International journal of cardiology · 2026
Addition of high-sensitivity troponin to the T-Amylo score for the diagnosis of transthyretin cardiac amyloidosis in acute heart failure: TnT-Amylo.
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Burgos Lucrecia María, Spaccavento Ana, Baro Vila Rocio Consuelo, De Bortoli María Antonella, Malano Damian Jesus, Nachman Tomas, Meretta Alejandro Horacio, Seia Ivana, Elissamburu Pablo, Diez Mirta, Costabel Juan Pablo
Аннотация
BACKGROUND: Identifying specific aetiologies during hospitalization for acute heart failure (AHF) remains challenging, particularly conditions with important therapeutic and prognostic implications such as transthyretin cardiac amyloidosis (ATTR-CM). Clinical risk scores may aid early suspicion; however, many patients are classified as intermediate risk, limiting bedside decision-making in the acute care setting. High-sensitivity cardiac troponin T (hs-TnT) may improve diagnostic stratification.
METHODS: We conducted a prospective single-centre study including consecutive patients aged ≥60 years hospitalized with AHF between 2022 and 2024. All patients underwent bone-tracer scintigraphy; ATTR-CM was defined by myocardial uptake grade ≥ 2 and exclusion of plasma cell dyscrasia. The T-Amylo score was calculated blinded to diagnosis. hs-TnT was incorporated into a revised model (TnT-Amylo) using regression-derived weighting. Patients were categorized as low (0-2), intermediate (3-6), or high (7-11) risk. Diagnostic performance and reclassification were evaluated.
RESULTS: Among 138 patients (63% male; mean age 80 ± 6.9 years), ATTR-CM prevalence was 15.9%. The T-Amylo score showed good discrimination (AUC 0.93). hs-TnT was significantly higher in ATTR-CM than in non-ATTR-CM patients (median 68 vs 29 ng/L; p < 0.001; AUC 0.80). In the intermediate-risk group (n = 87), hs-TnT reclassified 15.7% to high risk (72.7% ATTR-CM) and 84.3% to low risk (5% ATTR-CM). The TnT-Amylo model achieved 72.3% sensitivity and 94.9% specificity, with a net reclassification improvement of 135%.
CONCLUSIONS: In AHF patients, integrating hs-TnT into a clinical risk score improves bedside diagnostic stratification, particularly among intermediate-risk patients. This approach may facilitate early aetiological identification and more efficient use of advanced imaging in the acute cardiovascular care setting.
TRANSLATIONAL PERSPECTIVE: This study translates pathophysiological insights of chronic myocardial injury in transthyretin cardiac amyloidosis into a simple bedside diagnostic tool. By integrating high-sensitivity cardiac troponin T-an inexpensive and universally available biomarker-into a clinical risk score, this approach bridges mechanistic myocardial damage with pragmatic decision-making, facilitating early identification of ATTR-CM and more efficient allocation of advanced imaging resources in acute heart failure care.
METHODS: We conducted a prospective single-centre study including consecutive patients aged ≥60 years hospitalized with AHF between 2022 and 2024. All patients underwent bone-tracer scintigraphy; ATTR-CM was defined by myocardial uptake grade ≥ 2 and exclusion of plasma cell dyscrasia. The T-Amylo score was calculated blinded to diagnosis. hs-TnT was incorporated into a revised model (TnT-Amylo) using regression-derived weighting. Patients were categorized as low (0-2), intermediate (3-6), or high (7-11) risk. Diagnostic performance and reclassification were evaluated.
RESULTS: Among 138 patients (63% male; mean age 80 ± 6.9 years), ATTR-CM prevalence was 15.9%. The T-Amylo score showed good discrimination (AUC 0.93). hs-TnT was significantly higher in ATTR-CM than in non-ATTR-CM patients (median 68 vs 29 ng/L; p < 0.001; AUC 0.80). In the intermediate-risk group (n = 87), hs-TnT reclassified 15.7% to high risk (72.7% ATTR-CM) and 84.3% to low risk (5% ATTR-CM). The TnT-Amylo model achieved 72.3% sensitivity and 94.9% specificity, with a net reclassification improvement of 135%.
CONCLUSIONS: In AHF patients, integrating hs-TnT into a clinical risk score improves bedside diagnostic stratification, particularly among intermediate-risk patients. This approach may facilitate early aetiological identification and more efficient use of advanced imaging in the acute cardiovascular care setting.
TRANSLATIONAL PERSPECTIVE: This study translates pathophysiological insights of chronic myocardial injury in transthyretin cardiac amyloidosis into a simple bedside diagnostic tool. By integrating high-sensitivity cardiac troponin T-an inexpensive and universally available biomarker-into a clinical risk score, this approach bridges mechanistic myocardial damage with pragmatic decision-making, facilitating early identification of ATTR-CM and more efficient allocation of advanced imaging resources in acute heart failure care.