Cardiac pathology in COVID-19: a single center autopsy experience

Abstract

Background: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is commonly associated with myocardial injury and heart failure. The pathophysiology behind this phenomenon remains unclear, with many diverse and multifaceted hypotheses. To contribute to this understanding, we describe the underlying cardiac findings in fifty patients who died with coronavirus disease 2019 (COVID-19).

Methods: Included were autopsies performed on patients with a positive SARS-CoV-2 reverse-transcriptase-polymerase-chain reaction test from the index hospitalization. In the case of out-of-hospital death, patients were included if post-mortem testing was positive. Complete autopsies were performed according to a COVID-19 safety protocol, and all patients underwent both macroscopic and microscopic examination. If available, laboratory findings and echocardiograms were reported.

Results: The median age of the decedents was 63.5 years. The most common comorbidities included hypertension (90.0%), diabetes (56.0%) and obesity (50.0%). Lymphocytic inflammatory infiltrates in the heart were present in eight (16.0%) patients, with focal myocarditis present in two (4.0%) patients. Acute myocardial ischemia was observed in eight (16.0%) patients. The most common findings were myocardial fibrosis (80.0%), hypertrophy (72.0%), and microthrombi (66.0%). The most common causes of death were COVID-19 pneumonia in 18 (36.0%), COVID-19 pneumonia with bacterial superinfection in 12 (24.0%), and COVID-19 pneumonia with pulmonary embolism in 10 (20.0%) patients.

Conclusions: Cardiovascular comorbidities were prevalent, and pathologic changes associated with hypertensive and atherosclerotic cardiovascular disease were the most common findings. Despite markedly elevated inflammatory markers and cardiac enzymes, few patients exhibited inflammatory infiltrates or necrosis within cardiac myocytes. A unifying pathophysiologic mechanism behind myocardial injury in COVID-19 remains elusive, and additional autopsy studies are needed.

Keywords: Cardiac pathology; Cardiovascular disease; Coronavirus disease 2019; Severe acute respiratory syndrome coronavirus 2.

Fig. 1

Gross cardiac pathology. (A) Specimen with biventricular dilation and straightening of the interventricular septum as a result of increased pulmonary pressure. (B) Acute transmural hemorrhagic infarction extending from the apex to base with involvement of the anterior and lateral walls and interventricular septum.

Fig. 2

(A) Acute ischemic injury with irreversible contraction band necrosis (H&E 20x) in a patient with moderate atherosclerotic stenosis of the left anterior descending coronary artery. (B) Hypereosinophilic myocytes with contraction bands and nuclear loss surrounding an area of granulation tissue and myocardial fibrosis (H&E 20x). (C) Reversible vacuolar degeneration of myocytes typical of myocardial ischemia (H&E 40x).

Fig. 3

(A) Mild interstitial lymphocytic infiltration without myocyte damage (H&E 20x). (B) Focal myocarditis characterized by mononuclear cell infiltrate with myocyte damage (H&E 10x). (C) Fibrinous pericarditis (H&E 20x). (D) Pulmonary artery with subendothelial inflammatory infiltrate (H&E 20x).

Fig. 4

(A) Microthrombus within pulmonary vasculature (H&E 20x). (B) Non-occlusive organizing thrombus of an intramural vessel of the lateral left ventricle (H&E 4x).

Fig. 5

Patchy and multifocal lymphocytes and intramyocardial giant cells compatible with a diagnosis of cardiac sarcoidosis. (H&E 4x (A); 10x (B)). The findings of sarcoidosis were incidental in the setting of known heart failure with reduced ejection fraction requiring ICD placement, atrial fibrillation requiring multiple cardioversions, and severe mitral regurgitation.