Arnold J Ranjit, Yeo Jian L, Budgeon Charley A, Shergill Simran, England Rachel, Shiwani Hunain, Artico Jessica, Moon James C, Gorecka Miroslawa, Roditi Giles, Morrow Andrew, Mangion Kenneth, Shanmuganathan Mayooran, Miller Christopher A, Chiribiri Amedeo, Alzahir Mohammed, Ramirez Sara, Lin Andrew, Swoboda Peter P, McDiarmid Adam K, Sykes Robert, Singh Trisha, Bucciarelli-Ducci Chiara, Dawson Dana, Fontana Marianna, Manisty Charlotte, Treibel Thomas A, Levelt Eylem, Young Robin, McConnachie Alex, Neubauer Stefan, Piechnik Stefan K, Davies Rhodri H, Ferreira Vanessa M, Dweck Marc R, Berry Colin, McCann Gerry P, Greenwood John P
University of Leicester and The NIHR Leicester Biomedical Research Centre, Glenfield Hospital, Leicester, UK.
Cardiovascular Epidemiology Research Centre, School of Population and Global Health, University of Western Australia, Perth, Australia.
Int J Cardiovasc Imaging. 2025 Feb;41(2):247-256. doi: 10.1007/s10554-024-03304-7. Epub 2024 Dec 30.
The pathophysiology of myocardial injury following COVID-19 remains uncertain. COVID-HEART was a prospective, multicentre study utilising cardiovascular magnetic resonance (CMR) to characterise COVID-related myocardial injury. In this pre-specified analysis, the objectives were to examine (1) the frequency of myocardial ischaemia following COVID-19, and (2) the association between ischaemia and myocardial injury. We studied 59 patients hospitalised with COVID-19 and elevated serum troponin (COVID + /troponin + , age 61 ± 11 years) and 37 control subjects without COVID-19 or elevated troponin and similar by age and cardiovascular comorbidities (COVID -/comorbidity + , 64 ± 10 years). Subjects underwent multi-parametric CMR (comprising assessment of ventricular volumes, stress perfusion, T1/T2 mapping and scar). The primary endpoint was the frequency of inducible myocardial ischaemia. Inducible ischaemia was evident in 11 (19%) COVID + /troponin + patients and in 8 (22%) control subjects (p = 0.72). In COVID + /troponin + patients with ischaemia, epicardial coronary disease pattern ischaemia was present in eight patients and microvascular disease pattern, in three patients. There was no significant difference in the frequency of inducible ischaemia in COVID + /troponin + patients with previous myocardial infarction and/or revascularisation compared to those without (2/12 [17%] vs. 9/47 [19%] respectively, p = 0.84), or in those with and without scar (7/27 [26%] vs. 4/32 [13%] respectively, p = 0.19). Myocardial ischaemia was present in ~ 20% of patients recently hospitalised with COVID-19 and with elevated cardiac troponin, but this was not different to matched comorbid controls. This finding coupled with the lack of an association between ischaemia and myocardial scar suggests that coronary artery abnormalities are unlikely to be the predominant mechanism underlying COVID-19 induced myocardial injury.
新型冠状病毒肺炎(COVID-19)后心肌损伤的病理生理学仍不明确。COVID-HEART研究是一项前瞻性、多中心研究,利用心血管磁共振成像(CMR)来描述与COVID-19相关的心肌损伤。在这项预先设定的分析中,目标是研究:(1)COVID-19后心肌缺血的发生率;(2)缺血与心肌损伤之间的关联。我们研究了59例因COVID-19住院且血清肌钙蛋白升高的患者(COVID+/肌钙蛋白+,年龄61±11岁)和37例无COVID-19或肌钙蛋白升高且年龄和心血管合并症与之相似的对照受试者(COVID-/合并症+,64±10岁)。受试者接受了多参数CMR检查(包括心室容积评估、负荷灌注、T1/T2成像和瘢痕检测)。主要终点是可诱导性心肌缺血的发生率。11例(19%)COVID+/肌钙蛋白+患者和8例(22%)对照受试者出现可诱导性缺血(p = 0.72)。在有缺血的COVID+/肌钙蛋白+患者中,8例为心外膜冠状动脉疾病型缺血,3例为微血管疾病型缺血。既往有心肌梗死和/或血运重建的COVID+/肌钙蛋白+患者与无此类情况的患者相比,可诱导性缺血的发生率无显著差异(分别为2/12 [17%] 对9/47 [19%],p = 0.84),有瘢痕和无瘢痕的患者之间也无显著差异(分别为7/27 [26%] 对4/32 [13%],p = 0.19)。近期因COVID-19住院且心肌肌钙蛋白升高的患者中约20%存在心肌缺血,但这与匹配的合并症对照无差异。这一发现加上缺血与心肌瘢痕之间缺乏关联,表明冠状动脉异常不太可能是COVID-19诱导心肌损伤的主要机制。