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Many studies have reported myocardial involvement in COVID-19, but questions remain about how often this occurs and what the consequences are. Investigators studied 828 consecutive patients with COVID-19 discharged from London hospitals through April 2020.
Overall, 586 patients (71%) had an elevated high-sensitivity troponin T (hsTnT) level. Of those with an elevated hsTNT, 41% died, compared with 8% of the other patients (P<0.001). Among patients with an elevated hsTNT, 6 had an acute coronary syndrome and 12 had a pulmonary embolus.
There were 29 people without a specific identifiable cause of elevated hsTNT who underwent cardiovascular magnetic resonance (CMR). Late gadolinium enhancement (LGE) patterns suggestive of myocarditis were identified in 45% of these people. These individuals had normal systolic function (left ventricular ejection fraction, 70%) without regional wall motion abnormalities. The median extent of LGE was 2 segments.
Knight DS et al. COVID-19: Myocardial injury in survivors. Circulation 2020 Jul 14; [e-pub]. (https://doi.org/10.1161/CIRCULATIONAHA.120.049252)
Comment
Emblematic of where we are in the pandemic, these early and rather incomplete reports still have value. I found notable the high percentage of people with elevated troponin levels and the presence in some people of CMR-detectable myocarditis that did not affect ejection fraction or produce regional wall motion abnormalities — indicating that a screening echocardiogram would not have identified the myocardial damage. Whether that damage is transient or confers any prognostic information is yet to be determined.