American Heart Journal
Volume 141, Issue 2, Supplement , Pages S58-S62, February 2001

Effect of menopause on plaque morphologic characteristics in coronary atherosclerosis☆☆

Washington, DC, and New Orleans, La

From the Department of Cardiovascular Pathology, Armed Forces Institute of Pathology, Washington, DC,a and the bDepartment of Pathology, Louisiana State University, New Orleans

Abstract 

Background Coronary artery disease in women appears 10 to 15 years later than in men. To test the hypothesis that the effects of estrogen may manifest themselves as histologic differences in coronary plaques, we examined the hearts of premenopausal and postmenopausal women who died suddenly from coronary artery disease. Methods We studied 51 cases of sudden coronary death and 47 deaths in women who died from noncoronary causes. Coronary deaths were classified on the basis of histologic features. The number of acute plaque ruptures, healed plaque ruptures, vulnerable plaques, and acute plaque erosions were compared between groups. Postmortem values of serum total cholesterol, HDL cholesterol, and thiocyanate were measured, and menopausal status was confirmed by calculating body mass index. Results Women older than 50 years of age were much more likely to have a ruptured plaque than were younger, premenopausal women. Plaque rupture was significantly associated with elevated total cholesterol level. In the 51 women who died of coronary disease, the mean number of vulnerable plaques increased significantly as women advanced into the postmenopausal years. Conclusions Our data suggest that estrogen has an anti-inflammatory effect on atherosclerotic plaques, resulting in plaque stabilization. Plaque erosion, the major substrate for thrombosis in premenopausal women, does not appear to be inhibited by estrogen. Because plaque progression may result both from repeated rupture and repeated erosion, a better understanding of the effect of estrogen on atherosclerosis may yield insights into the nature of coronary artery disease. (Am Heart J 2001;141:S58-62.)

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 Supported in part by research grant RO1HL61799-02 from the National Institutes of Health.

☆☆ The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or reflecting the views of the Department of the Army, the Department of the Air Force, or the Department of Defense.

 Reprint requests: Renu Virmani, MD, Department of Cardiovascular Pathology, Armed Forces Institute of Pathology, Washington, DC 20306-6000. E-mail: virmani@afip.osd.mil

PII: S0002-8703(01)70045-2

American Heart Journal
Volume 141, Issue 2, Supplement , Pages S58-S62, February 2001