Biopsy-proven lymphocytic myocarditis following first mRNA COVID-19 vaccination in a 40-year-old male: case report

Abstract

We report a 40-year-old, previously healthy man who was admitted to our emergency unit by his family doctor because of fever (till 39 °C), headache, chest pain and shortness of breath. Six days ago, he got the first dose of the mRNA COVID-19 vaccine Comirnaty® (BioNTech/Pfizer). Two days after vaccination, he developed fever and headache and another 2 days later, he suffered from resting dyspnea and angina pectoris. Physical examination on admission revealed no pathologies. The first resting electrocardiogram (ECG 1) showed sinus rhythm with 82 beats per minute without any signs of acute ischemia (Fig. 1). Laboratory tests showed a highly increased high-sensitive Troponin T concentration of 952 ng/l (rising to 1030 ng/l after three hours; normal range < 15 ng/l), increased concentrations of creatine kinase (CK) (666 U/l, rising to 763 U/l three hours later; normal range < 190 U/l) and CK-MB isoenzyme (68 U/l; 75 U/l after three hours; normal range < 25 U/l), an increased D-dimer level (0.87 mg/l; normal range < 0.55 mg/l) and an elevated C-reactive protein (50.9 mg/l; normal range < 5 mg/l) without leukocytosis; creatinine clearance, hemoglobin concentration, eosinophilic and platelet count and liver enzymes were all normal. Blood cultures remained sterile. The SARSCoV-2 PCR of a nasopharyngeal swap was negative as well as SARS-CoV-2 antibody testing (IgG and IgA). Pulmonary embolism was ruled out by CT angiography and sinus vein thrombosis was excluded by a cranial MRI scan. Transthoracic echocardiograpy in the emergency unit showed a normally sized left ventricle (end-diastolic diameter 52 mm) with a moderately reduced ejection fraction of 45% (biplane Simpson method) without regional wall motion abnormalities. The thickness of the basal septum was slightly increased to 13 mm. Pericardial effusion could be ruled out as well as a valvular heart disease. The patient was transferred to the intermediate care unit with the working diagnosis of “non-ST segment elevation myocardial infarction (NSTEMI)” versus “myocarditis”, and therapy with acetylsalicylic acid, unfractionated heparin, an ACE inhibitor, a beta-blocker and a mineralocorticoid antagonist was started. On the next morning, chest pain worsened and ECG showed ST elevations in leads I, II, aVL, V5-V6 and ST depression in leads III and aVR (ECG 2 in Fig. 2), which prompted emergency coronary angiography using transradial access. As no coronary artery disease could be diagnosed and laevo-cardiography showed a globally reduced ejection fraction of 43% (see supplementary data file), left ventricular endomyocardial biopsy was performed to exclude a potentially life-threatening type of myocarditis. Histology and immuno-histology of the biopsies revealed acute lymphocytic myocarditis (Fig. 3). (RT-)PCRs for common cardiotropic viruses or bacteria were negative. Conservative heart failure therapy achieved complete remission of all symptoms within two days. Left ventricular ejection fraction normalized to 60% forty-eight hours after admission. On day four after admission, the patient was discharged from hospital free of symptoms. Heart failure medication was continued. He was advised to refrain from * Michael Kindermann [email protected]