Transthyretin cardiac amyloidosis (ATTR-CM) is an increasingly recognized cause of heart failure and conduction disease in older adults. Resulting from either spontaneous (wild-type) or genetic variant–associated pathogenesis, this infiltrative cardiomyopathy is caused by deposition of amyloid fibrils within the myocardium, resulting in wall thickening and ensuing cardiac dysfunction. A left ventricular (LV) wall thickness threshold ≥1.2 cm in the absence of an alternative cause (eg, hypertension, aortic stenosis) serves as the principal imaging finding to develop clinical suspicion for cardiac amyloidosis (CA) in guideline documents and expert consensus statements.1-3 Subgroup analyses from trials demonstrate increased benefit in stabilizer and silencer therapy when initiated in less severe, less symptomatic disease.3-6 Although clinical trials have enrolled patients with earlier stage disease over time, real-world data suggests that more than half of new diagnoses are in those with NAC (National Amyloidosis Center) stage II and III disease with markedly elevated N-terminal pro–B-type natriuretic peptide (NT-proBNP) and/or declining renal function.7
