Post-COVID myocarditis simulating acute coronary syndrome: Case report

Abstract

Acute myocarditis corresponds to an acute inflammation of the myocardium whose origin is most often viral. Several viruses can be incriminated to note the parvovirus B19, the virus herpes of the group 6 and to a lesser degree the virus of the hepatitis C (VHC). Since 2019 and with the discovery of SARS COV2 some cases of myocarditis associated with COVID have been noted, this last association is rare and is present in only 5% of cases. The diagnosis of myocarditis is sometimes difficult and can lead to confusion with acute coronary syndrome, especially in cases of ST-segment elevation on the EKG, hence the interest of magnetic resonance imaging, which has made it possible in recent years to reduce the rate of unnecessary coronary angiography, especially in the case of young subjects with no cardiovascular risk factors. Here, we report the case of a 33-year-old patient with no cardiovascular risk factors and no medical or surgical antecedents who was admitted to the emergency department for the management of acute chest pain, the patient had initially undergone an electrocardiogram which showed an ST-segment elevation in the inferior territory and in the low lateral territory with a mirror image in the high lateral territory. In view of the typical character of the pain and based on the electrical data, it was decided to carry out a coronary angiography which came back without any particularity. As part of the etiological work-up, an MRI scan was performed, which showed an appearance compatible with viral myocarditis. This case shows diagnostic difficulties and management of this disease.

Introduction

Viruses are known as the most prevalent cause of myocarditis [1], and during previous viral outbreaks, which to date were mostly due to influenza A and B cases, autopsy series reported myocarditis prevalence ranging from 22% to 34% [2,3]. COVID-19 disease caused by severe acute respiratory coronavirus-2 (SARS-CoV-2) affects primarily the respiratory system and it is usually manifested by respiratory symptoms, but also affects other systems such as the cardiovascular system, which may be the first warning signs of Sars-CoV-2 infection [4].it is necessary to know that Multiple manifestations of cardiac pathology have been documented in autopsy studies of patients with fatal COVID-19, including microvascular thrombi, ischemic injury, right ventricular strain injury, pericarditis, myocardial inflammatory cellular infiltrates, and full myocarditis with myocyte destruction [5]. The association between myocarditis and COVID is rare and acute coronary syndrome is the main differential diagnosis, especially in case of elevation of the St-segment on the EKG.

In this paper, we will represent a case of a 33-year-old patient admitted to the emergency room for the management of acute chest pain the explorations revealed acute myocarditis with SARS-CoV-2 infection.

Our case report was written according to CARE guideline [6].

Case presentation

A 33-year-old patient was admitted to the emergency department of our hospital for the management of acute infarcted resting chest pain from the day before his admission. The interrogation found a patient with no cardiovascular risk factor, but he reported a flu syndrome associated with a fever in the week preceding the chest pain, treated with antipyretics. It should be noted that the patient had never been operated on. Moreover, there was no similar case in the patient's family. On examination, the patient was conscious, of normal weight and height with a BMI of 22 kg/m². His heart rate on admission was 60 beats/min, hemodynamically stable with a heart pressure that was 120/70 symmetrical to both limbs. He was eupneic with a respiratory rate of 16 breaths/min and an O₂ saturation of 90% on room air. There was no sign of right or left heart failure, the complementary physical examination was normal. The electrocardiogram showed a regular sinus rhythm with a CVM of 53 beats per minute, a constant PR of 160 ms and a fine QRS of 84 ms, a ST-segment shift of 1.5 mm in inferior and apical-lower lateral and of 1 mm in basal with ST-segment shift in lateral-high (Figs. 1 and 2). The differential diagnoses included all the etiologies of acute chest pain: acute coronary syndrome, pulmonary embolism, aortic dissection, pneumothorax, acute pericarditis.

Fig. 1.

Resting EKG showing 1.5 mm ST-segment elevation in apico-lateral low and inferior with ST-segment depression in lateral low.

Fig. 2.

Resting EKG right leads showing a 1 mm ST-segment elevation in basal.

The chest X-ray showed an appearance suggestive of COVID-19 lung damage, in view of the epidemiological context, a thoracic CT scan was carried out, which showed that the COVID-19 affected 40%-50% of the lungs (Figs. 3 and 4). The transthoracic echocardiography (TTE) showed a non-dilated LV with non-hypertrophied walls and a good radial LVEF of 61% (SBP); it should be noted that the global longitudinal strain was also normal at -18.6%. The biological assessment showed a very high ultra-sensitive troponin 21,888 ng/L (1200 times higher than normal); hyper leukocytosis at 12,000/Ul, C-reactive protein at 80 mg/L (normal between 0.00 and 5.00 mg/L), lipasemia at 60 IU/L (normal 8.00-78.00) IU/L, his renal function was correct.

Fig. 3.

Chest CT axial section showing 40%-50% COVID-19 lung involvement.

Fig. 4.

Chest CT sagittal section showing 40%-50% COVID-19 lung involvement.

It was decided to perform an emergency coronary angiography on the basis of the clinical, electrical and biological data that came back without any particularity (Figs. 5 and 6). A cardiac MRI was subsequently performed given the clinical history of the patient and the epidemiological context which had objectified an aspect compatible with acute myocarditis (Figs. 7 and 8).

Fig. 5.

Coronary angiography performed via the femoral route showing normal left coronary arteries.

Fig. 6.

Coronary angiography performed via the femoral route showing normal right coronary arteries.

Fig. 7.

Four-cavity cardiac MRI image showing late subepicardial enhancement at the lateral wall of the LV.

Fig. 8.

Short-axis cardiac MRI image showing late subepicardial enhancement at the lateral wall of the LV.

The patient was admitted to the cardiology intensive care unit where he was conditioned and scoped, the diagnosis the diagnosis of acute myocarditis was made on the basis of clinical, biological, and MRI evidence.

The patient was put on SARS-CoV-2 infection treatment: vitamin c, zinc, azythromicin, dexamethasone and preventive anticoagulation enoxaparin and paracetamol.

It should be noted that the patient remained stable throughout his hospitalization and his chest pain responded well to analgesics and disappeared on the second day of hospitalization, with a decrease of troponin numbers. He stayed 10 days in intensive care of cardiology, then transferred to clinical cardiology, thereafter he was declared discharged with an appointment of control in 1 month.

Discussion

The etiology of myocarditis often remains undetermined, a large variety of infectious agents, systemic diseases, drugs, and toxins can cause the disease. Diagnosis may be supported by an electrocardiogram, increased troponin and occasionally an endomyocardial biopsy. Cardiovascular magnetic resonance (CMR) has become the primary tool for non-invasive assessment of myocardial inflammation in patients with suspected myocarditis [7]. The COVID-19 has been found to cause the onset of new myocardial injury (defined as marked troponin elevation), cardiac dysfunction, myocarditis and death due to heart failure (HF) [8]. It remains unclear if the heart is being affected primarily by the virus or as a result of a secondary critical illness, it was demonstrated that high levels of troponin are associated with higher mortality rates of up to 50% [[9], [10], [11]]. It is essential to rule out other possible causes of the presentation, specifically acute coronary syndrome and other cardiovascular or extra-cardiac non-inflammatory diseases that could explain the clinical presentation [12]. Myocarditis mimicking ST-elevation myocardial infarction is rare, with an estimated clinical diagnostic incidence of 0.17 per 1000 man-years [13]. Nakashima et al. stated that myocarditis with pericardial involvement might contribute to ST elevations on ECG [14]. Furthermore, cell membrane leakage, accumulation of bioproducts, and a decrease in the inflamed myocardial tissue's oxygenation may further contribute to ST-segment changes [14,15].

Clinically suspected myocarditis is defined in presence of ≥1 clinical presentation and ≥1 diagnostic criteria from different categories in the absence of angiographically detectable coronary artery disease (coronary stenosis, ≥50%) and known preexisting cardiovascular dis-ease or extracardiac causes which could explain the syndrome (eg, valve disease, congenital heart disease, hyperthyroidism) [7]. Suspicion is higher with higher number of fulfilled criteria; if the patient is asymptomatic, ≥2 diagnostic criteria should be met [16].

Clinical presentation could include [16]:

• •Acute chest pain
• •New-onset dyspnea (days up to 3 months)
• •Subacute/chronic dyspnea [> 3 months]
• •Palpitations and/or unexplained arrhythmia symptoms
• •Unexplained cardiogenic shock.

Diagnostic criteria are defined as follow [16]:

• •ECG features of cardiac damage
• •Elevated markers of myocardial necrosis
• •Functional and/or structural abnormalities on cardiac imaging (echocardiogram or angiogram or CMR)
• •Tissue characterization by CMRI (edema and/or LGE of classical myocarditic pattern)

It should be noted that the treatment of acute viral myocarditis differs according to the severity and initial presentation of the patient, for example, in fulminant forms, the initial management is that of cardiogenic shock and is based on hospitalization in an intensive care unit, continuous monitoring of cardiac rhythm and invasive blood pressure, careful correction of possible hypovolemia, and the use of inotropic and vasopressor therapies, mainly dobutamine and noradrenaline. In acute and chronic forms, treatment is by analogy identical to the treatment of chronic heart failure. In the absence of signs of low output, treatment combines diuretics in case of pulmonary edema or signs of overload, converting enzyme inhibitors, beta blockers, and antialdosterone. However, no studies have specifically looked at myocarditis [17]. In recent years and with the appearance of COVID-19, the diagnosis of acute coronary syndrome based only on EKG has become difficult especially in cases where COVID-19 is complicated by acute myocarditis which leads to ST-segment elevation with sometimes a typical chest pain, in this context we decided to write this paper to know better how to manage this association which remains until now little described in the literature in terms of additional examinations, and therapeutic management.

In our case, the patient in question was 33 years old and had no pre-existing conditions or notable medical history. He was admitted for treatment of acute chest pain associated with an elevated ST-segment on EKG caused by acute myocarditis diagnosed by cardiac MRI. After being treated in the cardiology intensive care unit, he was discharged on under the therapeutic protocol of COVID-19 associated with an analgesic treatment and scheduled for a follow-up appointment in 1 month.

Conclusion

• -The COVID-19 represents a new entity that unfortunately we have not yet managed to treat and control well.
• -The pulmonary attack represents the principal attack of the COVID but it can also touch several vital organs among which the heart whose prognosis can go from the simple attack to the fulminant myocarditis with a high risk of death.
• -Acute post-COVID myocarditis requires a multidisciplinary approach to reduce the death rate.

Learning objectives

• 1)To get an idea of the clinical presentation and the electrical and imaging aspects of this rare entity.
• 2)To suggest the diagnosis of post-COVID myocarditis especially in young patients without cardiovascular risk factors and with a symptomatology consistent with COVID-19.
• 3)To reduce the rate of unnecessary invasive explorations.

Ethical approval

The ethical committee approval was not required give the article type (case report). However, the written consent to publish the clinical data of the patients was given and is available to check by the handling editor if needed.

Author contributions

Zakaria El Marraki: Study concept, Data collection, Data analysis, Writing the paper. Adam Bouzhir: Data collection, Data analysis. Jaouad Nguadi: Data collection. Abderrahmane Bouchaala: Data collection. Najat Mouine: Supervision and data validation. Atif Benyass: Supervision and data validation.

Rail registry number

This is not an original research project involving human participants in an interventional or an observational study but a case report. This registration is was not required.

Guarantor

Zakaria El Marraki.

Rovenance and peer review

Not commissioned, externally peer-reviewed.

Patient consent

Written informed consent was obtained from the patient for publication of this case report. CARE guidelines were applied for reporting this case report’ finding.