Fulminant myocarditis and cardiogenic shock during SARS-CoV-2 infection

To the Editor:

Myocarditis is defined as an inflammatory disease of the myocardium, diagnosed using the Dallas criteria, which include histological, (inflammatory infiltrate associated with degeneration and necrosis), immunological and immunohistochemical parameters.¹

The incidence of myocarditis is difficult to establish since its precise diagnosis relies on endomyocardial biopsies. In general terms, myocarditis is considered to affect 22/100,000 inhabitants.¹

Regarding its aetiology, there are many factors associated with the development of this pathology and these differ according to geographical location. The viral aetiology is found to be the most frequent cause in developed countries. Other causes such as toxic agents or autoimmune diseases are also frequently responsible for this clinical entity.¹

The clinical presentation includes numerous signs and symptoms (chest pain, heart failure, ventricular arrhythmias or dyspnoea), with most being nonspecific. A flu-like process is frequently present in the preceding days or weeks in most patients.

Different complementary tests are necessary for its diagnosis. Endomyocardial biopsy is the gold standard. The recommended imaging test is a transthoracic echocardiography. Cardiac magnetic resonance imaging may be helpful in identifying the course of myocarditis.^1–3

There is no specific treatment. Hemodynamic and respiratory support treatment is recommended. The use of anti-inflammatory agents is a controversial issue and antiretroviral therapy is not recommended.

50% of cases will experience full recovery while, on the contrary, with 25% it will lead to severe dysfunction.^1,2

In December 2019, the first cases appeared of an infection caused by SARS-CoV-2, a type of coronavirus that principally causes a respiratory disease. Cardiac involvement and the development of myocarditis were not frequent.^4,5

We present the case of a previously healthy, 53-year-old man, who came to the emergency department presenting dyspnoea and 38 °C fever for the past 10 days. He had been in contact with family members infected with SARS-CoV-2. The physical examination showed tachypnoea and work of breathing (WOB). Blood pressure: 94/59, 92% SatO₂. Cardiopulmonary auscultation was normal. Blood tests showed a high-sensitivity troponin T level of 555.1 ng/L, leucocytes 7.6 × 10³/mm³ (neutrophils 82.7%, lymphocytes 6.6%). Normal chest x-ray. ECG: sinus rhythm at 133 bpm with diffuse ST-segment elevation. A transthoracic echocardiogram showed a slightly dilated LV with global moderate-severe dysfunction (LVEF 35%). No valvular disease. Normal right cavities.

He was admitted to the intensive care unit with cardiomyopathy of probable viral origin. Cardiotrope virus serologies and blood and urine cultures were obtained - which all gave negative results - and the COVID-19 nasopharyngeal smear was positive.

Treatment was started with a 5.4 µg/kg/min dobutamine infusion. Orotracheal intubation was required due to respiratory compromise. The patient presented progressive hemodynamic deterioration, with clear hypotension, so norepinephrine treatment was started, as well as de novo atrial fibrillation which was treated with amiodarone and electrical cardioversion, which were ineffective.

In the following hours, he presented greater hemodynamic instability and increased cardiac enzymes. When a new transthoracic echocardiogram was compared to the previous one, it revealed a decline with LVEF < 10%. Anuria existed despite high doses of furosemide.

Given the poor evolution, a multidisciplinary team discussed the possibility of either implanting a cardiac assist device or the evaluation of placing the patient on the heart transplant list (grade 0 emergency). Finally, the patient died a few hours later in a situation of multi-organ failure.

The clinical presentation of acute myocarditis involves a wide spectrum of symptoms, from chest pain to cardiogenic shock.^1,2

Coronavirus-19 infection is a global challenge. The mortality of patients with previous cardiovascular disease has increased as a consequence of this infection.

In this case, the patient met the criteria for suspecting fulminant myocarditis: myocardial injury with elevated cardiac enzymes and ventricular dysfunction. The lack of respiratory symptoms despite the COVID-19 infection is an eye-opener, as this is usually the guiding symptom. It is possible that myocarditis has been under-diagnosed in these patients, as the symptoms coincide with cardiovascular alterations (QT lengthening and arrhythmias) described as secondary effects of the administered treatments.⁵

Thank you

To the Intensive Medicine Department of the Lozano Blesa University Clinical Hospital in Zaragoza.