Patti Giuseppe, Pasceri Vincenzo, Nusca Annunziata, Di Sciascio Germano
Dipartimento di Scienze Cardiovascolari, Università Campus Bio-Medico, Roma.
Ital Heart J Suppl. 2005 Sep;6(9):553-60.
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.
冠状动脉介入治疗期间心肌损伤发生率为10% - 40%,通常表现为心肌坏死标志物略有升高,无相关症状、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正可检测到的梗死的表现,且可能与更高的随访死亡率相关。手术并发症导致CK-MB升高的原因显而易见;然而,大多数CK-MB轻度升高的病例发生在手术过程顺利且最终血管造影结果良好的患者中。有人提出,在原本成功的冠状动脉介入治疗过程中,解释心肌坏死发生的主要机制可能是斑块成分的远端微栓塞、炎症状态增强、总斑块负荷和/或不稳定性。为预防冠状动脉介入治疗期间的心肌损伤,人们提出了不同的治疗方法,包括静脉输注硝酸酯类药物、冠状动脉内注射β受体阻滞剂、腺苷和IIb/IIa抑制剂,但这些方法(除了使用IIb/IIIa抑制剂外)均未常规应用于临床实践。以往的观察性研究表明,在此情况下他汀类药物预处理具有有益作用;ARMYDA(阿托伐他汀降低血管成形术期间心肌损伤)试验是第一项前瞻性、随机、安慰剂对照研究,评估了每日40mg阿托伐他汀治疗7天对接受经皮介入治疗的稳定型心绞痛患者术后心肌损伤标志物释放的影响。在这项研究中,阿托伐他汀治疗使围手术期心肌梗死的发生风险降低了80%,同时也使干预后所有心肌损伤标志物的峰值水平显著降低。阿托伐他汀有益作用的潜在机制可能是其具有抗炎作用,可减少微栓塞导致的心肌损伤坏死,改善微循环内皮功能,并提供直接的心肌保护。