Cardiac Inflammation Can Be Present After Mild COVID Infection
Myocardial inflammation is present in a small proportion of patients who have recovered from relatively mild cases of COVID-19 infection, a new study shows.
“Our findings suggest that even in patients who have had relatively mild cases of COVID-19, some will have inflammatory changes to the heart, and these changes can be present without any cardiac symptoms,” senior author, Paaladinesh Thavendiranathan, MD, University of Toronto, told theheart.org | Medscape Cardiology.
“While our data suggest that this inflammation improves over time and the outcomes seem positive, we don’t know if there will be any long-term consequences,” he added.
Noting than even a short period of inflammation in the heart may be associated with symptoms or arrhythmias in the longer term, Thavendiranathan said: “I would recommend that it is best to avoid getting the infection if there is any chance of heart inflammation.”
The study was published online in JAMA Cardiology on January 12.
The authors explain that among patients hospitalized with COVID, early studies suggested that approximately one in four experience cardiovascular injury, defined as an elevation in troponin levels, which was associated with a 5- to 10-fold increase in the risk for death. But there is limited information on cardiac injury in patients who do not require hospitalization.
Although a broad range of abnormal myocardial tissue has been reported in several cardiac MRI studies of patients recovered from COVID infection, there is little understanding of persistent changes in myocardial metabolism in recovered patients, which is a potential concern, given that COVID-19 is associated with systemic inflammation during the acute illness, they say.
For the current study, the researchers examined myocardial inflammation measured using two different methods — cardiac MRI and fluorodeoxyglucose–positron emission tomography (FDG-PET) — in individuals who had recovered from COVID-19 infection and looked at how this related to changes in inflammatory blood markers.
Lead author Kate Hanneman, MD, also from the University of Toronto, explained that FDG-PET imaging is more sensitive than MRI in detecting active inflammation. “Inflammatory cells have a higher uptake of glucose, and FDG-PET imaging is used to look for metabolically active inflammatory tissue that takes up glucose. It gives complementary information to MRI. Cardiac MRI shows structural or functional changes, such as scarring or edema, whereas FDG-PET imaging directly measures metabolic activity related to inflammatory cells.”
The study involved 47 individuals, 51% female, with a mean age of 43 years, who had recently recovered from COVID-19 infection. Of these, the majority had had relatively mild COVID disease, with 85% not requiring hospitalization.
Cardiac imaging was performed a mean of 67 days after the diagnosis of COVID-19. At the time of imaging, 19 participants (40%) reported at least one cardiac symptom, including palpitations, chest pain, and shortness of breath.
Results showed that eight patients (17%) had focal FDG uptake on PET consistent with myocardial inflammation. Compared with those without FDG uptake, patients with focal FDG uptake had higher regional T2, T1, and extracellular volume (colocalizing with focal FDG uptake), higher prevalence of late gadolinium enhancement indicating fibrosis, lower left ventricular ejection fraction, worse global longitudinal and circumferential strain, and higher systemic inflammatory blood markers including interleukin (IL)-6, IL- 8, an high-sensitivity C-reactive protein.
Of the 47 patients in the study, 13 had received at least one dose of a COVID-19 vaccine. There was no significant difference in the proportion of patients who were PET-positive among those who had received a COVID-19 vaccine and those who had not.
There was also no difference in inflammation in patients who had been hospitalized with COVID-19 and those who had managed their infection at home.
Among patients with focal FDG uptake, PET, MRI, and inflammatory blood markers improved at follow-up imaging performed a mean of 52 days after the first imaging. The authors say this suggests that these abnormalities were not related to pre-existing cardiovascular disease.
Of the eight patients with positive FDG-PET results, two did not show any MRI abnormalities. These two patients also had elevated inflammatory biomarkers. “PET is a more sensitive method of measuring cardiac inflammation, and our results show that these changes may not always translate into functional changes seen on MRI,” Thavendiranathan noted.
The only cardiac risk factor that was more common in participants with FDG uptake was hypertension. Although cardiac symptoms were nearly twice as common in participants with focal FDG uptake, this difference was not statistically significant.
“Given the growing number of survivors with similar symptoms, these interesting findings warrant further investigation,” the authors say.
Noting that FDG uptake corelated with elevations in systemic inflammatory biomarkers, the researchers suggest that “a more intense systemic inflammatory process may be contributing to cardiac inflammation and the consequential alteration to regional and global myocardial function in PET-positive participants.”
On repeat imaging 2 months later, all eight patients who showed FDG uptake showed improvement or resolution of inflammation without any treatment, although two patients still had some signs of inflammation. Blood biomarkers also improved on follow-up.
“This is encouraging information, but we need longer-term data to see if there are any long-term repercussions of this inflammation,” Hanneman said.
“Overall, the study findings suggest an imaging phenotype that is expected to have good prognosis. However, longer-term follow-up studies are required to understand the need for ongoing cardiac surveillance, relationship to cardiac symptoms, guidance for safe return to exercise and sports participation, and long-term cardiovascular disease risk,” the researchers state.
This study was funded by grants from the Joint Department of Medical Imaging Academic Incentive Fund, Peter Munk Cardiac Center Innovation Committee, and Ted Rogers Center for Heart Research. Hanneman reports personal fees from Sanofi Genzyme, Amicus, and Medscape outside the submitted work.
JAMA Cardiol. Published online January 12, 2022. Full text