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Oreoluwa Oladiran, Adeolu Oladunjoye, Olubunmi O. Oladunjoye, Anish Paudel, Ibiyemi Oke, Lisa Motz, Sarah Luber, Anthony Licata
(Cardiovascular Division, Department of Medicine, Tower Health Medical Group, Reading Hospital, West Reading, PA, USA)
Am J Case Rep 2020; 21:e927041
Cardiac amyloidosis is an infiltrative cardiomyopathy caused by the extracellular deposition of insoluble precursor protein amyloid fibrils. These depositions of protein amyloid fibrils are found on the atria and ventricles and can cause a wide array of arrhythmias; however, sustained ventricular arrhythmias are quite uncommon.
CASE REPORT: A 71-year-old man with a history of hypertension developed a sudden onset of shortness of breath, profuse diaphoresis, lightheadedness, and presyncope. Upon emergency medical services’ arrival, an initial electrocardiogram revealed wide complex tachycardia with a heart rate of 220 to 230 beats per min. He was subsequently given, in succession, magnesium, adenosine, and amiodarone with no change in heart rate or rhythm. Due to ongoing symptoms of diaphoresis and the development of dyspnea, he underwent direct current cardioversion and was converted from ventricular tachycardia to atrial fibrillation at controlled rates. A transthoracic echocardiogram and cardiac magnetic resonance imaging showed features suspicious for cardiac amyloidosis. A subsequent 99m technetium pyrophosphate single-photon emission computerized tomography scan revealed a grade 3 visual uptake and a heart-to-contralateral lung ratio of 1.92, consistent with transthyretin amyloidosis. The patient was treated with tafamidis and an implantable cardioverter-defibrillator for secondary prevention of ventricular arrhythmia.
CONCLUSIONS: This case highlights the need to consider cardiac amyloidosis in the differential diagnoses of patients with persistent ventricular arrhythmia and no prior history of heart disease.