Sex Differences in Blood Pressure Trajectories Over the Life Course | Cardiology | JAMA Cardiology | JAMA Network
[Skip to Navigation]
Access to paid content on this site is currently suspended due to excessive activity being detected from your IP address 35.170.64.36. Please contact the publisher to request reinstatement.
1.
Dean  J, Cruz  SD, Mehta  PK, Merz  CN.  Coronary microvascular dysfunction: sex-specific risk, diagnosis, and therapy.   Nat Rev Cardiol. 2015;12(7):406-414. doi:10.1038/nrcardio.2015.72PubMedGoogle Scholar
2.
Eaton  CB, Pettinger  M, Rossouw  J,  et al.  Risk factors for incident hospitalized heart failure with preserved versus reduced ejection fraction in a multiracial cohort of postmenopausal women.   Circ Heart Fail. 2016;9(10):e002883. doi:10.1161/CIRCHEARTFAILURE.115.002883PubMedGoogle Scholar
3.
Beale  AL, Meyer  P, Marwick  TH, Lam  CSP, Kaye  DM.  Sex differences in cardiovascular pathophysiology: why women are overrepresented in heart failure with preserved ejection fraction.   Circulation. 2018;138(2):198-205. doi:10.1161/CIRCULATIONAHA.118.034271PubMedGoogle Scholar
4.
Cheng  S, Xanthakis  V, Sullivan  LM, Vasan  RS.  Blood pressure tracking over the adult life course: patterns and correlates in the Framingham heart study.   Hypertension. 2012;60(6):1393-1399. doi:10.1161/HYPERTENSIONAHA.112.201780PubMedGoogle Scholar
5.
Forouzanfar  MH, Liu  P, Roth  GA,  et al.  Global burden of hypertension and systolic blood pressure of at least 110 to 115 mm Hg, 1990-2015.   JAMA. 2017;317(2):165-182. doi:10.1001/jama.2016.19043PubMedGoogle Scholar
6.
Daubert  MA, Douglas  PS.  Primary prevention of heart failure in women.   JACC Heart Fail. 2019;7(3):181-191. doi:10.1016/j.jchf.2019.01.011PubMedGoogle Scholar
7.
Mehta  LS, Beckie  TM, DeVon  HA,  et al; American Heart Association Cardiovascular Disease in Women and Special Populations Committee of the Council on Clinical Cardiology, Council on Epidemiology and Prevention, Council on Cardiovascular and Stroke Nursing, and Council on Quality of Care and Outcomes Research.  Acute myocardial infarction in women: a scientific statement from the American Heart Association.   Circulation. 2016;133(9):916-947. doi:10.1161/CIR.0000000000000351PubMedGoogle Scholar
8.
The ARIC investigators.  The Atherosclerosis Risk in Communities (ARIC) Study: design and objectives.   Am J Epidemiol. 1989;129(4):687-702. doi:10.1093/oxfordjournals.aje.a115184PubMedGoogle Scholar
9.
Yano  Y, Reis  JP, Tedla  YG,  et al.  Racial differences in associations of blood pressure components in young adulthood with incident cardiovascular disease by middle age: Coronary Artery Risk Development in Young Adults (CARDIA) Study.   JAMA Cardiol. 2017;2(4):381-389. doi:10.1001/jamacardio.2016.5678PubMedGoogle Scholar
10.
Bild  DE, Bluemke  DA, Burke  GL,  et al.  Multi-Ethnic Study of Atherosclerosis: objectives and design.   Am J Epidemiol. 2002;156(9):871-881. doi:10.1093/aje/kwf113PubMedGoogle Scholar
11.
O’Brien  E, Mee  F, Atkins  N, O’Malley  K.  Inaccuracy of the Hawksley random zero sphygmomanometer.   Lancet. 1990;336(8729):1465-1468. doi:10.1016/0140-6736(90)93177-QPubMedGoogle Scholar
12.
Ni  H, Wu  C, Prineas  R,  et al.  Comparison of Dinamap PRO-100 and mercury sphygmomanometer blood pressure measurements in a population-based study.   Am J Hypertens. 2006;19(4):353-360. doi:10.1016/j.amjhyper.2005.10.020PubMedGoogle Scholar
13.
Jacobs  DR  Jr, Yatsuya  H, Hearst  MO,  et al.  Rate of decline of forced vital capacity predicts future arterial hypertension: the Coronary Artery Risk Development in Young Adults Study.   Hypertension. 2012;59(2):219-225. doi:10.1161/HYPERTENSIONAHA.111.184101PubMedGoogle Scholar
14.
Tobin  MD, Sheehan  NA, Scurrah  KJ, Burton  PR.  Adjusting for treatment effects in studies of quantitative traits: antihypertensive therapy and systolic blood pressure.   Stat Med. 2005;24(19):2911-2935. doi:10.1002/sim.2165PubMedGoogle Scholar
15.
Wald  DS, Law  M, Morris  JK, Bestwick  JP, Wald  NJ.  Combination therapy versus monotherapy in reducing blood pressure: meta-analysis on 11,000 participants from 42 trials.   Am J Med. 2009;122(3):290-300. doi:10.1016/j.amjmed.2008.09.038PubMedGoogle Scholar
16.
Wu  J, Kraja  AT, Oberman  A,  et al.  A summary of the effects of antihypertensive medications on measured blood pressure.   Am J Hypertens. 2005;18(7):935-942. doi:10.1016/j.amjhyper.2005.01.011PubMedGoogle Scholar
17.
Feinstein  M, Ning  H, Kang  J, Bertoni  A, Carnethon  M, Lloyd-Jones  DM.  Racial differences in risks for first cardiovascular events and noncardiovascular death: the Atherosclerosis Risk in Communities study, the Cardiovascular Health Study, and the Multi-Ethnic Study of Atherosclerosis.   Circulation. 2012;126(1):50-59. doi:10.1161/CIRCULATIONAHA.111.057232PubMedGoogle Scholar
18.
Vasan  RS, Short  MI, Niiranen  TJ,  et al.  Interrelations between arterial stiffness, target organ damage, and cardiovascular disease outcomes.   J Am Heart Assoc. 2019;8(14):e012141. doi:10.1161/JAHA.119.012141PubMedGoogle Scholar
19.
Franklin  SS, Gustin  W  IV, Wong  ND,  et al.  Hemodynamic patterns of age-related changes in blood pressure: the Framingham Heart Study.   Circulation. 1997;96(1):308-315. doi:10.1161/01.CIR.96.1.308PubMedGoogle Scholar
20.
Wills  AK, Lawlor  DA, Matthews  FE,  et al.  Life course trajectories of systolic blood pressure using longitudinal data from eight UK cohorts.   PLoS Med. 2011;8(6):e1000440. doi:10.1371/journal.pmed.1000440PubMedGoogle Scholar
21.
Shen  W, Zhang  T, Li  S,  et al.  Race and sex differences of long-term blood pressure profiles from childhood and adult hypertension: the Bogalusa Heart Study.   Hypertension. 2017;70(1):66-74. doi:10.1161/HYPERTENSIONAHA.117.09537PubMedGoogle Scholar
22.
Naqvi  S, Godfrey  AK, Hughes  JF, Goodheart  ML, Mitchell  RN, Page  DC.  Conservation, acquisition, and functional impact of sex-biased gene expression in mammals.   Science. 2019;365(6450):eaaw7317. doi:10.1126/science.aaw7317PubMedGoogle Scholar
23.
Heise  L, Greene  ME, Opper  N,  et al; Gender Equality, Norms, and Health Steering Committee.  Gender inequality and restrictive gender norms: framing the challenges to health.   Lancet. 2019;393(10189):2440-2454. doi:10.1016/S0140-6736(19)30652-XPubMedGoogle Scholar
24.
Arnold  AP, Cassis  LA, Eghbali  M, Reue  K, Sandberg  K.  Sex hormones and sex chromosomes cause sex differences in the development of cardiovascular diseases.   Arterioscler Thromb Vasc Biol. 2017;37(5):746-756. doi:10.1161/ATVBAHA.116.307301PubMedGoogle Scholar
25.
Gaillard  R, Steegers  EA, Tiemeier  H, Hofman  A, Jaddoe  VW.  Placental vascular dysfunction, fetal and childhood growth, and cardiovascular development: the generation R study.   Circulation. 2013;128(20):2202-2210. doi:10.1161/CIRCULATIONAHA.113.003881PubMedGoogle Scholar
26.
Lang  RM, Badano  LP, Mor-Avi  V,  et al.  Recommendations for cardiac chamber quantification by echocardiography in adults: an update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging.   J Am Soc Echocardiogr. 2015;28(1):1-39.e14. doi:10.1016/j.echo.2014.10.003PubMedGoogle Scholar
27.
Dickerson  JA, Nagaraja  HN, Raman  SV.  Gender-related differences in coronary artery dimensions: a volumetric analysis.   Clin Cardiol. 2010;33(2):E44-E49. doi:10.1002/clc.20509PubMedGoogle Scholar
28.
Rizzoni  D, Agabiti-Rosei  C, Agabiti-Rosei  E.  Hemodynamic consequences of changes in microvascular structure.   Am J Hypertens. 2017;30(10):939-946. doi:10.1093/ajh/hpx032PubMedGoogle Scholar
29.
Weber  T, Wassertheurer  S, O’Rourke  MF,  et al.  Pulsatile hemodynamics in patients with exertional dyspnea: potentially of value in the diagnostic evaluation of suspected heart failure with preserved ejection fraction.   J Am Coll Cardiol. 2013;61(18):1874-1883. doi:10.1016/j.jacc.2013.02.013PubMedGoogle Scholar
30.
Guzik  TJ, Touyz  RM.  Oxidative Stress, Inflammation, and Vascular Aging in Hypertension.   Hypertension. 2017;70(4):660-667. doi:10.1161/HYPERTENSIONAHA.117.07802PubMedGoogle Scholar
31.
Paulus  WJ, Tschöpe  C.  A novel paradigm for heart failure with preserved ejection fraction: comorbidities drive myocardial dysfunction and remodeling through coronary microvascular endothelial inflammation.   J Am Coll Cardiol. 2013;62(4):263-271. doi:10.1016/j.jacc.2013.02.092PubMedGoogle Scholar
Original Investigation
January 15, 2020

Sex Differences in Blood Pressure Trajectories Over the Life Course

Author Affiliations
  • 1Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts
  • 2Framingham Heart Study, Framingham, Massachusetts
  • 3Department of Cardiology, Shanghai Tenth People’s Hospital, Tongji University, Shanghai, China
  • 4Barbra Streisand Women’s Heart Center, Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, California
  • 5Hypertension Center of Excellence, Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, California
  • 6National Institute for Health and Welfare, Helsinki, Finland
  • 7Turku University Hospital, Department of Medicine, University of Turku, Turku, Finland
JAMA Cardiol. 2020;5(3):255-262. doi:10.1001/jamacardio.2019.5306
Key Points

Question  How do patterns of blood pressure (BP) change over the life course and differ between sexes?

Findings  In this analysis of 4 community cohort studies, trajectories of BP elevation in 32 833 individuals (54% women) were examined serially over 4 decades (age span, 5 to 98 years). Women compared with men exhibited a steeper increase in BP measures that began as early as in the third decade and continued throughout the life course.

Meaning  Sex differences in BP trajectories, which begin early and persist with aging, may set the stage for later-life cardiovascular diseases that frequently present differently in women vs men.

Abstract

Importance  If we assume that women and men exhibit variations of the same fundamental vascular physiology, then conventional analyses of subclinical measures would suggest that women catch up to men by midlife in the extent of potentially important vascular disease. Alternatively, under the assumption that vascular physiology may fundamentally differ between women and men, a sex-specific analysis of existing data could offer new insights and augment our understanding of sex differences in cardiovascular diseases.

Objective  To evaluate whether longitudinal patterns of blood pressure (BP) elevation differ between women and men during the life course when considering baseline BP levels as the reference.

Design, Setting, and Participants  We conducted sex-specific analyses of longitudinal BP measures (144 599 observations) collected for a period of 43 years (1971 to 2014) in 4 community-based US cohort studies. The combined total included 32 833 participants (54% female) spanning ages 5 to 98 years. Data were analyzed between May 4, 2019, and August 5, 2019.

Exposures  Age and serially assessed longitudinal BP measures: systolic BP, diastolic BP, mean arterial pressure (MAP), and pulse pressure (PP).

Main Outcomes and Measures  Sex-specific change in each primary BP measure compared with baseline BP levels, derived from multilevel longitudinal models fitted over the age span, and new-onset cardiovascular disease events.

Results  Of the 32 833 participants, 17 733 were women (54%). Women compared with men exhibited a steeper increase in BP that began as early as in the third decade and continued through the life course (likelihood ratio test χ2 = 531 for systolic BP; χ2 = 123 for diastolic BP; χ2 = 325 for MAP; and χ2 = 572 for PP; P for all <.001). After adjustment for multiple cardiovascular disease risk factors, these between-sex differences in all BP trajectories persisted (likelihood ratio test χ2 = 314 for systolic BP; χ2 = 31 for diastolic BP; χ2 = 129 for MAP; and χ2 = 485 for PP; P for all <.001).

Conclusions and Relevance  In contrast with the notion that important vascular disease processes in women lag behind men by 10 to 20 years, sex-specific analyses indicate that BP measures actually progress more rapidly in women than in men, beginning early in life. This early-onset sexual dimorphism may set the stage for later-life cardiovascular diseases that tend to present differently, not simply later, in women compared with men.

×