Two separate studies, published in the journal JAMA Cardiology, have provided more insight into how Covid-19 may have a prolonged impact on heart health in those who have recovered from illness and may have caused cardiac infection in those who died.
Outcomes of Cardiovascular Magnetic Resonance Imaging in Patients Recently
One of the JAMA Cardiology studies found that, among 100 adults who recently recovered from Covid, 78% showed some type of cardiac involvement in MRI scans and 60% had ongoing inflammation in the heart.
In this cohort study including 100 patients recently recovered from COVID-19 identified from a COVID-19 test center, cardiac magnetic resonance imaging revealed cardiac involvement in 78 patients (78%) and ongoing myocardial inflammation in 60 patients (60%), which was independent of preexisting conditions, severity and overall course of the acute illness, and the time from the original diagnosis.
These findings indicate the need for ongoing investigation of the long-term cardiovascular consequences of COVID-19.
A number of case reports and small series suggested that COVID-19 prominently affects the cardiovascular system by exacerbating heart failure in patients with preexisting cardiac conditions and troponin elevation in critically ill patients.
Fulminant myocarditis was suspected in 7% of patients with lethal outcome.
The proposed pathophysiological mechanisms of cardiac injury include inflammatory plaque rupture, stent thrombosis, cardiac stress due to high cardiac output, and infection via the angiotensin-converting enzyme 2 receptors causing systemic endothelitis
Analysis of Autopsies
In the other JAMA Cardiology study, an analysis of autopsies found that coronavirus could be identified in the heart tissue of Covid-19 patients who died.
The study included data from 39 autopsy cases from Germany between April 8 and April 18. The patients, ages 78 to 89, had tested positive for Covid-19 and the researchers analyzed heart tissue from their autopsies.
ardiac tissue from 39 consecutive autopsy cases were included. The median (interquartile range) age of patients was 85 (78-89) years, and 23 (59.0%) were women. SARS-CoV-2 could be documented in 24 of 39 patients (61.5%). Viral load above 1000 copies per μg RNA could be documented in 16 of 39 patients (41.0%).
None of the patients in the study were diagnosed as having clinically fulminant myocarditis. Comorbidities such as hypertension, coronary artery disease, and diabetes were frequent and diagnosed in 17 (43.6%), 32 (82.0%), and 7 patients (17.9%), respectively.
Fifteen of 39 autopsies (38.5%) had no SARS-CoV-2 RNA in the myocardium. In 8 of 24 patients (33.3%) with viral presence, the virus load was lower than 1000 copies per μg RNA. In the remaining 16 patients, virus load was above 1000 copies.
Virus replication of SARS-CoV-2 defined by detection of the (−) strand replicate of the RNA genome was documented in the myocardium of the 5 patients with the highest virus load. The median (interquartile range) copy number of those 5 patients was 135 584 (84 949-474 675) per μg RNA.
