Abstract
Cardiac amyloidosis is a rare disease caused by the accumulation of protein-based fibrils that deposit into the myocardium, causing disease. The accumulation of amyloid in the heart tissue causes the heart to become increasingly stiff, reducing compliance, with the eventual decline of the heart’s systolic function over time as the disease progresses. The restrictive physiology of the disease usually prompts investigation; however, if allowed to progress, the systolic function becomes affected in the later stages of the disease. We present a case of late-stage transthyretin-related amyloidosis (ATTR).