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Infarct size estimated from peak creatine kinase is reduced in patients using beta‐blockers at the onset of chest pain

机译:在胸痛发作时使用 β 受体阻滞剂的患者中,根据肌酸激酶峰值估计的梗死面积减少

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AbstractIn 418 patients (median 67 years) with acute myocardial infarction (AMI) we examined if ongoing β‐blocker treatment at the onset of AMI (n= 63) had beneficial effects on infarct size as judged from peak creatine kinase (CKmax) activity. The study had an observational exposed/non‐exposed design where we investigated the possible association between β‐blocker treatment and CKmax. Both crude and adjusted effects were looked for, in the latter adjusting for the effect of confounders such as thrombolytic treatment and age during AMI.Crude effects: β‐blocker treatment significantly (p= 0.003) reduced CKmax, from 1171 U/1 to 790 U/1 (median values). In the 25 of patients with the largest infarcts, β‐blockers reduced the incidence of large infarcts by 61 (odds ratio = 0.39) (p= 0.015). Previous coronary heart disease reduced CKmax(p= 0.0001), whereas thrombolytic treatment significantly increase CKmax(p= 0.0001), probably due to reperfusion.Adjusted effects: β‐blocker treatment significantly reduced CKmax(p= 0.03), and reduced the incidence of large infarcts by 54 (odds ratio = 0.46).Thus, when adjusting for confounders, β‐blocker treatment at the onset of AMI reduced infarct size as well as the incidence of large infarcts. These observational results suggest real
机译:摘要在418例急性心肌梗死(AMI)患者(中位67岁)中,我们研究了在AMI发作时正在进行的β阻滞剂治疗(n=63)是否对梗死面积有有益影响,从肌酸激酶峰值(CKmax)活性判断。该研究采用观察性暴露/非暴露设计,我们研究了β阻滞剂治疗与CKmax之间的可能关联。研究了粗略效应和调整效应,后者调整了混杂因素的影响,例如溶栓治疗和 AMI 期间的年龄。粗制滥造效应:β阻滞剂处理显著(p=0.003)降低了CKmax,从1171 U/1降低到790 U/1(中位值)。在 25% 的最大梗死患者中,β阻滞剂可将大面积梗死的发生率降低 61%(比值比 = 0.39)(p= 0.015)。既往冠心病降低了CKmax(p=0.0001),而溶栓治疗显著提高了CKmax(p=0.0001),可能是由于再灌注所致。调整效果:β阻滞剂治疗显著降低了CKmax(p=0.03),大面积梗死发生率降低了54%(比值比=0.46)。因此,在调整混杂因素时,AMI开始时的β阻滞剂治疗减少了梗死面积以及大面积梗死的发生率。这些观察结果表明,这些结果是真实的

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