Hospitalized COVID-19 patients with high troponin levels are twice as likely to have cardiac abnormalities than those with normal troponin, with or without COVID-19, a multicenter U.K. study suggests.
The causes were diverse, myocarditis prevalence was lower than previously reported, and myocardial scar emerged as an independent risk factor for adverse cardiovascular outcomes at 12 months.
“We know that multiorgan involvement in hospitalized patients with COVID-19 is common ... and may result in acute myocardial injury, detected by an increase in cardiac troponin concentrations,” John P. Greenwood, PhD, of the University of Leeds (England), told this news organization. “Elevated cardiac troponin is associated with a worse prognosis.”
“Multiple mechanisms of myocardial injury have been proposed and ... mitigation or prevention strategies likely depend on the underpinning mechanisms,” he said. “The sequelae of scar may predispose to late events.”
The study, published online in Circulation, also identified a new pattern of microinfarction on cardiac magnetic resonance (CMR) imaging, highlighting the pro-thrombotic nature of SARS-CoV-2, Dr. Greenwood said.
Injury patterns different
Three hundred and forty-two patients with COVID-19 and elevated troponin levels (COVID+/troponin+) across 25 centers were enrolled between June 2020 and March 2021 in COVID-HEART, deemed an “urgent public health study” in the United Kingdom. The aim was to characterize myocardial injury and its associations and sequelae in convalescent patients after hospitalization with COVID-19.
Enrollment took place during the Wuhan and Alpha waves of COVID-19: before vaccination and when dexamethasone and anticoagulant protocols were emerging. All participants underwent CMR at a median of 21 days after discharge.
Two prospective control groups also were recruited: 64 patients with COVID-19 and normal troponin levels (COVID+/troponin−) and 113 without COVID-19 or elevated troponin matched by age and cardiovascular comorbidities (COVID−/comorbidity+).
Overall, participants’ median age was 61 years and 69% were men. Common comorbidities included hypertension (47%), obesity (43%), and diabetes (25%).
The frequency of any heart abnormality – for example, left or right ventricular impairment, scar, or pericardial disease – was twice as great (61%) in COVID+/troponin+ cases, compared with controls (36% for COVID+/troponin− patients versus 31% for COVID−/comorbidity+ patients).
Specifically, more cases than controls had ventricular impairment (17.2% vs. 3.1% and 7.1%) or scar (42% vs. 7% and 23%).
The myocardial injury pattern differed between cases and controls, with cases more likely to have infarction (13% vs. 2% and 7%) or microinfarction (9% vs. 0% and 1%).
However, there was no between-group difference in nonischemic scar (13% vs. 5% and 14%).
The prevalence of probable recent myocarditis was 6.7% in cases, compared with 1.7% in controls without COVID-19 – “much lower” than in previous studies, Dr. Greenwood noted.
During follow-up, four COVID+/troponin+ patients (1.2%) died, and 34 (10%) experienced a subsequent major adverse cardiovascular event (MACE; 10.2%), which was similar to controls (6.1%).
Myocardial scar, but not previous COVID-19 infection or troponin level, was an independent predictor of MACE (odds ratio, 2.25).
“These findings suggest that macroangiopathic and microangiopathic thrombosis may be the key pathologic process for myocardial injury in COVID-19 survivors,” the authors conclude.
Dr. Greenwood added, “We are currently analyzing the 6-month follow-up CMR scans, the quality-of-life questionnaires, and the 6-minute walk tests. These will give us great understanding of how the heart repairs after acute myocardial injury associated with COVID-19. It will also allow us to assess the impact on patient quality of life and functional capacity.”