Psaltis Peter J, Nguyen Mau T, Singh Kuljit, Sinhal Ajay, Wong Dennis T L, Alcock Richard, Rajendran Sharmalar, Dautov Rustem, Barlis Peter, Patel Sanjay, Salagaras Thalia, Marathe Jessica A, Bursill Christina A, Montarello Nicholas J, Nidorf Stefan M, Thompson Peter L, Butters Julie, Cuthbert Alana R, Yelland Lisa N, Ottaway Juanita L, Kataoka Yu, Di Giovanni Giuseppe, Nicholls Stephen J
Vascular Research Center, Lifelong Health Theme, South Australian Health and Medical Research Institute, North Terrace, Adelaide 5000, Australia.
Department of Cardiology, Central Adelaide Local Health Network, Port Road, Adelaide 5000, Australia.
Cardiovasc Res. 2025 Apr 29;121(3):468-478. doi: 10.1093/cvr/cvae191.
Low-dose colchicine reduces the risk of cardiovascular events after myocardial infarction (MI). The purpose of this study was to assess the effect of colchicine post-MI on coronary plaque morphology in non-culprit segments by optical coherence tomography (OCT).
COCOMO-ACS was a double-blind, placebo-controlled trial that randomized 64 patients (median age 61.5 years; 9.4% female) with acute non-ST-segment elevation MI to colchicine 0.5 mg daily or placebo for a median of 17.8 months in addition to guideline-recommended therapy. Participants underwent serial OCT imaging within a matched segment of non-culprit coronary artery that contained at least one lipid-rich plaque causing ≥20% stenosis. The primary outcome was the change in minimum fibrous cap thickness (FCT) in non-culprit segments from baseline to final visit. Of those randomized, 57 (29 placebo, 28 colchicine) had evaluable imaging at baseline and follow-up. Overall, colchicine had no effect on relative (placebo +48.0 ± 35.1% vs. colchicine +62.4 ± 38.1%, P = 0.18) or absolute changes in minimum FCT (+29.2 ± 20.9 µm vs. + 37.2 ± 21.3 µm, P = 0.18), or change in maximum lipid arc (-38.8 ± 32.2° vs. -54.8 ± 46.9°, P = 0.18) throughout the imaged non-culprit segment. However, in patients assigned colchicine, cap rupture was less frequent (placebo 27.6% vs. colchicine 3.6%, P = 0.03). In post hoc analysis of 43 participants who had been followed for at least 16 months, minimum FCT increased to a greater extent in the colchicine group (placebo +38.7 ± 25.4% vs. colchicine +64.7 ± 34.1%, P = 0.005).
In this study, OCT failed to detect an effect of colchicine on the minimum FCT or maximum lipid arc of plaques in non-culprit segments post-MI. The post hoc observation that minimum FCT increased to a greater extent with colchicine after more prolonged treatment suggests that longer-term studies may be required to detect the effect of anti-inflammatory therapies on plaque morphology by OCT.
Australian New Zealand Clinical Trials Registry Identifier, ACTRN12618000809235, registered on the 11 May 2018.
低剂量秋水仙碱可降低心肌梗死(MI)后心血管事件的风险。本研究的目的是通过光学相干断层扫描(OCT)评估MI后秋水仙碱对非罪犯节段冠状动脉斑块形态的影响。
COCOMO-ACS是一项双盲、安慰剂对照试验,将64例急性非ST段抬高型MI患者(中位年龄61.5岁;9.4%为女性)随机分为每日服用0.5mg秋水仙碱组或安慰剂组,除指南推荐的治疗外,中位治疗17.8个月。参与者在非罪犯冠状动脉的匹配节段内进行了系列OCT成像,该节段包含至少一个导致≥20%狭窄的富含脂质斑块。主要结局是从基线到末次随访时非罪犯节段最小纤维帽厚度(FCT)的变化。随机分组的患者中,57例(29例安慰剂组,28例秋水仙碱组)在基线和随访时有可评估的成像。总体而言,秋水仙碱对最小FCT的相对变化(安慰剂组增加48.0±35.1%,秋水仙碱组增加62.4±38.1%,P=0.18)或绝对变化(增加29.2±20.9µm vs.增加37.2±21.3µm,P=0.18),或整个成像的非罪犯节段最大脂质弧的变化(减少38.8±32.2° vs.减少54.8±46.9°,P=0.18)均无影响。然而,在服用秋水仙碱的患者中,帽破裂的发生率较低(安慰剂组为27.6%,秋水仙碱组为3.6%,P=0.03)。在对43例至少随访16个月的参与者进行的事后分析中,秋水仙碱组最小FCT的增加幅度更大(安慰剂组增加38.7±25.4%,秋水仙碱组增加64.7±34.1%,P=0.005)。
在本研究中,OCT未能检测到秋水仙碱对MI后非罪犯节段斑块的最小FCT或最大脂质弧有影响。事后观察发现,经过更长时间治疗后,秋水仙碱组最小FCT增加幅度更大,这表明可能需要进行长期研究,以通过OCT检测抗炎治疗对斑块形态的影响。
澳大利亚和新西兰临床试验注册标识符,ACTRN12618000809235,于2018年5月11日注册。