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

Abstract

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.

Keywords: COVID-19; Cardiovascular magnetic resonance; Myocardial infarction; Myocardial oedema; Myocarditis; SARS-CoV-2.

Graphical abstract

Figure 1

Consort diagram. CMR, cardiovascular magnetic resonance.

Figure 2

Patterns of myocardial scar and cardiovascular magnetic resonance diagnoses. CMR, cardiovascular magnetic resonance; LGE, late gadolinium enhancement; MI, myocardial infarction.

Figure 3

Example of patient with a myocarditis-pattern late gadolinium enhancement and evidence of active inflammation. Native T1 and myocardial T2 were elevated in the inferolateral wall (T1 1261 ms, T2 56 ms) and normal in the basal inferoseptum (T1 983 ms, T2 50 ms). Late gadolinium enhancement imaging shows patchy areas of subepicardial enhancement in the lateral wall and basal inferior wall, and mid-wall enhancement in the distal septum and distal anterior wall (white arrows).

Figure 4

Example of patient admitted with COVID-19 infection and associated troponin rise. Late gadolinium enhancement (bright blood left two panels and dark blood third panel) shows a lateral infarct (white arrows). Coronary angiography (right panel) showed an occluded obtuse marginal branch (black arrow).

Figure 5

Example of patient admitted with COVID-19 infection and associated troponin rise. Cardiovascular magnetic resonance with adenosine stress perfusion mapping showed inducible ischaemia in the inferior wall, basal inferoseptum, anterior, and anterolateral walls. Coronary angiography showed occluded right coronary artery and severe disease in proximal-mid LAD (black arrows).

Figure 6

Example of patient with dual pathology. Late gadolinium enhancement showed mid-wall late gadolinium enhancement in the basal inferolateral wall (myocarditis-pattern, red arrow) and sub-endocardial late gadolinium enhancement in the mid-anterior and part of the distal lateral wall (myocardial infarction pattern, white arrows). Native T1 and T2 were normal within the area of myocarditis-pattern late gadolinium enhancement (T1 1061 ms, T2 52 ms).

Figure 7

Native T1 (left panel) and myocardial T2 (right panel) measured in the remote myocardium. There was no significant difference in native T1 or T2 in the remote myocardium between COVID-19 patients and controls.