Abstract
Amyloidosis is a rare disease with an incidence of only 16.6 per 100,000 patients per year. A high grade of clinical suspicion is required to suspect an atypical cause of left ventricular hypertrophy or new-onset heart failure. A transthoracic echocardiogram (TTE) is the initial evaluation that may yield clues pointing towards an etiology of cardiac amyloidosis. Due to the subjective nature of TTE interpretations, suspicion for cardiac amyloidosis may be missed. Once suspicion arises, additional tests, such as serum and urine electrophoresis and technetium-99m pyrophosphate myocardial perfusion imaging, can further aid in establishing a diagnosis. The pathophysiology in transthyretin amyloidosis (ATTR) involves the misfolding of the transthyretin/prealbumin protein, which leads to an inherent propensity to aggregate. These proteins can accumulate in the extracellular space between cardiac myocytes, which may thicken sections of the heart, leading to ventricular restriction. Here, we explore the case of an 83-year-old man with chronic, treatment-resistant heart failure with preserved ejection fraction, New York Heart Association class III, who presented with multiple ruptured bullae in the bilateral lower extremity, leading to a new diagnosis of ATTR cardiac amyloidosis.