Role of advanced imaging in COVID-19 cardiovascular complications

Fig. 1. Hypothetical pathophysiology patterns concurring in cardiovascular involvement in COVID-19. SARS-CoV-2 enters cells via ACE2 receptor in type 2 in pneumocytes, endothelial cells, pericytes and cardiac myocytes, causing direct damage. Systemic inflammation and uncontrolled immune cell activation lead to a ‘cytokine storm’ which can contribute to destabilize atherosclerotic plaques and potentially trigger the onset of myocarditis trough T cells and macrophages infiltrations. Direct viral cardiac injury can provoke the development of arrhythmias, as well as several medications used in COVID-19 patients

Fig. 2. Myocarditis. 51-year-old man hospitalized for COVID‐19 pneumonia and sudden onset of tachyarrhythmias. STIR images revealed no edema (a), although LGE was evident on infero-lateral segments of basal-mid planes with a subepicardial pattern of distribution (b, c orange arrows) and native T1 was increased on LGE + segments (d). T2 mapping sequences revealed the presence of edema on infero-lateral segments of mid-ventricular planes (e). ECV confirmed those findings with implemented values on infero-lateral wall (f). Chest CT showed GGO predominantly distributed on inferior lobes with a peripheral distribution (g). STIR short tau inversion recovery, LGE late gadolinium enhancement, ECV extracellular volume, CT computed tomography, GGO ground glass opacity

Fig. 3. Suggested CMR protocol for myocarditis diagnosis in COVID-19 patients. STIR short tau inversion recovery; MOLLI modified look-locker imaging; FLASH-3D fast low angle shot three-dimensional; SSFP steady-state free precession; MR magnetic resonance; IR-CE inversion recovery contrast enhanced; LGE late gadolinium enhancement; Gd gadolinium

Fig. 4. Pericarditis. 36-year-old in-hospital COVID-19 patient with chest discomfort and evidence of pericardial effusion at bedside Echo. a Evidence a slight hyperintensity of the pericardial layers, with no myocardial edema. LGE sequences confirm the presence on pericardial layers enhancement and moderate pericardial effusion (b, c orange arrows). Native T1 values were mildly increased (d) as well as T2 mapping (e) and ECV values (f). Coronal and axial chest CT revealed peripheral posterior areas of parenchymal consolidation (g). Echo echocardiography; STIR short tau inversion recovery; LGE late gadolinium enhancement; ECV extracellular volume; CT computed tomography

Fig. 5. STEMI. 45-year-old male patient with no CV history admitted to ER with acute chest pain, elevation of TnT and ST elevation at ECG. Nasopharyngeal swab tested positive for SARS-CoV-2 and chest CT showed a mild pulmonary involvement (a). Occlusion of proximal DA was detected and treated at ICA (b). CMR, performed 7 days after revascularization, showed antero-septal edema of mid and apical planes at STIR images (c, d orange arrows). LGE sequences evidenced necrosis with subendocardial distribution on antero-septal segments and transmural extension on anterior segments on mid planes (e, f blue arrows). Increased values of native T1 (g), T2 mapping (h) and ECV fraction (i) confirmed the presence of edema and necrosis on anterior and antero-septal segments on mid and apical planes. CV cardiovascular; ER emergency room; TnT t-troponin; CT computed tomography; DA descending coronary artery; ICA invasive coronary angiography; CMR cardiac magnetic resonance; STIR short tau inversion recovery; LGE late gadolinium enhancement, ECV extracellular volume

Fig. 6. Takotsubo cardiomyopathy. COVID-19 female patient with chest pain and no CAD. Cine-SSFP showed a diffuse hypokinesia of mid and apical segments with «apical ballooning» sign (a). Diffuse edema of mid-ventricular and apical segments on 2-chambers STIR was found (b red asterisk). PSIR sequences evidenced no LGE (c). Native T1, T2 mapping and ECV fraction values were all increased (d–f). Chest CT showed a low-grade pulmonary involvement with peripheral interstitial thickening (g). CAD coronary artery disease; SSFP steady-state free precession; STIR short tau inversion recovery; PSIR phase sensitive inversion recovery; LGE late gadolinium enhancement; ECV extracellular volume; CT computed tomography

Fig. 7. Pulmonary Embolism. COVID-19 patient with dyspnea, increased D-dimer levels and O2 saturation < 93. Chest CT evidenced GGO with interstitial thickening of the interlobular and intralobular septa, together with pleural effusion (a, b). After contrast media injection, PE was found in the left upper lobar branch, the left inferior lobar branch and the segmental arteries for the left inferior pulmonary lobe and PE of the interlobar arteries for the inferior right lobe, probably extended to the subsegmentary arteries (d, e). CT computed tomography; GGO ground glass opacity; PE pulmonary embolism

Fig. 8. Suggested flowchart for imaging management of suspected cardiac injury in COVID-19 patients. (*) CCTA can be considered to triple rule-out CAD, interstitial pneumonia and pulmonary embolism in selected patients. TnT T-troponin; Echo echocardiography; ICA invasive coronary angiography; CCTA cardiac computed tomography angiography; CMR cardiac magnetic resonance