Tozinameran

Author Information

An event is serious (based on the ICH definition) when the patient outcome is:

• * death

• * life-threatening

• * hospitalisation

• * disability

• * congenital anomaly

• * other medically important event

A 50-year-old man developed fulminant myocarditis following immunisation with tozinameran against COVID-19.

The man presented with syncope and resting chest pain 10 days after receiving the second dose of tozinameran [COVID-19 mRNA BNT162b2; route and dosage not stated] vaccine and was admitted to the hospital. He was referred to another hospital due to hypotension and worsening chest pain. The RT-PCR assay was negative for SARS-CoV-2, while antibodies against SARS-CoV-2 were present. Electrocardiography showed sinus tachycardia and ST-segment elevation in leads V1−V4 with complete right bundle branch block. Laboratory blood tests revealed elevated levels of cardiac troponin-I and creatine kinase-MB. The brain natriuretic peptide level was 248 pg/mL. Chest radiography and chest CT showed mild pulmonary oedema but no pneumonia lesions. Echocardiography showed a left ventricular ejection fraction (LVEF) of 35% with diffuse hypokinesis. Cardiac MRI late gadolinium enhancement imaging revealed linear mid-myocardial enhancement of the septum walls at the base of the mid-left ventricle, and T2-weighted short-axis inversion recovery imaging showed a high intensity of the global walls of the left ventricle. Coronary angiography showed no obstructive coronary artery disease. An endomyocardial biopsy specimen showed multifocal cardiomyocyte damage with severe inflammation of lymphocytes and macrophages. The diagnosis of fulminant myocarditis attributed to tozinameran was confirmed by histopathological examination. He developed cardiogenic shock and was transferred to the ICU.

The man was treated with methylprednisolone pulse therapy and required unspecified inotropes, even after pulse steroid therapy. On day 6 of admission, an advanced atrioventricular block was observed, and a temporary transvenous pacemaker was placed. After the first pulse methylprednisolone therapy, the cardiac troponin-I level rapidly increased. Subsequently, a second methylprednisolone pulse therapy was administered, following a daily dose of of prednisolone, which was gradually reduced. On day 8, he did not require unspecified inotropes as blood pressure had improved. On day 9, the temporary transvenous pacemaker was removed and on day 18, prednisolone treatment course was completed, and no atrioventricular block was detected. He then received guideline-directed medical therapy for heart failure including bisoprolol, spironolactone and sacubitril/valsartan. On day 21, his cardiac troponin-I level decreased to the normal range and echocardiography showed a recovered LVEF of 60% with no regional wall motion abnormalities. He was discharged 22 days after admission. At the 2 week follow-up, he presented with syncope and exacerbation of congestive heart failure. Electrocardiography revealed atrioventricular dissociation and an echocardiogram showed an LVEF of 60% with no regional wall motion abnormalities. The cardiac troponin-I level slightly increased. He was hospitalised because of heart failure, and unspecified diuretics were administered. Eventually, he was discharged one week later.