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.

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SEcho is superior to ExECG in the risk stratification of patients with suspected ACS but negative troponin. SEcho resulted in less diagnostic uncertainty, fewer referrals for further investigation, and hence, a significant cost benefit over ExECG.

Background— Distinguishing ischemic from nonischemic origin in patients presenting with acute heart failure (AHF) not resulting from acute myocardial infarction has both therapeutic and prognostic implications. The aim of the study was to assess whether myocardial contrast echocardiography (MCE) can identify underlying coronary artery disease (CAD) as the cause of AHF. Methods and Results— Fifty-two consecutive patients with AHF with no prior clinical history of CAD and no clinical evidence of acute myocardial infarction underwent resting echocardiography and MCE both at rest and after dipyridamole stress at a mean of 9±2 days after admission. All patients underwent coronary arteriography before discharge. Of the 52 patients, 22 demonstrated flow-limiting CAD (>50% luminal diameter narrowing). Sensitivity, specificity, and positive and negative predictive values of MCE for the detection of CAD were 82%, 97%, 95%, and 88%, respectively. Among clinical, ECG, biochemical, resting echocardiographic, and MCE markers of CAD, MCE was the only independent predictor of CAD ( P <0.0001). Quantitative MCE demonstrated significantly ( P <0.0001) lower myocardial blood flow velocity reserve in vascular territories subtended by >50% CAD (0.59±0.46) compared with patients with normal coronary arteries (1.99±1.00). However, myocardial blood flow velocity reserve in patients with no significant CAD was significantly ( P =0.03) lower compared with control (2.91±0.41). Myocardial blood flow velocity reserve correlated significantly ( P <0.0001) with increasing severity of CAD. Conclusions— MCE, which is a bedside technique, may be used to detect CAD in patients presenting with AHF without a prior history of CAD or evidence of acute myocardial infarction. Quantitative MCE may further risk-stratify patients with AHF but no CAD.