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SARS-COV-2 infects the heart and leads to lasting heart damage in many patients: JAMANETWORK.

em coronavirus from NIAID– CC license

This study from JAMA Cardiology posted on JAMANETWORK on July 27 looked at cardiac MRI scans of 100 people who had recovered from COVID-19. Their median age was 49; a third of them had been hospitalized, and all had been diagnosed between two and three months before they were examined. Many of these patients had been infected during a ski vacation, so they were not sedentary prior to their disease onset.

Only 5% of the patients had increased cardiac troponin T levels (a sign of heart damage often observed in myocardial infarction or “heart attack”) and none of them had active symptoms. This from the abstract:

Compared with healthy controls and risk factor–matched controls, patients recently recovered from COVID-19 had lower left ventricular ejection fraction, higher left ventricle volumes, higher left ventricle mass, and raised native T1 and T2. A total of 78 patients recently recovered from COVID-19 (78%) had abnormal CMR findings, including raised myocardial native T1 (n = 73), raised myocardial native T2 (n = 60), myocardial late gadolinium enhancement (n = 32), and pericardial enhancement (n = 22). … . Endomyocardial biopsy in patients with severe findings revealed active lymphocytic inflammation.

JAMA Cardiol. Published online July 27, 2020. doi:10.1001/jamacardio.2020.3557

In conclusion, the MRI findings showed: “cardiac involvement in 78 patients (78%) and ongoing myocardial inflammation in 60 patients (60%)…” This is astounding and indicates that most patients in this age group (roughly 50 year olds) had heart damage from COVID-19 that was not resolved 2-3 months after diagnosis.

The second heart study, of autopsies, was also from JAMANETWORK on July 27. 39 consecutive autopsies, with a median age of 85, were examined. The presence of SARS-COV-2 was documented in 24 patients, with elevated virus RNA in 16. From the results section:

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%). A cytokine response panel consisting of 6 proinflammatory genes was increased in those 16 patients compared with 15 patients without any SARS-CoV-2 in the heart. Comparison of 15 patients without cardiac infection with 16 patients with more than 1000 copies revealed no inflammatory cell infiltrates or differences in leukocyte numbers per high power field.

JAMA Cardiol. Published online July 27, 2020. doi:10.1001/jamacardio.2020.3551

This autopsy showed high levels of viral replication in heart tissue and definite signs that cells were “transformed” into virus factories, getting ready to die and release their viral loads. These results explain the frequent observations of acutely ill patients with elevated cardiac troponins and the 70% incidence of echocardiographic evidence of myocardial dysfunction (hearts not working right.)

One difference in the autopsy study was that they didn’t see an “inflammatory cell infiltrate” whereas the MRI study mentioned a finding of “active lymphocytic inflammation”– perhaps this is a late finding, and the older autopsied patients died before this could occur.

A clinical presentation compatible with myocarditis or heart inflammation (abnormal heart rhythm, palpitations, swelling in ankles, increased shortness of breath on lying down) as opposed to the usual cough, headache, chest pain, shortness of breath, weakness, and dizziness, is unusual. This suggests that infection of the heart is relatively silent compared to the obvious lung infection.

This does account for the devastating presentations of patients with severe COVID-19 if both the heart and lungs are affected.

This heart damage is shocking but not really surprising, given that a large proportion of patients with even mild disease have prolonged symptoms of fatigue or weakness and dizziness. Patients who have recovered from COVID-19 often complain of symptoms compatible with “mild heart failure” like exercise intolerance and shortness of breath.

Only time will tell how long these lingering symptoms will last and whether they will lead to a large population of chronic heart failure patients.

We learn something new about SARS-COV-2 almost every day.

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