SARS-CoV-2 is an emerging cause of viral myocarditis that generates multiple complications, such as dilated cardiomyopathy. We describe a young, obese male patient with severe myocardial involvement by the SARS-CoV-2 virus, who presented with chest pain, elevated cardiac enzymes, non-specific electrocardiographic findings, echocardiogram with evidence of dilated heart disease with reduced ejection fraction, and subsequent verification using magnetic resonance imaging (MRI). The results of the cardiac MRI were typical of viral myocarditis. The patient did not respond to a short course of systemic steroids and the standard management for heart failure, had multiple re-admissions, and, unfortunately, died.
Introduction
Since its appearance in December 2019 in Wuhan (Hubei, China), more than 300 million people worldwide have been infected with the SARS-CoV-2 virus1 (which generates multi-systemic involvement and is an emerging cause of myocardial compromise). This article presents an illustrative case of dilated cardiomyopathy as a complication of viral myocarditis due to SARS-CoV-2.
Case presentation
Table 1. Most relevant laboratory findings
| Test | Result | Reference values |
|---|---|---|
| Leukocytes | 13,400/µL | 4,200–10,400/µL |
| Lymphocytes | 1,300/µL | 300–1,500/µL |
| Haemoglobin | 14 g/dL | 11.7–15.5 g/dL |
| Platelets | 282,000/µL | 156,000–373,000/µL |
| Serum creatinine | 1.11 mg/dL | 0.44–1.2 mg/dL |
| D-dimer | 686.96 ng/ml | 0–255 ng/ml |
| Troponin I | 28.3 pg/ml initial and 40.5 pg/ml control | 0–19.8 pg/ml |
| CK-MB | 14 U/L | 9–27.3 U/L |
| Ferritin | 367 ng/ml | 11–306.8 ng/ml |
| GOT | 71 U/L | 10–42 U/L |
| GPT | 120 U/L | 10–40 U/L |
| LDH | 203 U/L | 81–234 U/L |
| CRP | 4.87 mg/dL | 0–0.748 mg/dL |
| ESR | 15 mm | 0–20 mm |
| Key: CK-MB = creatine kinase MB; CRP = C-reactive protein; ESR = erythrocyte sedimentation rate; GOT = glutamic oxalacetic transaminase; GPT = glutamic pyruvic transaminase; LDH = lactate dehydrogenase | ||
The patient was a 36-year-old man with a body mass index (BMI) of 35 kg/m2. The patient presented at the hospital with general malaise, fever, nausea and dyspnoea; vital signs included normal blood pressure, tachycardia, tachypnoea, desaturation and bi-basilar crackles. Laboratory testing showed leukocytosis with neutrophilia, mild elevation of transaminases, positive troponin I and elevated inflammatory markers (table 1). Thoracic computed tomography (CT) scan showed areas with limited extension of ground-glass opacification towards the lung apices. The patient was confirmed positive for SARS-CoV-2 by reverse transcriptase polymerase chain reaction (RT-PCR) and, therefore, an immunomodulatory management with dexamethasone dosage of 6 mg every 24 hours for 10 days was given, expecting improvement.
During his hospital stay, he presented with thoracic pain, electrocardiographic (ECG) findings of sinus tachycardia, premature ventricular complexes, left atrial abnormality and positive troponin I. Transthoracic echocardiogram revealed dilated cardiomyopathy with a left ventricular (LV) ejection fraction of 20%. Chagas serology was negative. The management of heart failure was improved with dapagliflozin, sacubitril/valsartan, spironolactone and metoprolol succinate.
The stress myocardial perfusion imaging showed a moderated ischaemia (approximately 15%) in the inferolateral and inferior wall. The coronary angiography revealed epicardial arteries without lesions.
Finally, cardiac magnetic resonance imaging (MRI) showed severe dilation of the four chambers with severe biventricular dysfunction, presence of oedema, late gadolinium enhancement (LGE), extensive fibrosis of the meso and lateral epicardium of inferolateral and inferior wall, tricuspid regurgitation and dilation of the pulmonary artery (figures 1, 2 and 3), which confirmed the diagnosis of myocarditis. After the initial consultation the patient had multiple hospitalisations, was monitored over time and treated for heart failure. Unfortunately, the patient developed decompensated heart failure and died.
Discussion
Viral myocarditis has been identified as one of the most frequent causes of dilated cardiomyopathy. Historically, it has been linked to several viral strains, with SARS-CoV-2 currently the most common global cause of myocardial dysfunction. This virus enters the cells through the angiotensin-converting 2 enzyme (ACE 2) receptor generating an inflammatory response with injury to multiple systems, including the cardiovascular system.2
Most patients are asymptomatic; however, respiratory symptomatology is the most common pathology (as described in this patient). The risk of complications is more significant in those with pre-existing cardiovascular diseases; in this patient, obesity was found as a comorbidity.3
SARS-CoV-2 infection, manifesting in acute cardiac injury, has been well documented. The mechanism of such injury may be multi-factorial, including ischaemia, toxicity of viral injury stress, inflammation, microvascular dysfunction, or atheromatous plaque rupture. It has been documented that arrhythmias, such as sustained ventricular tachycardia and ventricular fibrillation, heart failure, myocardial dysfunction, severe cases of cardiogenic shock and fulminant myocarditis; with a reduction in left ventricular systolic function (in the absence of obstructive coronary disease) produce a high rate of mortality in these patients.4-6
Echocardiographic findings are non-specific for the diagnosis of myocarditis, although they may demonstrate regional or global dysfunction and, occasionally, pericardial effusion. The standard test for the diagnosis of myocarditis is an endomyocardial biopsy, which is considered an invasive test. However, a non-invasive test that allows the diagnosis of acute myocarditis is a cardiac MRI. In this case, the patient was given a cardiac MRI which revealed significant oedema and delayed gadolinium enhancement, showing an extensive area of fibrosis, all of which is consistent with myocarditis.7,8
Conclusion
The case illustrated in this article represents an unusual case of dilated cardiomyopathy due to viral myocarditis triggered by SARS-CoV-2 with a fatal outcome. Emphasis is placed on the findings and utility of the cardiac MRI in the diagnosis of the described pathology.
Conflicts of interest
None declared.
Funding
None.
Patient consent
For the publication of this case, we have the endorsement of the ethics committee of San José Hospital Universitario de Popayán, Colombia, instead of the consent of the relatives because contact with them was not achieved after patient’s death.
Disclaimer
The data and opinions expressed in the article are those of the authors and not an official position of the institution.
References
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