Montréal Heart Institute, Université de Montréal, Montréal, Québec, Canada.
St. Michael's Hospital, University of Toronto, Ontario, Canada; Canadian Heart Research Centre, Toronto, Ontario, Canada; Canadian VIGOUR Centre, University of Alberta, Edmonton, Alberta, Canada.
Can J Cardiol. 2021 Nov;37(11):1837-1845. doi: 10.1016/j.cjca.2021.08.009. Epub 2021 Aug 18.
A better understanding of the central role of inflammation in the development of coronary artery disease (CAD) has been the impetus for the evaluation of therapeutic strategies targeting the interleukin-1ß/interleukin-6 cytokine signaling pathway, involved in both chronic atherogenesis and in triggering of atherosclerotic plaque rupture. As an inexpensive pharmacologic agent with relatively few adverse effects that tend to be mild and tolerable, the role of colchicine in secondary prevention of atherothrombotic events has been the focus of multiple recent large-scale randomized controlled trials involving patients with stable CAD (Low-Dose Colchicine [LoDoCo] and LoDoCo2 trials), a recent myocardial infarction (Colchicine Cardiovascular Outcome Trial [COLCOT], Colchicine in Patients With Acute Coronary Syndrome [COPS], and Colchicine and Spironolactone in Patients With Myocardial Infarction/Synergy Stent Registry [CLEAR SYNERGY] trials), and undergoing percutaneous coronary interventions (Colchicine in Percutaneous Coronary Intervention [COLCHICINE-PCI] trial). Based on this evidence, low-dose colchicine (0.5 mg once daily) should be considered in patients with recent myocardial infarctions-within 30 days and, ideally, within 3 days-or with stable CAD to improve cardiovascular outcomes. Colchicine should not be used in patients with severe renal or hepatic disease because of the risk of severe toxicity. No serious adverse effect was associated with the combined use of colchicine and high-intensity statin therapy in large trials. The impact of colchicine in high-risk populations of patients with peripheral arterial disease and in those with diabetes for the primary prevention of CAD remains to be established.
更好地理解炎症在冠状动脉疾病 (CAD) 发展中的核心作用，是评估靶向白细胞介素-1β/白细胞介素-6 细胞因子信号通路治疗策略的动力，该通路参与慢性动脉粥样硬化形成和触发动脉粥样硬化斑块破裂。秋水仙碱作为一种廉价的药物，副作用相对较少，且往往较为轻微且可耐受，因此，其在动脉粥样血栓事件二级预防中的作用一直是多个最近的大规模随机对照试验的重点，这些试验涉及稳定型 CAD 患者（低剂量秋水仙碱 [LoDoCo] 和 LoDoCo2 试验）、近期心肌梗死患者（秋水仙碱心血管结局试验 [COLCOT]、急性冠状动脉综合征患者的秋水仙碱 [COPS] 和心肌梗死后的秋水仙碱和螺内酯试验 [CLEAR SYNERGY]）和接受经皮冠状动脉介入治疗的患者（经皮冠状动脉介入治疗中的秋水仙碱 [COLCHICINE-PCI] 试验）。基于这一证据，对于近期心肌梗死患者（心肌梗死后 30 天内，理想情况下为 3 天内）或稳定型 CAD 患者，应考虑使用低剂量秋水仙碱（每天一次 0.5 毫克）以改善心血管结局。由于严重毒性的风险，秋水仙碱不应在严重肾功能或肝功能不全的患者中使用。在大型试验中，秋水仙碱与高强度他汀类药物联合使用没有出现严重不良事件。秋水仙碱在有外周动脉疾病和糖尿病的高危人群中预防 CAD 的作用仍有待确定。
