**2. Case Report**

A six-year-old boy was diagnosed with left ventricular noncompaction cardiomyopathy with severe heart failure and underwent heart transplantation at nine months. His postoperative course was complicated by severe hypoxic-ischemic injury, gastrostomy, and tracheostomy, and he remained on mechanical ventilation. He had no clinical rejection evidence with maintenance immunosuppression (tacrolimus and mycophenolate sodium) and was doing well. He encountered SARS-CoV-2 infection and presented with fever and cyanosis. His chest-X ray (CXR) showed bilateral perihilar infiltrations (Figure 1A). Pseudomonas aeruginosa was isolated from tracheal aspirate and was sensitive to Imipenem, Amikacin, and Ofloxacin. The polymerase chain reaction for the viral respiratory panel was negative for other viral pathogens. His tracheal aspirate for aspergillus filament and pneumocystis carinii were negative. He was admitted to the hospital for supportive care and treated with intravenous Imipenem, and discharged home to complete a ten-day course with oral Ofloxacin. His father was also positive for SARS-CoV-2. Both were quarantined at home as per the center for disease control (CDC) guidelines. His father tested negative

**Citation:** Das, B.B. Presentation of SARS-CoV-2 in a Pediatric Heart Transplant Recipient with Multiple Underlying Comorbidities. *Transplantology* **2021**, *2*, 87–91. https://doi.org/10.3390/ transplantology2010009

Academic Editor: Taisto Sarkola

Received: 15 February 2021 Accepted: 4 March 2021 Published: 22 March 2021

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**Copyright:** © 2021 by the author. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https:// creativecommons.org/licenses/by/ 4.0/).

for SARS-CoV-2 after initial positive test subsequently, but the patient continued to be positive at three weeks.

**Figure 1.** (**A**): Chest X-Ray (CXR): (Initial presentation) Perihilar infiltrates (Expiratory film) vs. (**B**): Second CXR with improvement in infiltrations.

> The patient had a fever (38.3 ◦C) recurrence 23 days after initial positive SARS-CoV-2 and presumed pseudomonas pneumonia. He was hemodynamically stable but noted to have tachycardia (180 beats/min), frequent premature ventricular contractions, cyanosis (oxygen saturation was in the 80 s) for which he was admitted to the cardiac intensive care unit. A repeat CXR (Figure 1B) showed improved lung infiltrations compared to the previous one (Figure 1A). His electrocardiogram showed sinus tachycardia, and non-specific ST changes (Figure 2A) compared to his baseline (Figure 2B). His laboratory tests revealed a white blood cell count of 2.8 × 109/L, hemoglobin 10.5 g/L, platelets <sup>161</sup> × <sup>10</sup>9/L, and 23% of lymphocytes on the differential count. A complete metabolic panel showed no end-organ damage with normal creatinine and liver enzymes. His C-reactive protein was 88.45 mg/L (<10.01 mg/L), erythrocyte sedimentation rate 88 mm/h (2–34 mm/h), pro-calcitonin 1.5 ng/L (<0.05 ng/L), sedimentation rate 88 mm/h (2–34 mm/h), ferritin 35 ng/mL (22–322 ng/mL), brain natriuretic peptide 4218 pg/mL (0–124 pg/Ml), and troponin 1.2 ng/mL (<0.1 ng/mL). His echocardiogram showed normal biventricular systolic function and normal coronaries. His repeat blood, endotracheal aspirate, and urine cultures were negative. His repeat tracheal swab was negative for adenovirus, metapneumovirus, enterovirus, influenza A and B virus, parainfluenza type1-4 virus, bordetella pertussis, parapertusis, chlamydia, and mycoplasma. The differential diagnoses were presumed SARS-CoV-2 myocarditis or acute cardiac allograft rejection. He was treated with intravenous methylprednisolone 10 mg/kg/dose twice daily for three days. After starting the steroid, within 48 h, his heart rate returned to its baseline (60 s–70 s/min), and his inflammatory markers decreased significantly (erythrocyte sedimentation rate 32 mm/h, C-reactive protein 19 mg/L, and procalcitonin 0.07 ng/mL). His daily troponin trended downward, and at the end of the third day of the steroid pulse, troponin was 0.05 ng/mL, and brain natriuretic peptide was 52 pg/mL. His repeat echocardiogram showed no change in function. No changes to his immunosuppression regimen were made. His tacrolimus trough level was 4.8 ng/mL. He was discharged home four days after hospitalization on his home immunosuppression regimens and oral prednisone, which was tapered over two weeks and stopped. On follow-up after two weeks, he was doing well without recurrence of fever or tachycardia, and inflammatory markers and troponin were normal. His repeat tests for SARS-CoV-2 were positive at six weeks and then three months from his initial positivity. His CD4, CD8, CD3, CD19 cell counts, CD4:CD8 ratio, and immunoglobulin levels were within the normal limit. His serology returned positive for SARS-CoV-2 IgM, but IgG was negative three months from his first positive test for SARS-CoV-2. He became finally SARS-CoV-2 negative four months after his initial positive test and underwent

cardiac magnetic resonance (CMR) imaging as a part of surveillance that showed no myocardial edema, myocardial perfusion defects, or regional wall motion abnormalities at rest (Figure 3A). There was no evidence of delayed enhancement to suggest myocardial fibrosis or scarring (Figure 3B).

**Figure 2.** (**A**): A 12-lead ECG showing sinus tachycardia (150 bpm) and non-specific ST changes vs. baseline ECG (**B**): sinus rhythm with heart rate 70 bpm.

**Figure 3.** Short-axis T2-weighted image through the left ventricle base showing no early (**A**) or late-gadolinium enhancement (**B**).
