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Population Heterogeneity in Trajectories of Midlife Blood Pressure

Wills, Andrew K.a; Lawlor, Debbie A.b; Muniz-Terrera, Gracielac; Matthews, Fionac; Cooper, Rachela; Ghosh, Arjun K.a; Kuh, Dianaa; Hardy, Rebeccaa; on behalf of the FALCon Study Team

doi: 10.1097/EDE.0b013e3182456567

Background: We investigated whether there are subgroups with different underlying (latent) trajectories of midlife systolic blood pressure (BP), diastolic BP, and pulse pressure in a UK cohort.

Methods: Data are from 1840 men and 1819 women with BP measured at ages 36, 43, and 53 years. We used unconditional growth mixture models to test for the presence of latent trajectory classes. Extracted classes were described in terms of a number of known lifetime risk factors, and linked to the risk of undiagnosed angina (Rose questionnaire) at age 53 years.

Results: In both sexes for systolic BP, diastolic BP, and pulse pressure, there was a large “normative” class (>90% of the sample) characterized by gentle annual increases (eg, an increase in male systolic BP of 0.9 mm Hg/year [95% confidence interval = 0.9 to 1.0]), with a smaller class for whom the rate of increase was high (eg, an increase in male systolic BP of 3.1 mm Hg/year [2.8 to 3.4]). In women, there was an additional class for whom BP was high at age 36 and remained high. Persons in the “normative” classes were, on average, heavier at birth and taller at age 7 years, had a lower midlife body mass index, and were less likely to be on antihypertensive medication compared with those in other classes. Among those with no diagnosed cardiovascular disease, those in the classes with more strongly increasing systolic BP and pulse pressure were at greatest risk of angina.

Conclusion: Our study suggests that in midlife the majority of the population have a gentle underlying increase in BP, but that there also exists an important subgroup in whom BP increases much more markedly. These classes may be useful for identifying those most at risk for cardiovascular disease.

Author Information

From the aMRC Unit for Lifelong Health and Ageing, University College London, London, United Kingdom; bMRC Centre for Causal Analyses in Translational Epidemiology, School of Social Medicine, University of Bristol, Bristol, United Kingdom; and cMRC Biostatistics Unit, University of Cambridge, Cambridge, United Kingdom.

Submitted 19 January 2011; accepted 25 October 2011; posted online 16 January 2012.

Supported by the UK Medical Research Council (MRC) Population health sciences research network (PHSRN29), which funded this research and the salary of A.K.W., D.K., R.H., G.M. ((MRC) WBS U.1052.00.013.00003) and F.M. (U.1052.00.013.00001). R.C. is receiving support from the HALCyon programme funded by the New Dynamics of Ageing (RES-353-25-0001). The UK MRC and the University of Bristol provide core funding for the MRC Centre of Causal Analyses in Translational Epidemiology where DAL works. The UK MRC has provided funding for the NSHD since 1962. The authors reported no other financial interests related to this research.

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Correspondence: Andrew K. Wills, MRC Unit for Lifelong Health and Ageing, University College London, 33 Bedford Place, London, United Kingdom, WC1B 5JU. E-mail:

© 2012 Lippincott Williams & Wilkins, Inc.