Differences between males and females in blood pressure changes during their lifetimes
Authors:
Murín J. 1; Bulas J. 1; Wawruch M. 2; Gašpar Ľ. 1,3
Authors‘ workplace:
I. interná klinika LF UK a UN Bratislava
1; Ústav farmakológie a klinickej farmakológie, LF UK Bratislava
2; Inštitút fyzioterapie, balneológie a liečebnej rehabilitácie Piešťany, UCM Trnava
3
Published in:
Kardiol Rev Int Med 2020, 22(2): 72-74
Overview
In the last three decades, epidemiological data have showed us that women suffer from similar cardiovascular (CV) diseases as men, but that these diseases start later and their symptoms are more often atypical. In ischaemic heart disease and in heart failure (HF) women suffer more often from coronary microvascular dysfunction and from HF with normal ejection fraction in comparison with men. CV pathophysiology of disease development may therefore be different in each sex.A recent analysis looked at the differences in blood pressure (BP) changes as well as in serum lipids and other risk factors during the patients’ lifetimes. They concentrated more on BP changes, as these are presented in all clinical studies and hypertension contributes to the development of ischaemic heart disease and to HF. They analysed data from the Framingham, ARIC, CARDIA and MESA studies, concentrated on the ages of 5–98 years and looked at the presence of other risk factors. The results are: 32,833 patients, 54% of whom were women, follow-up of 43 years, 8,130 (24.8%) major CV events. Systolic blood pressure values in women reached the male values in the age subgroup of around 48–50 years and later they exceeded them. During the ageing process all blood pressure components increased more in women. The trends in blood pressure developments were not changed by other risk factors or by the treatment of hypertension. The occurrence of major CV events was higher in men (29.7%) than it was in women (20.5%). In women, the increase in BP is more progressive than in men and the same applies to vascular atherosclerotic changes. The pathogenesis of development of CV disease is different in each sex, possibly due to hormonal and genetic changes but also due to a complex set of social factors.
Keywords:
cardiovascular diseases – risk factors – blood pressure – differences between sexes
Sources
1. Dean J, Cruz SD, Mehta PK et al. Coronary microvascular dysfunction: sex-specific risk, diagnosis, and therapy. Nat Rev Cardiol 2015; 12(7): 406–414. doi: 10.1038/ nrcardio.2015.72.
2. Eaton CB, Pettinger M, Rossouw J et al. Risk factors for inicident hospitalized heart failure patients with preserved versus reduced ejection fraction in a multiracial cohort of postmenopausal women. Circ Heart Fail 2016; 9(10): e002883. doi: 10.1161/ CIRCHEARTFAILURE.115.002883.
3. Beale AL, Mayer P, Marwick TH et al. 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.118.034271
4. Ji H, Kim A, Ebinger JE et al. Sex differences in blood pressure trajectories over the life course. JAMA Cardiol 2020; 5(3): 19–26. doi: 10.1001/ jamacardio.2019.5306.
5. Cheng S, Xanthakis V, Sullivan LM et al. Blood pressure tracking over the adult life course: patterns and correlates in the Framingham heart study. Hypertension 2012; 60(60): 1393–1399. doi: 10.1161/ HYPERTENSIONAHA.112.201780.
6. 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.2016.19043.
7. Daubert MA, Douglas PS. Primary prevention of heart failure in women. JACC Heart Fail 2019; 7(3): 181–191. doi: 10.1016/ j.jchf.2019.01.011.
8. 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.0000000000000351.
9. The ARIC investigators. The Atherosclerosis Risk In Communities (ARIC) Study: design and objective. Am J Epidemiol 1989; 129(4): 687–702.
10. Yano, 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.2016.5678.
11. Bild DE, Bluemke DA, Burke GL et al. Multi-ethnic study of atheroclerosis: objectives and design. Am J Epidemiol 2002; 156(9): 871–881. doi: 10.1093/ aje/ kwf113.
12. Wills AK, Lawlor S, 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.1000440.
13. 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.117.09537.
14. Arnold AP, Cassis LA, Eghbali M et al. Sex hormones and sex chromosomes cause sex differences in the development of cardiovascular diseases. Artrioscler Thromb Vasc Biol 2017; 37(5): 746–756. doi: 10.1161/ ATVBAHA.116.307301.
15. Naqvi S, Godfrey AK, Hughes JF et al. Conservation, acquisition, and functional impact of sex-biased gene expression in mammals. Science 2019; 365(6450): eaaw7317. doi: 10.1126/ science.aaw7317.
16. Heise L, Greene ME, Opper N et al. Gender inequality and restrictive gender norms: Framing the challenges to health. Lancet 2019; 393(10189): 2440–2454. doi: 10.1016/ S0140-6736(19)30652-X.
17. 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.2014.10.003.
18. 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.20509.
19. 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/ hpx032.
20. 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.2013.02.013.
21. Guzik TJ, Touyz RM. Oxidative stress, inflammation, and vascular aging in hypertension. Hypertension 2017; 70(4): 660–667. doi: 10.1161/ HYPERTENSIONAHA.117.07802.
22. 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.2013.02.092.
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Paediatric cardiology Internal medicine Cardiac surgery CardiologyArticle was published in
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