Table 4.
Studies reporting cardiac tissue findings in COVID-19 patients.
| Study (year) | Number of patients | Design | Findings |
|---|---|---|---|
| Basso et al. (92) | 21 | Multicenter pathology study, post-mortem | Increased interstitial macrophage infiltration was present in 86% of the cases, whereas lymphocytic myocarditis was present in 14% of the cases |
| Varga et al. (48) | 3 | Case reports, post-mortem | Lymphocytic endotheliitis in lung, heart, kidney, and liver but no sign of lymphocytic myocarditis. |
| Menter et al. (93) | 21 | Multicenter, post-mortem | Myocardial hypertrophy (71% of cases), senile amyloidosis (29% of cases), peracute myocardial necrosis (14% cases), acute myocardial infarction (5% cases) |
| Lax et al. (94) | 11 | Single-center, prospective study, post-mortem | Myocardial hypertrophy (100%), coronary small vessel disease (54%), myocardial fibrosis (91%), focal lymphocytic infiltrate (9%) |
| Buja et al. (95) | 3 | Multicenter, post-mortem | Lymphocytic myocarditis was reported in 1 case. |
| Duarte-Neto et al. (96) | 10 | Single-center, case series, post-mortem | Cardiomyocyte hypertrophy (90%), myocardial fibrosis (90%), previous myocardial infarction (40%), interstitial oedema (90%) myocarditis (20%), and fibrin thrombi (20%) |
| Bradley et al. (97) | 14 | Multicenter, case series, post-mortem | Cardiac findings were mostly non-specific: fibrosis (100%) and myocyte hypertrophy (93%). Myocarditis was present with aggregates of lymphocytes surrounding necrotic myocytes in 7% |
| Rapkiewicz et al. (98) | 7 | Single-center, case series, post-mortem | 1 case had focal acute lymphocyte-predominant inflammation in the myocardium. Otherwise, cardiac histopathological changes were limited to minimal epicardial inflammation (n = 1), early ischemic injury (n = 3), and mural fibrin thrombi (n = 2) |
| Grosse et al. (99) | 14 | Single-center, case series, post-mortem | Myocardial hypertrophy (92.9%), acute myocardial infarction (21.4%), focal myocardial fibrosis (42.9%), amyloidosis (7.1%), mononuclear inflammatory cells in the myocardial interstitium (100%) |
| Hanley et al. (100) | 10 | Multicenter, case series, post-mortem | Acute coronary thrombosis (10%), thrombi in the microcirculation (56%), aright atrial thrombus (11%). Pericarditis (22%); marantic endocarditis in 11% |
| Oprinca et al. (101) | 3 | Single-center, case series, post-mortem | Mild to moderate perivascular edema, vascular congestion, small number of scattered lymphocytes between the myocardial fibers |
| Sala et al. (86) | 1 | Case report with EMB | Diffuse T-lymphocytic inflammatory infiltrates with huge interstitial oedema and limited foci of necrosis. No replacement fibrosis |
| Tavazzi et al. (88) | 1 | Case report with EMB | Low-grade interstitial and endocardial inflammation, with macrophages containing virions of coronaviruses. Cardiac myocytes showed non-specific features consisting of focal myofibrillar lysis and lipid droplets. |
| Escher et al. (102) | 104 | Multicenter, EMB study | 5 EMBs were positive for SARS-CoV-2 E-gene-specific sequences. Other findings were active myocarditis (13.4%), inflammatory cardiomyopathy (32.6%), borderline myocarditis (2.9 %); dilated cardiomyopathy (41.3%), and amyloidosis (9.6%) |
| Lindner et al. (63) | 39 | Cohort study, post-mortem | Viral presence within the myocardium could be documented in 41% but was not associated with an influx of inflammatory cells |
| Kawakami et al. (103) | 15 | Literature review, post-mortem | None of the cases met the criteria of myocarditis, although in 3 cases microvascular infarction was described. In 2 cases, the virus was detected by RT-PCR in the atria, but no inflammation was described. |
| Haslbauer et al. (104) | 23 | Multicenter, post-mortem | 60% of cases had myocardial RT-PCR positivity by SARS-CoV-2 PCR. Significantly higher levels of capillary fibrin deposition, capillary dilatation, and parenchymal microhemorrhages (consistent with microvascular dysfunction) compared with 10 autopsies without SARS-CoV-2. Five cases presented with increased cardioinflammatory infiltrate presented but without cardiomyocyte necrosis. Only while 1 case presented with active lymphohistiocytic myocarditis. |
| Bearse et al. (105) | 41 | Single-center, consecutive cases, post-mortem | Cardiac infection by SARS-CoV-2 (assessed by RT-PCR) was present in 30/41 cases. Cardiac infection by SARS-CoV-2 is associated with more cardiac inflammation (monocytes and macrophages). Four cases met criteria for myocarditis. |
| Fox et al. (106) | 10 | Single-center, case series, post-mortem | No evidence of lymphocytic myocarditis. In the COVID-19-affected cases, diffuse number of infiltrative cells of monocytes/macrophage lineage was noticed, with upper quantiles as compared to both matched control hearts. |
EMB, endomyocardial biopsy; SARS-CoV-2, severe acute respiratory syndrome coronavirus 2; RT-PCR, reverse transcriptase-polymerase chain reaction.