Comorbidities may explain myocardial abnormalities seen in patients with COVID-19
Compared with comorbidity-matched volunteers, patients recovering from severe COVID-19 did not show evidence of left ventricular dysfunction or a major excess in persistent myocardial injury, researchers reported.
The findings indicated that a high prevalence of CV comorbidities may explain much of the reported myocardial abnormalities on cardiac MRI.
“However, some patients recovering from COVID-19 did have evidence of mild persistent right ventricular dysfunction,” Trisha Singh, BM, clinical research fellow at the University of Edinburgh, Scotland, and colleagues wrote.
In the prospective, two-center observational study, Singh and colleagues sought to better understand the contribution of comorbidities on the reported widespread myocardial abnormalities in patients with recent COVID-19.
The study included patients hospitalized with confirmed COVID-19 who received gadolinium and manganese-enhanced MRI and coronary CTA. After masked analysis, researchers compared these patients with healthy and comorbidity-matched volunteers.
According to results, of the 52 patients (median age, 54 years; 25% women) who recovered from COVID-19, 29% were admitted to intensive care and 21% were ventilated. Additionally, among the 23 patients undergoing coronary CTA, 35% had underlying CAD.
Results revealed that compared with younger healthy volunteers (n = 10), patients with COVID-19 demonstrated reductions in LV ejection fraction (57.4% vs. 66.3%; P = .02) and right ventricular EF (51.7% vs. 60.5%; P .0001). Patients with COVID-19 also displayed elevated native T1 values (1,225 ms vs. 1,197 ms; P = .04) and extracellular volume fraction (31% vs. 24%; P < .0003), whereas myocardial manganese uptake was reduced (6.9 mL/100 g/min vs. 7.9 mL/100 g/min; P = .01).
Compared with comorbidity-matched volunteers (n = 26), patients with COVID-19 exhibited preserved LV function but decreased RV systolic function (51.7% vs. 59.3%; P = .0005). Researchers also reported similar native T1 values (1,225 vs. 1,227 ms; P = .99), extracellular volume (31% vs. 29%; P = .35), late gadolinium enhancement presence and manganese uptake between the two groups.
Singh and colleagues noted that the findings were irrespective of COVID-19 disease severity, myocardial injury presence or ongoing symptoms.
“Concomitant comorbidities and risk factors play a major role in prior reports of left ventricular abnormalities associated with COVID-19,” the researchers wrote. “In patients who recovered from severe COVID-19, there was evidence of persistent right ventricular dysfunction that presumably reflects the recent severe viral pneumonia and consequent pulmonary hypertension.”
They added that future research is needed to “establish the true extent of cardiac abnormalities in patients who have suffered severe COVID-19 and to determine whether this is likely to impact on their long-term clinical outcome.”