Acute myocarditis associated with Covid-19 vaccination

A 26-year-old man with no remarkable past medical history presented to the Emergency Department with a 24-hour history of left parasternal chest pain. No fever, cough or dyspnea. EKG was normal but blood work showed elevated troponin and C-reactive protein values. Echocardiography was performed and showed hypokinetic movement of the lateral wall. He was then referred for cardiac magnetic resonance (CMR) imaging. The patient had received immunization for COVID (Moderna) 3 weeks prior to the event.

CMR showed normal biventricular volumes with preserved systolic function. Normal left ventricular mass and wall thickness with mild hypokinesia of mid anterior segment.

T2-mapping showed increased T2 relaxation time in keeping with myocardial oedema affecting basal and mid anterior segments. There was no evidence of hypoperfusion.

Estimated extracellular volume was 30%.

On viability series there was late gadolinium subepicardial enhancement in basal inferoseptal, anterolateral and inferolateral segments, as well as midwall enhancement in mid inferior segment.

There was no evidence of pericardial effusion.

These findings are consistent with acute myocarditis. Most common causes of myocarditis were clinically excluded: there was no evidence of systemic infection and the patient had no history of immunological disorder or recent drug use.

Functional parameters of the left ventricle (body mass-indexed values in parenthesis):

- End-diastolic volume (EDV) 149 ml (78 ml/m²). Normal values (NV) for male patients aged 20-29: 126-208 ml

- End-systolic volume (ESV) 57 ml (30 ml/m²). NV: 35-80 ml

- Systolic volume (SV) 92 ml (48 ml/m²). NV: 81-137 ml

- Ejection fraction (EF) 62%. NV: 57-74%

- Cardiac output 6.5 l/min (3.3 l/(min*m²)). NV: 4-8 l/min

- Myocardial mass 93 g. NV: 109-186 g

Functional parameters of the right ventricle:

- EDV 116 ml (61 ml/m²). NV: 127-227 ml

- ESV 36 ml (19 ml/m²). NV: 38-98 ml

- SV 80 ml (42 ml/m²). NV: 74-143 ml

- EF 60%. NV: 48-74%

Myocarditis is defined as the nonischemic inflammation of the myocardium.

Many triggers have been described in its pathogenesis, although most cases in developed countries are attributable to viral infection.

Symptoms are nonspecific and can mimic myocardial infarction [1],  typically affecting young male patients, and it has been estimated that it may be responsible for 20% of deaths in adults younger than 40 years of age [2].

Although rare, immunization can also cause myocarditis and there is recent evidence that COVID-19 vaccination can increase the risk, particularly after the second booster of mRNA vaccines by cross-reaction mechanism [3], [4], [5].

Myocarditis is often clinically suspected by exclusion of other entities, and endomyocardial biopsy is only recommended in selected number of cases [6], [7].

Evaluation and management of these patients vary depending on clinical factors although most patients can be managed medically [8].

CMR has become the imaging modality of choice in patients with suspected acute nonischemic cardiomyopathy [9].

MR findings are commonly assessed using the Lake Louise criteria (LLC) [10]. To make the diagnosis, high clinical pretest probability is required, as well as a T2-based marker of myocardial oedema and a T1-based marker of myocardial damage [11].

Findings include:

• Oedema: high T2 signal intensity of the myocardium or increase in T2 relaxation time. It can be assessed visually or quantitatively by comparison with normal myocardium or skeletal muscle. In the absence of LGE, oedema reflects reversible injury [12].
• Hyperemia:  increased regional volume of distribution as compared to normal muscle tissue [9], [13]. Studies have demonstrated that omitting this step may decrease sensitivity [14].

• Scarring and/or necrosis: late gadolinium enhancement (LGE) in a nonischemic pattern. Presence of scarring or necrosis can also be demonstrated by increase of myocardial native T1 or extracellular volume values. In COVID-19 vaccination-induced myocarditis, enhancement may have a predilection for the basal to mid-lateral wall, with infrequent septal involvement [15].

• Regional wall motion abnormalities and/or ventricular dysfunction: nonspecific and not commonly present. Associated with a more severe form of the disease.
• Pericardial inflammation: pericardial enhacement or effusion.

In this case, there is evidence of myocardial oedema (T2-based marker) and of myocardial damage in the form of late gadolinium enhancement (T1-based marker).

Most recent studies show that myocardial inflammation secondary to COVID-19 vaccination may have milder MR abnormalities as compared to other causes of myocarditis [15].

CMR in myocarditis can provide valuable prognostic data and guide the decision-making process in terms of therapeutic options. Furthermore, in around 11% of cases, it provides an alternative diagnosis [16].

Take-Home Message / Teaching Points

There is evidence that COVID-19 vaccination can induce acute myocardial inflammation, especially after the second booster of mRNA vaccines and most commonly in young males.

CMR is the diagnostic modality of choice for its assessment due to its capability to noninvasively detect and quantify myocardial alterations like oedema, hyperemia, scarring or necrosis as well as wall motion abnormalities or ventricular dysfunction in more severe cases.

Written informed patient consent for publication has been obtained.