Key result
Baseline native T1 ≥ 1447 ms predicts markedly higher one-year worsening heart failure in tafamidis-treated ATTR-CM.
Why the study?
Data were lacking regarding short-term outcomes and treatment responsiveness of CMR myocardial T1 mapping in patients with ATTR-CM undergoing tafamidis therapy.
Do baseline myocardial T1 mapping parameters predict one-year worsening heart failure in patients with wild-type ATTR-CM undergoing tafamidis treatment?
Cohort (n=60)
Do baseline myocardial T1 mapping parameters predict one-year worsening heart failure in patients with wild-type ATTR-CM undergoing tafamidis treatment?
Effect estimate: HR 15.2 and 9.3
Elevated baseline T1 mapping parameters, specifically T1 native ≥ 1447 ms, strongly predict one-year worsening heart failure in wild-type ATTR-CM patients treated with tafamidis, and may track treatment-induced myocardial changes.
Baseline T1 mapping may stratify WHF risk on tafamidis in ATTR-CM; leaves open serial monitoring value pending prospective validation.**[[1]](https://www.sciencedirect.
There is a paucity of data regarding short-term outcomes and treatment responsiveness of myocardial T1 mapping via cardiac magnetic resonance (CMR) in patients with transthyretin amyloid cardiomyopathy (ATTR-CM) undergoing tafamidis therapy. We retrospectively studied 60 wild-type ATTR-CM patients who underwent baseline CMR to measure native myocardial T1 value (T1 native ) and extracellular volume fraction (ECV), followed by tafamidis treatment. Cardiac biomarkers, including high-sensitivity cardiac troponin T and N-terminal pro-B-type natriuretic peptide (NT-proBNP), were measured at baseline. We followed a one-year composite of worsening heart failure (WHF; hospitalization and/or intensification of diuretic therapy for heart failure). Additionally, 51 patients underwent follow-up CMR and measurements of cardiac biomarkers one-year after the initiation of tafamidis treatment. Patients with WHF (n = 12) exhibited significantly elevated baseline T1 native and ECV than those without WHF, and their optimal cutoffs in predicting WHF were 1447 ms and 48.7 %, respectively. Multivariate analysis adjusted for Mayo or National Amyloidosis Center stages identified T1 native of ≥ 1447 ms as an independent predictor of WHF, with hazard ratios of 15.2 and 9.3, respectively. A notable proportion of patients exhibited a reduction in T1 native (39 %) and ECV (47 %) after one year of tafamidis treatment. Post-treatment changes in T1 native were correlated positively with changes in NT-proBNP concentration (r = 0.40, p = 0.0036). In wild-type ATTR-CM patients receiving tafamidis, elevated baseline T1 mapping parameters were associated with one-year WHF. T1 mapping parameters, particularly T1 native , may offer imaging-based evidence of alterations in myocardial characteristics induced by tafamidis.
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Kitagawa et al. (2026) conducted a cohort in Wild-type transthyretin amyloid cardiomyopathy (ATTR-CM) (n=60). Tafamidis was evaluated on One-year composite of worsening heart failure (hospitalization and/or intensification of diuretic therapy) (HR 15.2 and 9.3). Baseline native T1 ≥ 1447 ms independently predicted one-year worsening heart failure in wild-type ATTR-CM patients treated with tafamidis (HR 15.2 and 9.3 depending on staging adjustment).
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