A plea for a clinical trial of anticoagulation in dilated cardiomyopathy.
A plea for a clinical trial of anticoagulation in dilated cardiomyopathy.
复制标题
呼吁对扩张型心肌病进行抗凝临床试验。
DOI:
10.1016/0002-9149(90)91436-a
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发表时间:
1990
期刊:
影响因子:
--
通讯作者:
Rodney H. Falk
中科院分区:
文献类型:
--
作者:
Rodney H. Falk
D ilated cardiomyopathy is believed to be a pre-disposing factor for stroke.’Autopsy studies of hearts with dilated cardiomyopathy demonstrate the presence of ventricular thrombus or mural endocardial plaques (which are considered to be due to organized thrombi) in up to 75% of cases2 Features of systemic embolization are common and may not have been suspected during life. Although autopsy data represent a highly selected subgroup, retrospective studies in dilated cardiomyopathy suggest that clinically apparent embolism is common, occurring with an annual incidence of about 3.5%.’Long-term anticoagulation with warfarin has been recommended to reduce the risk of embolization,‘, 3+ 4 but this conclusion is retrospectively derived from selected patient groups and no data are available to estimate the risk-to-benefit ratio in an unselected population. It is my personal impression that many physicians are reluctant to prescribe long-term warfarin for their patients with dilated cardiomyopathy. For example, in a recent study only 6 of 40 patients with dilated cardiomyopathy were receiving anticoagulation. The reluctance may be because of a lack of convincing, prospectively derived data on the risk-to-benefit ratio. It may also stem from concern that anticoagulation may be more hazardous in this group of patients-in whom fluctuating degrees of hepatic congestion may result in changing warfarin requirements and an increased risk of bleeding.‘jT’In the past few years our knowledge of thromboembolism and its prevention after acute myocardial infarction has greatly expanded. Important differences exist between thrombus formation in myocardial infarction and dilated cardiomyopathy. They will be discussed herein, as will possibilities for assessing and safely reducing thromboembolic events originating from the myopathic ventricle.