TOPIC: Cardiovascular Disease TYPE: Medical Student/Resident Case Reports INTRODUCTION: Amyloidosis is characterized by the deposition of insoluble abnormal protein in the extracellular space that results in the organ's abnormal functioning. The incidence of cardiac amyloidosis is 55 /100,000 person-years while prevalence is 17/100,000 person–years. (1) It can manifest with heart failure, (HF) conduction abnormalities, or pericardial effusion. (2) Early diagnosis is imperative as it is a life-threatening disease. We report a case of a patient who presented with heart failure. CASE PRESENTATION: A 73-year-old man with a history significant for hypertension, atrial fibrillation, and chronic kidney disease stage 4, presented with complaints of worsening shortness of breath. Physical exam was notable for elevated jugular venous pulse and hypotension. Lab workup was unremarkable except for elevated BNP (910 pg/ml). He underwent right and left heart catheterization that was remarkable for low cardiac output and increased filling pressure in the right and left heart, without any coronary artery obstruction. Nuclear technetium pyrophosphate scan showed diffuse uptake in the left ventricle suggestive of transthyretin cardiac amyloidosis. (Fig 1) He was treated with IV diuretics and milrinone for blood pressure support. He was deemed not a suitable candidate for a heart transplant given multiple comorbidities. His kidney function deteriorated and with intractable HF, he died of cardiac arrest after his discharge. DISCUSSION: Cardiac amyloidosis can be diagnosed with the help of different imaging modalities including EKG, echocardiography, cardiac MRI, and radionuclide bone scintigraphy. Cardiac MRI and radionuclide bone scintigraphy are the imaging of choice in diagnosing amyloidosis given the two modalities' sensitivity and specificity. (3). The therapy for transthyretin amyloidosis with cardiac involvement is aimed at treating congestive heart failure and preventing the progression of amyloid deposits. Heart failure associated with cardiac amyloidosis is treated by fluid, and salt restriction, and diuretics. Beta-blockers and ACE inhibitors should be avoided as they exacerbate the symptoms of cardiac amyloidosis. Unfortunately, for many with end-organ damage treatment is limited. The definitive treatment of transthyretin cardiac amyloidosis is heart transplantation. (4) CONCLUSIONS: Clinicians should keep the diagnosis of cardiac amyloidosis in their minds while treating newly diagnosed heart failure in people who do not have coronary artery disease. REFERENCE #1: 1)Gilstrap LG, Dominici F, Wang Y, et al. Epidemiology of Cardiac Amyloidosis-Associated Heart Failure Hospitalizations Among Fee-for-Service Medicare Beneficiaries in the United States. Circ Heart Fail. 2019;12(6): e005407. doi:10.1161/CIRCHEARTFAILURE.118.005407 REFERENCE #2: 2)Castaño A, Narotsky DL, Hamid N, et al. Unveiling transthyretin cardiac amyloidosis and its predictors among elderly patients with severe aortic stenosis undergoing transcatheter aortic valve replacement. Eur Heart J. 2017;38(38):2879-2887. doi:10.1093/eurheartj/ehx350 REFERENCE #3: 3) Fontana M, Martinez-Naharro A, Hawkins PN. Staging Cardiac Amyloidosis With CMR: Understanding the Different Phenotypes. JACC Cardiovasc Imaging. 2016;9(11):1278-1279. DOI: 10.1016/j.jcmg.2016.02.035. 4) Yamamoto H, Yokkaichi T. Transthyretin cardiac amyloidosis: an update on diagnosis and treatment. ESC Heart Fail. 2019;6(6):1128-1139. doi:10.1002/ehf2.12518 DISCLOSURES: No relevant relationships by Junaid mir, source=Web Response No relevant relationships by Sharon Scott, source=Admin input