[Prevention of periprocedural myocardial damage in patients undergoing percutaneous coronary intervention].

Giuseppe Patti, Vincenzo Pasceri, Annunziata Nusca, Germano Di Sciascio
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Abstract

Myocardial injury during coronary intervention occurs in 10-40% of cases and is often characterized by a slight increase in the markers of myocardial necrosis, without symptoms, electrocardiographic changes or impairment of cardiac function. However, even small increases in creatine kinase (CK)-MB levels are an expression of a true and detectable infarction and may be associated with a higher follow-up mortality. The cause of CK-MB elevation in case of procedural complications is obvious; however, most cases of minor CK-MB elevation occur in patients with uncomplicated procedures with excellent final angiographic results. It has been suggested that the main mechanism explaining the occurrence of myocardial necrosis during otherwise successful coronary intervention may be distal microembolization of plaque components, an enhanced inflammatory state or total plaque burden and/or instability. Different treatments have been proposed to prevent myocardial injury during coronary intervention, including nitrate infusion, intracoronary beta-blockers, adenosine and IIb/IIa inhibitors, but none of these (apart from the use of IIb/IIIa inhibitors) have been routinely introduced into clinical practice. Previous observational studies suggested a beneficial effect of pre-treatment with statins in this setting; the ARMYDA (Atorvastatin for Reduction of Myocardial Damage During Angioplasty) trial is the first prospective, randomized, placebo-controlled study, evaluating the effects of 7-day therapy with 40 mg/day of atorvastatin on post-procedural release of markers of myocardial damage in patients with stable angina undergoing percutaneous intervention. In this study therapy with atorvastatin was associated with an 80% risk reduction in the occurrence of periprocedural myocardial infarction, as well as with a significant reduction in post-intervention peak levels of all markers of myocardial damage. The mechanisms underlying the beneficial effects of atorvastatin may be an inflammatory action reducing myocardial injury necrosis due to microembolization, an improvement in endothelial function on microcirculation, and direct myocardial protection.

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经皮冠状动脉介入治疗患者术中心肌损害的预防。
10-40%的病例在冠状动脉介入治疗期间出现心肌损伤,通常表现为心肌坏死标志物轻微升高,无症状、心电图改变或心功能损害。然而,即使肌酸激酶(CK)-MB水平的小幅升高也是真实和可检测的梗死的表达,并且可能与较高的随访死亡率相关。手术并发症时CK-MB升高的原因明显;然而,大多数轻微CK-MB升高的病例发生在手术简单且最终血管造影结果良好的患者中。有研究表明,在冠脉介入治疗期间心肌坏死的主要机制可能是斑块成分远端微栓塞、炎症状态或斑块总负荷增强和/或不稳定。为了预防冠状动脉介入治疗期间的心肌损伤,已经提出了不同的治疗方法,包括硝酸盐输注、冠状动脉内β -受体阻滞剂、腺苷和IIb/IIa抑制剂,但除了使用IIb/IIIa抑制剂外,这些方法都没有被常规引入临床实践。先前的观察性研究表明,在这种情况下,他汀类药物的预处理效果是有益的;ARMYDA(阿托伐他汀血管成形术中心肌损伤减少)试验是首个前瞻性、随机、安慰剂对照研究,评估了经皮介入治疗的稳定型心绞痛患者接受40mg /天阿托伐他汀7天治疗后心肌损伤标志物释放的影响。在这项研究中,阿托伐他汀治疗与围手术期心肌梗死发生风险降低80%相关,并且与干预后所有心肌损伤标志物峰值水平的显著降低相关。阿托伐他汀有益作用的机制可能是炎症作用,减少微栓塞引起的心肌损伤坏死,改善微循环内皮功能,直接保护心肌。
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