Effect of menopause on plaque morphologic characteristics in coronary atherosclerosis
Effect of menopause on plaque morphologic characteristics in coronary atherosclerosis
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DOI：
10.1067/mhj.2001.109946
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发表时间：
2001-02-01
影响因子：
4.8
通讯作者：
Virmani, R
中科院分区：
文献类型：
--
作者：
Burke, AP;Farb, A;Virmani, R
背景 女性冠状动脉疾病的出现比男性晚 10 至 15 年。为了验证雌激素的影响可能表现为冠状动脉斑块组织学差异的假设，我们检查了因冠状动脉疾病突然死亡的绝经前和绝经后女性的心脏。方法我们研究了 51 例冠心病猝死病例和 47 例死于非冠状动脉疾病的女性死亡病例。冠状动脉死亡根据组织学特征进行分类。比较各组之间急性斑块破裂、愈合斑块破裂、易损斑块和急性斑块糜烂的数量。测量死后血清总胆固醇、HDL 胆固醇和硫氰酸盐的值，并通过计算体重指数来确认绝经状态。结果 50 岁以上的女性比年轻的绝经前女性更有可能出现斑块破裂。斑块破裂与总胆固醇水平升高显着相关。在 51 名死于冠状动脉疾病的女性中，随着女性进入绝经后年龄，易损斑块的平均数量显着增加。结论我们的数据表明，雌激素对动脉粥样硬化斑块具有抗炎作用，从而稳定斑块。斑块糜烂是绝经前妇女血栓形成的主要基质，雌激素似乎不会抑制斑块糜烂。由于斑块的进展可能是由反复破裂和反复侵蚀引起的，因此更好地了解雌激素对动脉粥样硬化的影响可能有助于深入了解冠状动脉疾病的本质。
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.