Is there a risk of fatal Fulminant Necrotizing Eosinophilic Myocarditis Following Pfizer mRNA technology based COVID Vaccine? Yes! Ameratunga reported this; is this idiosyncratic? or a real concern?
by Paul Alexander
The clinical and pathological observations from a case of fatal fulminant necrotising myocarditis in a 57-year-old woman, following the first dose of the Pfizer-BioNTech vaccine, are described.
A previously well 57-year-old woman received the first Pfizer-BioNTech vaccine in July 2021. The following day she experienced increasing lethargy and had to leave work early because of worsening fatigue. She had one episode of breathlessness and complained of a stiff neck as well as upper limb pain. She had a sore throat but pointed to her sternum. During the remainder of the day, she became increasingly unwell. The following day she consulted her primary care physician with a sore throat, back pain, fatigue and an episode of haematuria, which had occurred the previous night. She had difficulty getting out of the car and experienced a fall at the family physician’s surgery. She did not complain of palpitations.
On day 2, a complete blood count (CBC) was normal but she was noted to have an increased C-reactive protein (CRP) (Table 1). She had a raised ferritin and alanine transaminase (ALT) but the aspartate aminotransferase (AST) was not undertaken, although the other liver enzymes were normal. There was no eosinophilia. On the third day, she was diagnosed with an Escherichia coli urinary tract infection, which was treated with trimethoprim. During that night, she was found deceased in bed. Apart from long-term omeprazole and the recently commenced trimethoprim, she was on no other treatment. There was no history of autoimmunity or allergic disease.
The body was that of a small-built adult female of Chinese descent, consistent with the stated age of 57 years (height 155 cm; weight 40 kg). External examination was unremarkable. On internal examination, the most striking finding was a tan, solid lobulated mass originating from the mediastinum and situated in the left pleural cavity (Fig. 1, top left and top right). This mass was 130 × 120 × 90 mm and weighed 710 g. Mild splenomegaly (240 g) was noted. There was no pericardial effusion and there was no intracardiac thrombosis. The remainder of the autopsy examination was unremarkable. There were no abnormalities of other organs.
Histology and Ancillary Tests
Histological examination of the heart sections showed fulminant necrotizing eosinophilic myocarditis (Fig. 1, bottom left and bottom right). There were multifocal aggregates of lymphoid cells, histiocytes and abundant eosinophils with focal myocyte necrosis in the free walls of both ventricles, inter-ventricular septum and around the conduction system (sino-atrial and atrio-ventricular nodes). No parasitic organisms or giant cells were identified. The eosinophilic infiltrate would make autoimmune myocarditis less likely. There was no evidence of eosinophils in other organs or eosinophilic vasculitis. Histological examination of the left pleural space mass showed a thymoma, WHO subtype AB.
There was a limited amount of post mortem serum for diagnostic studies. Antibodies to SARS-CoV-2 were negative on histological paraffin blocks and she had a mild reduction in IgG 4.54 (7–14 g/L), IgA 0.72 (0.8–4.0 g/L) and IgM 0.26 (0.4–2.5 g/L) levels, post mortem. T cell receptor excision circle numbers from peripheral blood DNA were normal, as was a tryptase level. She had a borderline parvovirus PCR test from the myocardium, below quantifiable levels. Other viral PCR tests including enterovirus, metapneumovirus, parainfluenza (1–4), rhinovirus, adenovirus, respiratory syncytial virus, SARS-CoV-2, parechovirus and influenza A and B were negative. A toxicology screen was negative. Complement studies and cytokine studies were not undertaken as there was no ante-mortem blood available.’