Over the last decade, transthyretin amyloid cardiomyopathy (ATTR-CM) has shifted toward earlier recognition and routine use of disease-modifying therapy, heightening the need for biomarkers that are inexpensive, reproducible, and clinically actionable [1]. TTR has long been used as a nutrition/inflammation marker, and has re-emerged in this setting because its circulating concentration plausibly integrates systemic biology and amyloidogenesis [2]. TTR circulates as a tetramer that transports thyroxine and, via retinol-binding protein, vitamin A; its concentrations typically range between 20 and 40 mg/dL and decrease with inflammation and malnutrition [2].
