Abstract

Background/Aims Constrictive pericarditis occurs most commonly after idiopathic pericarditis (in less than 1%) in the developed world. Other uncommon aetiologies include tuberculosis, rheumatological diseases and post-viral pericarditis. Methods We present a case of an 80-year-old Caucasian man admitted with shortness of breath (NYHA III), skin rash, loss of weight and peripheral oedema. He had no other features of connective tissue disease (CTD) or vasculitis. His past medical history included atrial fibrillation, gout, hiatus hernia and he was on rivaroxaban, ramipril, digoxin, allopurinol, bumetanide, ranitidine and finasteride. Investigations showed NT pro BNP at 6473 ng/L, CRP at 78 mg/ dL and lymphopenia (0.42 10*9/L). He has persistent hyponatraemia at 117 mmol/L with normal kidney function. His liver function test showed alkaline phosphatase of 239 U/L and globulin at 41 g/L. His COVID-19 swab test was positive whereas mycobacterial culture and hepatitis screen were both negative. He had weakly positive ANA at 0.7 but otherwise normal autoimmune profile. The level of immunoglobulin G was 25 g/L and paraprotein of 2 g/L. His electrophoresis showed a monoclonal IgG; Kappa/Lambda ratio was 2.03. CT chest and cardiac MRI: shows constrictive pericarditis, pericardial effusion and thickening, moderate pleural effusion and ground-glass changes scattered throughout the right lung which suggested probably inflammatory origin. Thoracoscopic surgery (RVATS) was done for drainage of pleural effusion, excision of fat pad and anterior partial pericardectomy. The pericardial biopsy concluded chronic fibrous pericarditis with focal submesothelial mononuclear cell infiltrate with numerous plasma cells and lymphocytes .There was no amyloid or immunoglobulin deposition or malignancy. After the operation, there was both clinical and biochemical improvement (CRP- 28 mg/ dL). He did not need any immunomodulatory therapy. Results Cardiac involvement is rapidly emerging in COVID -19 diseases with case reports of myopericarditis, atrial fibrillation, heart failure, Kawasaki disease, thromboembolism, cardiogenic shock and aortitis. The mechanism remains unexplained but it could be related to direct endothelial inflammation or the cytokine storm sequelae. In our case, pericardial biopsy concluded features suggestive of autoimmune or immunoglobulin associated disease, although there was no clinical evidence of autoimmune disease. There were no lytic lesions and MGUS was diagnosed and scheduled for six monthly monitoring. Conclusion We report a case of constrictive pericarditis with COVID-19, although this remained a differential among the co-existed immunoglobulin and autoimmune syndrome. Appropriate imaging, biomarkers and histology investigations need to be considered for rapid evaluation and escalation of treatment. Cardiac manifestations are an important feature of COVID- 19. Further research is required to guide the management plans for similar cases. Disclosure Z. Alkutobi: None. G. Ansari: None. A. Nandagudi: None.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call