A 63-year-old male was admitted to the hospital due to the expectoration of white sticky sputum, a fever of 39.3 ℃, and shortness of breath and chest tightness after activity. He had no history of heart disease or hypertension. He had allergic cough for 5 years and a previous smoking history. He had a recent history of travel to Hubei Province, China.
Blood gas analysis after admission showed a pH of 7.049, PCO2 of 76.4 mmHg, PO2 of 66.2 mmHg, and SaO2 at 91.8%. Nasal and pharyngeal swabs, bronchoalveolar lavage fluid (BALF), and sputum were tested for common respiratory viruses, and the results were all negative. In addition, blood samples showed increased alanine aminotransferase (ALT) (97 U/L) and creatinine (157 μmol/L) combined with hematuria, indicating deranged liver and renal function. Bedside chest radiographs showed typical ground-glass changes indicative of viral pneumonia (Fig. 1). On the first day of admission, he was genetically confirmed to have COVID-19 according to sputum testing, as shown in Table 1.
Markers of myocardial injury included elevated troponin I (Trop I) (11.37 g/L), myoglobin (Myo) (390.97 ng/mL), and n-terminal brain natriuretic peptide (NTBNP) (22,600 pg/mL) (Fig. 2). An electrocardiogram showed sinus tachycardia and no ST-segment elevation (Fig. 3). Bedside echocardiography showed an enlarged left ventricle (61 mm), diffuse myocardial dyskinesia along with a low left ventricular ejection fraction (LVEF) (32%), pulmonary hypertension (44 mmHg), and no decrease in right cardiac function (Figs. 4, 5). No pericardial effusion was observed.
The diagnosis was considered severe pneumonia, ARDS, fulminant myocarditis, and multiple organ dysfunction syndrome (MODS). The treatment regimen was ventilatory support, high-flow oxygen, lopinavir–ritonavir antiviral therapy, interferon α-1b, methylprednisolone, immunoglobulin, piperacillin–tazobactam, and continuous renal replacement therapy (CRRT). Notably, 11 days after admission, the patient’s lung lesions continued to progress, and the ventilator was unable to maintain oxygen saturation. The ventricular septum thickened to 14 mm, and interleukin-6 (IL-6) increased to 272.40 pg/mL. Therefore, extracorporeal membrane oxygenation (ECMO) was used to reduce the cardiopulmonary burden. The rotating speed of ECMO was 3500 rpm, the blood flow rate was 4.30 L/min, the air-flow rate was 4.00 L/min, and FiO2 was 100%. At one time, the patient's condition improved. A blood test 3 days later revealed that Trop I was reduced to 0.10 g/L, NTBNP was 750 pg/mL, and IL-6 was 7.63 pg/mL. After treatment, the LVEF of the patient gradually recovered to 68%, the left ventricle and wall thickness returned to within their normal ranges, and the bedside chest film suggested that the lesion had decreased. However, infection-related markers increased gradually from the 26th day, and vasoactive drugs were needed to maintain blood pressure. Candida, human α-herpesvirus, and β-herpesvirus were detected in BALF on the 29th day, and blood culture was positive for Bacteroides ovalus, indicating the aggravation of secondary infection. Pulmonary artery systolic pressure (PASP) and tricuspid annular plane systolic excursion (TAPSE) showed sudden declines on the 26th and 29th days, suggesting impaired right cardiac function. After consultation with the expert group, anti-infection treatment was strengthened, but the effect was not good. Septic shock and disseminated intravascular coagulation (DIC) gradually developed, and ecchymosis was widely observed in the skin. The patient died on the 33rd day of hospitalization.