Becker R C, Hochman J S, Cannon C P, Spencer F A, Ball S P, Rizzo M J, Antman E M
Cardiovascular Thrombosis Research Center, University of Massachusetts Medical School, Worcester 01655-0214, USA.
J Am Coll Cardiol. 1999 Feb;33(2):479-87. doi: 10.1016/s0735-1097(98)00582-8.
The purpose of this study was to determine the incidence and demographic characteristics of patients experiencing cardiac rupture after thrombolytic and adjunctive anticoagulant therapy and to identify possible associations between the mechanism of thrombin inhibition (indirect, direct) and the intensity of systemic anticoagulation with its occurrence. BACKGROUND Cardiac rupture is responsible for nearly 15% of all in-hospital deaths among patients with myocardial infarction (MI) given thrombolytic agents. Little is known about specific patient- and treatment-related risk factors. METHODS Patients (n = 3,759) with MI participating in the Thrombolysis and Thrombin Inhibition in Myocardial Infarction 9A and B trials received intravenous thrombolytic therapy, aspirin and either heparin (5,000 U bolus, 1,000 to 1,300 U/h infusion) or hirudin (0.1 to 0.6 mg/kg bolus, 0.1 to 0.2 mg/kg/h infusion) for at least 96 h. A diagnosis of cardiac rupture was made clinically in patients with sudden electromechanical dissociation in the absence of preceding congestive heart failure, slowly progressive hemodynamic compromise or malignant ventricular arrhythmias. RESULTS A total of 65 rupture events (1.7%) were reported-all were fatal, and a majority occurred within 48 h of treatment Patients with cardiac rupture were older, of lower body weight and stature and more likely to be female than those without rupture (all p < 0.001). By multivariable analysis, age >70 years (odds ratio [OR] 3.77; 95% confidence interval [CI] 2.06, 6.91), female gender (OR 2.87; 95% CI 1.44, 5.73) and prior angina (OR 1.82; 95% CI 1.05, 3.16) were independently associated with cardiac rupture. Independent predictors of nonrupture death included age >70 years (OR 3.68; 95% CI 2.53, 5.35) and prior MI (OR 2.14; 95%, CI 1.45, 3.17). There was no association between the type of thrombin inhibition, the intensity of anticoagulation and cardiac rapture. CONCLUSIONS Cardiac rupture following thrombolytic therapy tends to occur in older patients and may explain the disproportionately high mortality rate among women in prior dinical trials. Unlike major hemorrhagic complications, there is no evidence that the intensity of anticoagulation associated with heparin or hirudin administration influences the occurrence of rupture.
本研究的目的是确定接受溶栓及辅助抗凝治疗后发生心脏破裂的患者的发生率及人口统计学特征，并确定凝血酶抑制机制（间接、直接）与全身抗凝强度及其发生之间的可能关联。背景：在接受溶栓药物治疗的心肌梗死（MI）患者中，心脏破裂导致了近15%的院内死亡。关于特定的患者及治疗相关危险因素知之甚少。方法：参与心肌梗死溶栓及凝血酶抑制9A和9B试验的MI患者（n = 3759）接受静脉溶栓治疗、阿司匹林，并接受肝素（5000 U静脉推注，1000～1300 U/h输注）或水蛭素（0.1～0.6 mg/kg静脉推注，0.1～0.2 mg/kg/h输注）治疗至少96小时。对于无前驱性充血性心力衰竭、缓慢进展的血流动力学损害或恶性室性心律失常而突然发生电机械分离的患者，临床诊断为心脏破裂。结果：共报告65例破裂事件（1.7%），均为致命事件，大多数发生在治疗后48小时内。与未发生破裂的患者相比，发生心脏破裂的患者年龄更大、体重和身高更低，且更可能为女性（所有p < 0.001）。通过多变量分析，年龄>70岁（比值比[OR] 3.77；95%置信区间[CI] 2.06，6.91）、女性（OR 2.87；95% CI 1.44，5.73）和既往心绞痛（OR 1.82；95% CI 1.05，3.16）与心脏破裂独立相关。未发生破裂死亡的独立预测因素包括年龄>70岁（OR 3.68；95% CI 2.53，5.35）和既往心肌梗死（OR 2.14；95%，CI 1.45，3.17）。凝血酶抑制类型、抗凝强度与心脏破裂之间无关联。结论：溶栓治疗后心脏破裂倾向于发生在老年患者中，这可能解释了既往临床试验中女性不成比例的高死亡率。与主要出血并发症不同，没有证据表明与肝素或水蛭素给药相关的抗凝强度会影响破裂的发生。
