Systemic amyloidosis is a disease caused by misfolded proteins forming amyloid fibrils, which deposit in tissues and organs, impairing their structure and function .1 When fibrillar material is deposited in the heart, it leads to cardiac amyloidosis (CA), an infiltrative cardiomyopathy typically presenting as heart failure .2 Among over 30 amyloidogenic proteins, only nine are cardiotropic, with immunoglobulin light chains (AL) and transthyretin (ATTR) accounting for 98 % of CA cases.3,4 ATTR-CA, particularly its wild-type form (ATTRwt), primarily affects men over 65 and is increasingly recognized due to advances in diagnostic techniques and an aging population .5

Non-invasive diagnosis is often guided by bone scintigraphy in patients with increased ventricular wall thickness and clinical red flags .6 However, these criteria may lack specificity, leading to unnecessary imaging. The T-Amylo model was developed to estimate pre-test probability of ATTR-CA using accessible clinical, electrocardiographic, and echocardiographic variables .7 As prediction models are developed in specific populations, they are subject to potential overfitting and may not generalize well. Therefore, external validation in independent cohorts is essential .8 This study aimed to evaluate the diagnostic performance of the T-Amylo model in an external cohort of patients with clinical suspicion of ATTR-CA in a Latinoamerican center.