Premature diagnostic closure after pericarditis treatment delays recognition of ATTR cardiomyopathy: a multimodality case report.

BACKGROUND

Cardiac amyloidosis can present with troponin-positive chest pain and non-obstructive coronary arteries, mimicking acute coronary syndrome. When a concurrent treatable diagnosis, such as pericarditis, is identified, symptomatic improvement may lead to premature diagnostic closure and failure to pursue confirmatory testing for an underlying infiltrative cardiomyopathy.

CASE SUMMARY: A man in his 70s presented with pleuritic chest pain and troponin-T of 1840 ng/L. Coronary angiography was normal. Echocardiography revealed left ventricular hypertrophy with apical sparing on longitudinal strain. Cardiac magnetic resonance showed diffuse subendocardial late gadolinium enhancement and elevated extracellular volume (48%). Positron emission tomography (18F-FDG-PET) confirmed active pericarditis but no myocardial inflammation. Endomyocardial biopsy confirmed amyloid deposits; 99mTechnetium pyrophosphate scintigraphy confirmed transthyretin amyloid (ATTR) cardiomyopathy. He was treated for myopericarditis and referred for ATTR therapy.

DISCUSSION: This case highlights how symptomatic resolution after treatment of acute pericarditis can obscure a co-existing infiltrative cardiomyopathy, and why persistent imaging red flags, including apical sparing on strain, diffuse subendocardial late gadolinium enhancement, and markedly elevated extracellular volume, should prompt definitive testing regardless of clinical improvement.