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Platelet reactivity and thrombogenicity in postmenopausal women

Singla, Anand MD; Bliden, Kevin P. MBA; Jeong, Young-Hoon MD, PhD; Abadilla, Katrina MD; Antonino, Mark J. MS; Muse, William C. BS; Mathew, Denny P. MBBS; Bailon, Oscar MD; Tantry, Udaya S. PhD; Gurbel, Paul A. MD

doi: 10.1097/gme.0b013e31825ebafd
Original Articles

Objective: Age-adjusted incidence of cardiovascular disease, including myocardial infarction, is significantly lower in premenopausal women than in men, which is thought to be caused by the cardioprotective effects of estrogen. However, there is a consistent increase in the incidence of coronary artery disease in postmenopausal women in comparison with premenopausal women. The protective benefit of hormone therapy has not been observed in postmenopausal women. It is unknown whether measures of platelet reactivity and clot strength contribute to the disproportionate incidence of cardiovascular disease between premenopausal and postmenopausal women.

Methods: Fifty healthy volunteers, including 25 premenopausal women and 25 postmenopausal women, aged between 40 and 65 years were enrolled. Total estradiol and follicle-stimulating hormone levels were measured for confirmation of menopausal state and comparison testing. Platelet reactivity was assessed using light transmission aggregometry and P-selectin, and glycoprotein IIb/IIIa receptor expression was assessed using flow cytometry. Thrombelastography was used to measure clot strength, clotting time, and fibrinogen activity. Serum cholesterol, C-reactive protein, complete blood count, and comprehensive metabolic panel were also measured.

Results: Platelet reactivity did not differ among menopausal states or hormone levels. Clotting time was increased in postmenopausal women (6.6 ± 2.0 vs 7.8 ± 1.2 min, P = 0.013) and significantly correlated with estradiol levels (r = 0.68, P < 0.001). A significantly higher low-density lipoprotein cholesterol level was observed in postmenopausal women (P = 0.05). Mean C-reactive protein levels were numerically higher in the postmenopausal group.

Conclusions: The thrombotic risk profile between premenopausal and postmenopausal women is similar. However, improved management of cholesterol may be of clinical benefit. Large-scale studies are required to validate these findings.

This is the first study to comprehensively compare measures of platelet reactivity, thrombogenecity, lipids, and inflammation between menopausal states, and estradiol and FSH hormone levels. This pilot study demonstrates that the prevalence of cardiovascular disease after menopause may not be attributable to platelet mediated factors but more likely related to increases in LDL cholesterol, systemic inflammation and an imbalance in pro-and anti-coagulant factors.

From the Sinai Center for Thrombosis Research, Baltimore, MD.

Received December 20, 2011; revised and accepted April 19, 2012.

Funding/support: The study was supported by Sinai Hospital (Baltimore, MD).

Financial disclosure/conflicts of interest: Dr. Gurbel has received research grants, honoraria, and consultant fees from AstraZeneca, Merck, Medtronic, Lilly/Daiichi Sankyo Inc., Sanofi Aventis/Bristol Myers, Portola/Novartis, Boston Scientific, Bayer, Accumetrics, Boehringer Ingelheim, and Johnson and Johnson. Dr. Jeong has received honoraria for lectures from Sanofi Aventis, Daiichi Sankyo Inc., and Otsuka. The other authors report no conflicts of interest.

Address correspondence to: Paul A. Gurbel, MD, Cardiac Catheterization Laboratory, 2401 West Belvedere Avenue, Baltimore, MD 21215. E-mail: pgurbel@lifebridgehealth.org

© 2013 by The North American Menopause Society.