Patterns of myocardial injury in recovered troponin-positive COVID-19 patients assessed by cardiovascular magnetic resonance

Kotecha, Tushar; Knight, Daniel S; Razvi, Yousuf; Kumar, Kartik; Vimalesvaran, Kavitha; Thornton, George; Patel, Rishi; Chacko, Liza; Brown, James T; Coyle, Clare; Leith, Donald; Shetye, Abhishek; Ariff, Ben; Bell, Robert; Captur, Gabriella; Coleman, Meg; Goldring, James; Gopalan, Deepa; Heightman, Melissa; Hillman, Toby; Howard, Luke; Jacobs, Michael; Jeetley, Paramjit S; Kanagaratnam, Prapa; Kon, Onn Min; Lamb, Lucy E; Manisty, Charlotte H; Mathurdas, Palmira; Mayet, Jamil; Negus, Rupert; Patel, Niket; Pierce, Iain; Russell, Georgina; Wolff, Anthony; Xue, Hui; Kellman, Peter; Moon, James C; Treibel, Thomas A; Cole, Graham D; Fontana, Marianna

BACKGROUND: Troponin elevation is common in hospitalized COVID-19 patients, but underlying aetiologies are ill-defined. We used multi-parametric cardiovascular magnetic resonance (CMR) to assess myocardial injury in recovered COVID-19 patients. METHODS AND RESULTS: One hundred and forty-eight patients (64 ± 12 years, 70% male) with severe COVID-19 infection [all requiring hospital admission, 48 (32%) requiring ventilatory support] and troponin elevation discharged from six hospitals underwent convalescent CMR (including adenosine stress perfusion if indicated) at median 68 days. Left ventricular (LV) function was normal in 89% (ejection fraction 67% ± 11%). Late gadolinium enhancement and/or ischaemia was found in 54% (80/148). This comprised myocarditis-like scar in 26% (39/148), infarction and/or ischaemia in 22% (32/148) and dual pathology in 6% (9/148). Myocarditis-like injury was limited to three or less myocardial segments in 88% (35/40) of cases with no associated LV dysfunction; of these, 30% had active myocarditis. Myocardial infarction was found in 19% (28/148) and inducible ischaemia in 26% (20/76) of those undergoing stress perfusion (including 7 with both infarction and ischaemia). Of patients with ischaemic injury pattern, 66% (27/41) had no past history of coronary disease. There was no evidence of diffuse fibrosis or oedema in the remote myocardium (T1: COVID-19 patients 1033 ± 41 ms vs. matched controls 1028 ± 35 ms; T2: COVID-19 46 ± 3 ms vs. matched controls 47 ± 3 ms). CONCLUSIONS: During convalescence after severe COVID-19 infection with troponin elevation, myocarditis-like injury can be encountered, with limited extent and minimal functional consequence. In a proportion of patients, there is evidence of possible ongoing localized inflammation. A quarter of patients had ischaemic heart disease, of which two-thirds had no previous history. Whether these observed findings represent pre-existing clinically silent disease or de novo COVID-19-related changes remain undetermined. Diffuse oedema or fibrosis was not detected.