Department of Cardiology, Royal Perth Hospital, Perth and Faculty of Health and Medical Sciences, University of Western Australia; Heart Research Institute, Sydney, Department of Cardiology, Royal Prince Alfred Hospital, Sydney and Faculty of Medicine, University of Sydney.
Department of Cardiology, Royal Perth Hospital, Perth and Faculty of Health and Medical Sciences, University of Western Australia; Heart Research Institute, Sydney, Department of Cardiology, Royal Prince Alfred Hospital, Sydney and Faculty of Medicine, University of Sydney.
Am Heart J. 2019 Sep;215:62-69. doi: 10.1016/j.ahj.2019.06.003. Epub 2019 Jun 14.
Following an acute myocardial infarction (MI), patients with persistently elevated biomarkers of inflammation, in particular C-reactive protein (CRP), are at significantly increased risk of further cardiovascular events. Colchicine is a unique anti-inflammatory medication that has shown promise in reducing such events in patients with stable coronary heart disease. The current study tested the ability of low dose colchicine to reduce CRP levels at 30 days after an acute MI, a key marker of future outcome, and its safety and tolerability in this setting.
We conducted a randomized, double-blind, trial of low-dose colchicine (0.5 mg daily) or matching placebo in 237 patients admitted with an acute MI. The primary end-point was the proportion of patients with a residual high sensitivity CRP level ≥2 mg/L after 30 days of treatment, a threshold associated with a worse prognosis.
At 30-day follow-up, 44% of patients treated with colchicine had a CRP level ≥2 mg/L compared to 50% of those randomized to placebo (P = .35) and the median CRP in patients randomized to colchicine was 1.6 mg/L (interquartile range [IQR] 0.7-3.5) compared to 2.0 mg/L (IQR 0.9-4.0) in patients randomized to placebo (P = .11). The median absolute reduction in CRP levels was -4.3 mg/L (IQR -1.1 to -14.1) among colchicine treated patients and -3.3 mg/L (IQR -0.9 to -14.4, P = .44) in placebo treated patients. The relative reduction was a fall of 78% compared to a fall of 64% (P = .09). Low dose colchicine was well tolerated and did not reduce compliance with other secondary preventative medications at 30-days.
Treatment with low dose colchicine was safe and well tolerated, but was not associated with a significantly increased likelihood of achieving a CRP level <2 mg/L or lower absolute levels of CRP 30 days after an acute MI.
在急性心肌梗死（MI）后，持续存在炎症生物标志物升高的患者，特别是 C 反应蛋白（CRP），发生进一步心血管事件的风险显著增加。秋水仙碱是一种独特的抗炎药物，已显示出在稳定型冠心病患者中降低此类事件的潜力。本研究检测了低剂量秋水仙碱（每日 0.5mg）在 MI 后 30 天降低 CRP 水平的能力，这是未来结局的关键标志物，以及在此背景下的安全性和耐受性。
我们对 237 例急性 MI 住院患者进行了随机、双盲、试验，给予低剂量秋水仙碱（每日 0.5mg）或匹配安慰剂治疗。主要终点是治疗 30 天后残留高敏 CRP 水平≥2mg/L 的患者比例，这一阈值与预后较差相关。
在 30 天随访时，秋水仙碱治疗组有 44%的患者 CRP 水平≥2mg/L，而安慰剂组有 50%（P=0.35），随机接受秋水仙碱治疗的患者 CRP 中位数为 1.6mg/L（四分位距 [IQR] 0.7-3.5），而随机接受安慰剂治疗的患者为 2.0mg/L（IQR 0.9-4.0）（P=0.11）。秋水仙碱治疗组 CRP 水平的中位绝对降低值为-4.3mg/L（IQR -1.1 至 -14.1），安慰剂治疗组为-3.3mg/L（IQR -0.9 至 -14.4，P=0.44）。相对降低值为 78%，而安慰剂组为 64%（P=0.09）。低剂量秋水仙碱耐受良好，在 30 天时不会降低其他二级预防药物的依从性。
低剂量秋水仙碱治疗安全且耐受良好，但与 CRP 水平<2mg/L或急性 MI 后 30 天 CRP 绝对水平降低无关。
