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Hypertension. 2008;52:381-386
Published online before print June 23, 2008, doi: 10.1161/HYPERTENSIONAHA.108.113589
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(Hypertension. 2008;52:381.)
© 2008 American Heart Association, Inc.


Original Articles

Association of Parental Hypertension With Concentrations of Select Biomarkers in Nonhypertensive Offspring

Wolfgang Lieb; Michael J. Pencina; Thomas J. Wang; Martin G. Larson; Katherine J. Lanier; Emelia J. Benjamin; Daniel Levy; Geoffrey H. Tofler; James B. Meigs; Christopher Newton-Cheh; Ramachandran S. Vasan

From the Framingham Heart Study (W.L., M.J.P., T.J.W., M.G.L., E.J.B., D.L., C.N.-C., R.S.V.), Framingham, Mass; Department of Mathematics (M.J.P., M.G.L., K.J.L.) and Preventive Medicine and Cardiology Sections (E.J.B., R.S.V.), Boston University School of Medicine, Mass; Divisions of Cardiology (T.J.W., C.N.-C.) and General Medicine (J.B.M.), Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston; National Heart, Lung, and Blood Institute (D.L.), Bethesda, Md; Royal North Shore Hospital (G.H.T.), Sydney, Australia; and the Program in Medical and Population Genetics (C.N-C.), Broad Institute of Harvard and Massachusetts Institute of Technology, Cambridge, Mass.

Correspondence to Ramachandran S. Vasan, Framingham Heart Study, 73 Mount Wayte Ave, Framingham, MA 01702-5803. E-mail vasan{at}bu.edu

Children of parents with hypertension are at increased risk of developing high blood pressure. We hypothesize that circulating concentrations of putative biomarkers (that may play a role in development of high blood pressure) are higher in nonhypertensive offspring of parents with hypertension. We compared concentrations of 4 different biomarkers (urinary albumin:creatinine ratio, circulating C-reactive protein, aldosterone:renin ratio, and plasminogen activator inhibitor-1) in nonhypertensive Framingham offspring study participants with none (n=233), 1 (n=474), or both (n=322) parents with hypertension. Parental hypertension was defined as onset before age 60 years, based on longitudinal observations of the original Framingham cohort. Serum C-reactive protein concentrations were higher in nonhypertensive offspring with 1 (median: 1.7; Q1 to Q3: 0.8 to 3.6 mg/L) or both parents with hypertension (median: 1.8; Q1 to Q3: 0.7 to 3.6 mg/L) compared with offspring without parental hypertension (median: 1.4; Q1 to Q3: 0.7 to 3.2 mg/L). In multivariable analyses, parental hypertension was associated with higher serum C-reactive protein concentration in offspring (15% increase per parent with hypertension; P=0.004). Prospectively, the relation of parental hypertension to longitudinal changes in blood pressure in the nonhypertensive offspring was attenuated on adjustment for C-reactive protein (P=0.04 for attenuation). The levels of the other biomarkers evaluated did not significantly differ in offspring according to parental hypertension status. In conclusion, serum C-reactive protein concentrations are higher in nonhypertensive offspring of parents with hypertension. These data suggest that inflammation may partly mediate the familial influences on hypertension risk.


Key Words: hypertension • offspring • biomarkers • C-reactive protein