Paucisymptomatic post COVID-19 myocarditis in a young athlete during return to play workflow: possible usefulness of global longitudinal strain analysis

Background

COVID-19 infection is phenotypically expressed mainly with respiratory symptoms, but it is known that it also has a tropism for different organs and systems such as cardiac muscular tissue.1 2 Several observational studies documented the presence of subclinical inflammatory status even in asymptomatic or paucisymptomatic patients, accurately detectable with the use of cardiac MRI, where standard echocardiographic analysis often does not demonstrate significant anomalies.3

In the recent pandemic period, myocarditis in the young athlete showed a certain benignity. However, although rare, myocarditis is a cause of death in young athletes to whom a more detailed diagnostic process is adopted before returning to competitive practice.4

The MRI is not often quickly available to evaluate a post-COVID athlete for a safe return to competitive activity, nor can it be considered a large-scale screening method.

Echocardiographic analysis in COVID-19-hospitalised patients showed that the left ventricular global longitudinal strain (GLS) is significantly reduced5 as well as in post-COVID paucisymptomatic patients regardless of clinical presentation.6

A competitive cyclist underwent the diagnostic investigations protocol before returning to competitive practice (return to play protocol) after COVID-19 infection.

Despite the paucisymptomatic presentation of COVID-19 infection and the absence of relevant anomalies in standard first-level diagnostic investigations, echocardiographic examination findings especially speckle tracking analysis along with some modest clinical aspects suggested further second-level investigations eventually allowing the identification of myocardial damage.

Case presentation

A competitive cyclist in his 30s came to our attention after having contracted COVID-19 infection in May 2022. The course of the infection had been characterised by 48 hours of hyperpyrexia and 5 days of persistent coughing. COVID-19 test became negative on the 21st day.

The patient accessed our diagnostic centre to undergo the investigations required by the ‘return to play’ protocol before returning to competitive sports (figure 1).

Despite having tried to remain active during the entire isolation period, the patient still reported fatigue and dyspnoea on moderate efforts.

The physical examination was unremarkable. Blood pressure was 120/75 mm Hg and heart rate was 91 beats per minute.

ECG and spirometry examination did not show significant abnormalities.

Negative inflammation (high-sensitivity C reactive protein) and myocardial damage markers (high-sensitivity troponin) were observed.

The cycloergometer test was conducted up to stage 4 of Bruce protocol and showed no signs of myocardial distress, no induced relevant arrhythmias, rapid chronotropic increase, normal pressure increase and dyspnoea at 100 W workload. 24-hour Holter-ECG was performed showing 630 isolated premature ventricular complexes (PVC) with two prevalent morphologies and often early, not described in previous Holter-ECGs (figure 2).

Echocardiographic examination showed preserved left ventricular systolic function (LVEF) in the absence of segmental dyssynergies, normal pericardium and right sections’ findings (LVEF Simpson method 62% - E' 12 - E/E' 10 - TAPSE 23) and a reduced global longitudinal strain (GLS: −16.1%; figure 3).

Considering the referred symptoms and easy straining, although common symptoms in the post-COVID period, we performed a cardiopulmonary exercise test (CPET) that showed an early anaerobic threshold and a normal peak PVO₂ (21 mL/kg/min) not in line with the presumed range for a top-level athlete.

Considering the symptoms described, the CPET data, the evidence of early PVC and GLS reduction, despite the negative first-level investigations, the patient underwent MRI, which documented a myocardial oedema in the mid-basal region of inferior and posterior walls of the left ventricle (figures 4 and 5).

Treatment

Suitability for competitive practice was suspended, intense isometric efforts were not recommended, a gradual physical readaptation path was started, and therapy with low-dose bisoprolol was set. These precautionary measures were adopted despite it being known that the absence of inflammatory septal involvement generally implies a more benign prognosis.7

Outcome and Follow-up

The patient returned to our attention 6 months later. Gradual clinical improvement was reported during follow-up. The echocardiographic examination by speckle tracking analysis showed a GLS normalisation (GLS −23% - LVEF 64% - E' 15 - EE/E' 8; (figure 6).

The ergometric test with cardiopulmonary analysis showed a realignment of the HR/VCO₂ curve with a late threshold and increment of peak PVO₂ (39 mL/kg/min).

The 6-month control MRI examination showed almost no signs of myocardial inflammation and, for this reason, the patient was declared suitable for returning to competitive sport (figures 7 and 8).