CMR Assessment of Myocardial Injury in Recovered COVID-19

Quick Takes

  • In a cohort of 148 patients hospitalized with COVID-19 and positive serum troponins, nearly half had late gadolinium enhancement (LGE) on CMR, though only subepicardial LGE was more common in patients than in matched controls.
  • Among patients with CMR findings that would be suggestive of myocarditis in most clinical contexts, LV systolic function and wall motion remained normal.

Study Questions:

What are the patterns of myocardial injury in patients who have been hospitalized with troponin-positive coronavirus disease 2019 (COVID-19), based on evaluation with cardiovascular magnetic resonance (CMR)?


This prospective study was conducted at three hospitals in London, England. All patients admitted through late June 2020 with COVID-19 who had abnormal high-sensitivity troponin were considered for study enrollment and offered post-discharge CMR. Notable exclusion criteria were patient refusal and acute coronary syndrome as the primary admitting diagnosis. A historical control group of 40 patients was matched for age, gender, and presence/absence of diabetes and hypertension, and a group of 40 healthy controls was also used. The CMR protocol included standard cine imaging, native T1 and T2 mapping, and late gadolinium enhancement (LGE) imaging. When clinically indicated, patients also underwent adenosine stress perfusion imaging. An active myocarditis pattern on CMR was defined as the presence of nonischemic LGE with associated elevation in T1 and/or T2 in the same distribution as LGE, and healed myocarditis as nonischemic LGE with normal T2.


Of 820 troponin-positive patients discharged alive after COVID-19 admission, 148 underwent the CMR tissue characterization protocol, including 144 with gadolinium contrast and 76 with adenosine perfusion imaging, at a mean 56 days following hospital discharge. Mean age was 64 ± 12 years, 70% of patients were male, 50% were Caucasian, and 32% required intensive care unit admission. Common comorbidities included hypertension (57%), diabetes (34%), and hypercholesterolemia (46%). Prior myocardial infarction (MI) had occurred in 7% of patients, and 12% had undergone prior percutaneous coronary intervention or coronary artery bypass grafting.

Mean left ventricular ejection fraction (LVEF) in patients was 67%, no different from controls. LV systolic dysfunction was present in 17/148 patients (11%). LGE was present in 70/144 patients (49%), as compared with 45% of age- and comorbidity-matched controls (p = 0.80). LGE distributions in patients were as follows: subendocardial or transmural (suggestive of infarction) in 16%, subepicardial in 19%, mid-wall in 10%, and mixed pattern in 3%. Only subepicardial LGE was significantly more common in patients than in matched controls (5%, p = 0.018). Inducible ischemia without LGE was present in nine patients. Nonischemic CMR abnormalities were present in 26% of patients, ischemia/infarction in 22%, and dual pathology in 6%. Myocarditis-pattern injury was felt to be present in 40/148 (27%) patients (including 27 with healed myocarditis pattern), four of whom also had ischemia on stress imaging and three of whom also had infarction. Myocarditis-pattern injury was not accompanied by LV dysfunction or regional wall motion abnormalities in any of the patients imaged. There was no difference in mean native T1 in the remote myocardium in patients versus matched controls, but both had higher values than healthy controls.


Myocardial LGE in a nonischemic pattern was found to be common among COVID-19 convalescents who had elevated serum troponins at the time of acute illness. However, concomitant LV systolic dysfunction and regional wall motion abnormalities were not commonly seen in these patients.


This study adds to the growing body of CMR literature on myocardial injury in COVID convalescents. Prior work has suggested that diffuse myocardial edema may affect these patients (Puntmann VO, et al., JAMA Cardiol 2020;5:1265-73 and Huang L, et al., JACC Cardiovasc Imaging 2020;13:2330-9), though the current study does not support this idea. Limitations of the literature thus far include a paucity of biopsy correlation with CMR findings. Multiple processes cause myocardial injury in COVID-19, and most likely, only a small subset of patients have inflammatory cell infiltration of the myocardium. It is possible that some of the transmural LGE seen in this study actually represented nonischemic injury, though this pattern is not classic for myocarditis due to other etiologies. Conversely, some of the so-called nonischemic LGE could have represented small-vessel ischemic changes as a consequence of microthrombi. Long-term follow-up CMR studies are needed to see how much of the LGE in these patients is irreversible and therefore likely to represent scar. Other limitations of this study include survivor bias and incomplete characterization of the ischemic consequences of COVID-19, as patients with acute MI were excluded and only half underwent stress perfusion imaging.

Clinical Topics: Acute Coronary Syndromes, COVID-19 Hub, Dyslipidemia, Heart Failure and Cardiomyopathies, Noninvasive Imaging, Prevention, Homozygous Familial Hypercholesterolemia, Acute Heart Failure, Magnetic Resonance Imaging, Nuclear Imaging, Hypertension

Keywords: Acute Coronary Syndrome, Acute Disease, Adenosine, Comorbidity, Contrast Media, Coronavirus, COVID-19, Diabetes Mellitus, Diagnostic Imaging, Edema, Gadolinium, Heart Failure, Hypercholesterolemia, Hypertension, Magnetic Resonance Imaging, Myocardial Infarction, Myocarditis, Myocardium, Perfusion Imaging, Stroke Volume, Troponin, Ventricular Function, Left

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