Abstract
Introduction: The increase of cardiovascular risk in women coincides with the onset of menopause. Left ventricular hypertrophy (LVH), carotid atherosclerosis (CA) and chronic kidney disease are expressions of target organ damage in hypertension. This study evaluated whether menopause affects the development of target organ damage in hypertension.
Methods: We retrospectively analysed 963 hypertensive women referred to the Hypertension Clinic of the “Federico II” University, Naples, Italy, from October 1998 to July 2007.
Results: Postmenopausal women (n = 399) were older, had higher systolic blood pressure and worse metabolic profile compared with premenopausal women (n = 564). In postmenopausal women, prevalence of target organ damage was higher compared with premenopausal women. In particular, in premenopausal and postmenopausal patients, prevalence of LVH was 27% and 49% (p < 0.001), and of chronic kidney disease was 7% and 10% (p < 0.05), respectively. Similarly, prevalence of carotid thickening and carotid plaque was 34% and 28% in premenopausal women, and 37% and 48% (both p < 0.001) in postmenopausal women, respectively. Multiple stepwise regression analysis showed that menopause (adjusted odds ratio [OR] 2.14; 95% CI 1.13, 4.06; p = 0.02) and hypercholesterolaemia (adjusted OR 2.3; 95% CI 1.03, 5.17; p = 0.04) were independent predictors of CA.
Conclusions: Our results show that in hypertensive women menopause increases the risk of CA.
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Acknowledgements
This study was supported by the Italian National Minister of Health — Progetto Strategico-annuity 2006; S.C. was a recipient of a grant from the Italian Society of Hypertension (SIIA). The first two authors contributed equally to this manuscript. The authors have no conflicts of interest that are directly relevant to the content of this study.
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Crispo, S., De Gennaro, S., Buono, F. et al. Menopause Increases the Risk of Carotid Atherosclerosis in Essential Hypertension. High Blood Press Cardiovasc Prev 17, 31–36 (2010). https://doi.org/10.2165/11311740-000000000-00000
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DOI: https://doi.org/10.2165/11311740-000000000-00000