Myocardial ischaemia following COVID-19: a cardiovascular magnetic resonance study.

J Ranjit Arnold, Jian L Yeo, Charley A Budgeon, Simran Shergill, Rachel England, Hunain Shiwani, Jessica Artico, James C Moon, Miroslawa Gorecka, Giles Roditi, Andrew Morrow, Kenneth Mangion, Mayooran Shanmuganathan, Christopher A Miller, Amedeo Chiribiri, Mohammed Alzahir, Sara Ramirez, Andrew Lin, Peter P Swoboda, Adam K McDiarmid, Robert Sykes, Trisha Singh, Chiara Bucciarelli-Ducci, Dana Dawson, Marianna Fontana, Charlotte Manisty, Thomas A Treibel, Eylem Levelt, Robin Young, Alex McConnachie, Stefan Neubauer, Stefan K Piechnik, Rhodri H Davies, Vanessa M Ferreira, Marc R Dweck, Colin Berry, Gerry P McCann, John P Greenwood
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Abstract

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.

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COVID-19后心肌缺血:心血管磁共振研究
COVID-19后心肌损伤的病理生理学仍不确定。COVID-HEART是一项前瞻性多中心研究,利用心血管磁共振(CMR)来表征与covid相关的心肌损伤。在这个预先指定的分析中,目的是检查(1)COVID-19后心肌缺血的频率,以及(2)缺血与心肌损伤之间的关系。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相似的对照组(COVID -/合并症+,64±10岁)。受试者接受多参数CMR(包括心室容积评估、应激灌注、T1/T2制图和疤痕)。主要终点是诱发性心肌缺血的频率。诱导性缺血在11例(19%)COVID + /肌钙蛋白+患者和8例(22%)对照组中明显(p = 0.72)。在COVID + /肌钙蛋白+合并缺血的患者中,8例患者出现心外膜冠状动脉疾病型缺血,3例患者出现微血管疾病型缺血。有心肌梗死和/或血供重建史的COVID + /肌钙蛋白+患者与无心肌梗死和/或血供重建史的患者发生诱导性缺血的频率无显著差异(分别为2/12 [17%]vs. 9/47 [19%], p = 0.84),有疤痕和无疤痕患者发生诱导性缺血的频率分别为7/27 [26%]vs. 4/32 [13%], p = 0.19)。最近因COVID-19住院且心肌肌钙蛋白升高的患者中约有20%存在心肌缺血,但这与匹配的合并症对照组没有差异。这一发现加上缺血和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。
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