A 43-year-old male patient with unremarkable past medical history was admitted to the Infectious Diseases Unit for suspected respiratory infection by COVID-19. On arrival, the patient reported fever that started 14 days before and persisted for 10 days, dry cough, and haemoptoic sputum. Nasopharyngeal swabs were immediately obtained, confirming COVID-19 positivity.
On admission, he had a heart rate of 77 b.p.m., blood pressure of 135/80 mmHg, temperature of 36.8°C, and SpO2 of 91%.
Chest X-ray (Panel A) revealed a diffuse interstitial pattern with opacities in both lungs.
ECG (Panel B) showed sinus rhythm with minimal ST-segment elevation and extensive repolarization abnormalities.
Urgent portable transthoracic echocardiogram showed a left ventricle of normal dimensions with mild hypertrophy and overall hypokinesia, with LVEF 50–55%. A mild hyper-refringence pattern was also observed at the lateral wall of the left ventricle.
Laboratory results were: high-sensitivity troponin T curve of 29–24–24–18–15 ng/L (<14 ng/L) (Supplementary material online), NT-proBNP 456 pg/mL (<125 pg/mL), ferritin 1060 ng/mL (<300 ng/mL), D-dimer 790 ng/mL (<500 ng/mL), C-reactive protein 14 mg/L (<10 mg/L), leucocyte count 4.03 × 103/μL (> 4.8 × 103/μL), 83% neutrophils (<70%), and lymphocytes 0.42 × 103/μL (>0.9 × 103/μL), 10.4% (>19%).
Based on these findings, a cardiac magnetic resonance (CMR) study was requested to rule out the presence of acute myocarditis.
CMR at 1.5 T was performed 15 days after admission; right pulmonary condensation along with associated pleural effusion was seen in the multislice anatomical sequences (Supplementary material online). A left ventricle of normal volume with concentric hypertrophy and mild depressed systolic function (LVEF 53%) secondary to diffuse hypokinesia was observed (Supplementary material online, Videos S1–S4). Global longitudinal strain was decreased (Supplementary material online). Myocardial oedema with a predominant subepicardial pattern was seen in the lateral, anterior, inferior, and apical segments on T2 short tau inversion recovery (Panels C and D) and T2 mapping sequences (Panels E and F; average, 60 ms; mid-septum, 53 ms; lateral wall, 67 ms, reference value ∼50 ms), determining wall pseudo-hypertrophy. Pericardial oedema without associated effusion was also observed. Native T1 and extracellular volume (ECV) both were increased in relation to the acute inflammatory process (native T1, Panels G and H: average, 1110 ms; mid-septum, 1047 ms; lateral wall, 1204 ms, reference value ∼950 ms. ECV, Panels I and J: average, 33%; mid-septum, 29%; lateral wall, 39%; reference value ∼24%). Late gadolinium sequences showed extensive, patchy intramyocardial/subepicardial enhancement affecting the entire lateral, anterior, inferior, and apical septal walls and the pericardium (Panels K–M).
Viral serology by immunochromatography performed 15 days after onset of symptoms yielded IgM-negative and IgG-positive coronavirus 2019-nCoV. In conclusion, the final diagnosis was subacute perimyocarditis with mild systolic dysfunction associated with respiratory infection caused by COVID-19 (>15 days from the onset of symptoms). Hydroxychloroquine and azythromicin were administered but discontinued 2 days later due to QT interval prolongation. Bisoprolol, tocilizumab, and methylprednisolone were administered thereafter. During the hospital stay, the patient had no arrhythmias, chest pain, dyspnoea, dizziness, or palpitations at any time. The patient was discharged 8 days after hospital admission. After hospital discharge, a control CMR is scheduled to take place in ∼1 month.
Figure 1.
(A) Chest X-ray showing a diffuse interstitial pattern with opacities in both lungs. (B) Electrocardiogram showing sinus rhythm with minimal ST segment elevation and extensive repolarization abnormalities. (C and D) T2 short tau inversion recovery long-axis four-and two-chamber views, showing regional oedema of the lateral, anterior, inferior, and apical left ventricle predominantly, with subepicardial involvement. (E and F) T2 mapping long-axis images showing high values of T2 on average and predominantly in the lateral, anterior, inferior, and apical segments. (G–J) T1 native (above) and ECV (below) images reveal high values of T1 native and ECV. K–M Contrast-enhanced cardiac magnetic resonance long-axis imaging shows patchy intramyocardial/subepicardial enhance-ment affecting the entire lateral, anterior, inferior, and apical septal walls, and the pericardium.
Figure 2.
Time course of the high-sensitivity troponin T curve.
This case provides further evidence obtained with CMR of extensive myocardial inflammatory involvement secondary to SARS-CoV-2 infection that has been described in some patients but the mechanism of which is currently not fully understood.
The patient gave us his consent to publish the case. This form is available upon request.
Panel A. Chest X-ray showing a diffuse interstitial pattern with opacities in both lungs.
Panel B. Electrocardiogram showing sinus rhythm with minimal ST segment elevation and extensive repolarization abnormalities.
Panels C and D. T2 short tau inversion recovery long-axis four- and two-chamber views, showing regional oedema of the lateral, anterior, inferior, and apical left ventricle predominantly, with subepicardial involvement.
Panels E and F. T2 mapping long-axis images showing high values of T2 on average and predominantly in the lateral, anterior, inferior, and apical segments.
Panels G–J. T1 native (above) and ECV (below) images reveal high values of T1 native and ECV.
Panels K–M. Contrast-enhanced cardiac magnetic resonance long-axis imaging shows patchy intramyocardial/subepicardial enhancement affecting the entire lateral, anterior, inferior, and apical septal walls, and the pericardium.
Panels N and O. Coronal half-Fourier acquisition single-shot turbo spin-echo (HASTE) image (left) and axial steady-state free precession (SSFP) image (right) showing right pulmonary condensation along with associated pleural effusion.
Panels P–S. Strain analysis with a feature-tracking software (CircleCVI42®). From long-axis two- and four-chamber SSFP cine images, the longitudinal strain curve is derived. Both global values are impaired.
Video S1–S4 Two-chamber (S1), four-chamber (S2), three-chamber (S3), and short-axis (S4) cine images using SSFP showing a mild diffuse hypokinesia.
Supplementary material is available at European Heart Journal Case Reports online.
Supplementary Material
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