Literature DB >> 8626938

A composite view of cardiac rupture in the United States National Registry of Myocardial Infarction.

R C Becker1, J M Gore, C Lambrew, W D Weaver, R M Rubison, W J French, A J Tiefenbrunn, L J Bowlby, W J Rogers.   

Abstract

OBJECTIVES: This study was done to determine the incidence, timing and prevalence as a cause of death from cardiac rupture in patients with acute myocardial infarction.
BACKGROUND: Several clinical trials and overview analyses have suggested that the survival benefit conferred by thrombolytic therapy may be offset by a paradoxic increase in early deaths from cardiac rupture.
METHODS: Demographic, procedural and outcome data from patients with acute myocardial infarction were collected at 1,073 United States hospitals collaborating in the United States National Registry of Myocardial Infarction.
RESULTS: Among the 350,755 patients enrolled, 122,243 received thrombolytic therapy. In-hospital mortality for the overall patient population, those not treated with thrombolytics (n = 228,512) and those given thrombolytics were 10.4%, 12.9% and 5.9%, respectively (p<0.001). Cardiogenic shock was the most common cause of death in each patient group. Although the incidence of cardiac rupture was low (<1.0%), it was responsible for 7.3%, 6.1% and 12.1%, respectively, of in-hospital deaths (p<0.001). Death from rupture occurred earlier in patients given thrombolytic therapy, with a clustering of events within 24 h of drug administration. Despite the early risk, death rates were comparatively low in thrombolytic-treated patients on each of the first 30 days. By multivariable analysis, thrombolytics, prior myocardial infarction, advancing age, female gender and intravenous beta-blocker use were independently associated with cardiac rupture.
CONCLUSIONS: This large registry experience, including over 350,000 patients with myocardial infarction, suggests that thrombolytic therapy accelerates cardiac rupture, typically to within 24 to 48 h of treatment. The possibility that rupture represents an early hemorrhagic complication of thrombolytic therapy should be investigated.

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Year:  1996        PMID: 8626938     DOI: 10.1016/0735-1097(96)00008-3

Source DB:  PubMed          Journal:  J Am Coll Cardiol        ISSN: 0735-1097            Impact factor:   24.094


  57 in total

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10.  Olmesartan prevents cardiac rupture in mice with myocardial infarction by modulating growth differentiation factor 15 and p53.

Authors:  Baihe Chen; Di Lu; Yujuan Fu; Jingwen Zhang; Xiaobo Huang; Shiping Cao; Dingli Xu; Jianping Bin; Masafumi Kitakaze; Qiaobing Huang; Yulin Liao
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