department of Internal Medicine, Glostrup Hospital, Denmark (C.A.); Cardiology Clinic of San Antonio, TX (R.Q.); Department of Epidemiology (D.E., E.J.B., R.S.V.) and Department of Biostatistics (M.G.L.), Boston University School of Public Health, MA; Department of Mathematics and Statistics, Boston University, MA (M.G.L.); Whitaker Cardiovascular Institute (N.M.H., J.A.V., E.J.B., R.S.V.) and Section of Preventive Medicine and Epidemiology (E.J.B., R.S.V.), Boston University School of Medicine, MA; National Heart, Lung and Blood Institute, Bethesda, MD (D.L.); and Cardiovascular Engineering, Inc, Norwood, MA (G.F.M.). ca@heart.dk.
Insights
Children of parents with hypertension show increased arterial stiffness, a key factor in high blood pressure development. This suggests a hereditary link to early vascular changes, even before hypertension is diagnosed.
Area of Science:
- Cardiovascular Research
- Genetics of Hypertension
- Vascular Physiology
Background:
- High arterial stiffness is implicated in hypertension development.
- Hypertension is a heritable condition, suggesting a genetic predisposition.
- Early detection of vascular changes can inform preventative strategies.
Purpose of the Study:
- To investigate if offspring of hypertensive parents exhibit higher arterial stiffness.
- To determine if parental hypertension is associated with subclinical vascular changes in their nonhypertensive adult children.
- To explore the dose-dependent relationship between the number of hypertensive parents and offspring arterial stiffness.
Main Methods:
- Cross-sectional study of 1564 nonhypertensive adults from the Framingham Heart Study third-generation cohort.
- Arterial tonometry was used to measure arterial stiffness, including mean arterial pressure and forward pressure wave amplitude.
- Participants were categorized based on whether they had 0, 1, or 2 parents with hypertension.
Main Results:
- Offspring with one or two hypertensive parents had significantly higher mean arterial pressure and forward pressure wave amplitude.
- Carotid-femoral pulse wave velocity and augmentation index showed similar trends, though attenuated after adjustments.
- Individuals with a parent in the upper quartile of arterial stiffness measures had significantly higher values themselves.
Conclusions:
- Offspring of parents with hypertension demonstrate increased arterial stiffness.
- These findings suggest elevated vascular stiffness may be an early, heritable marker in hypertension pathogenesis.
- Early identification of at-risk individuals can aid in hypertension prevention efforts.
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.