Key result
Tafamidis maintains stable echocardiographic parameters over 12 months in patients with ATTR-CA.
Why the study?
Although tafamidis has demonstrated clinical benefit in transthyretin cardiac amyloidosis (ATTR-CA), real-world data regarding longitudinal echocardiographic evolution during therapy remain limited.
Does tafamidis therapy stabilize echocardiographic parameters over 12 months in patients with transthyretin cardiac amyloidosis?
Cohort (n=158)
No
Does tafamidis therapy stabilize echocardiographic parameters over 12 months in patients with transthyretin cardiac amyloidosis?
In a real-world cohort of patients with transthyretin cardiac amyloidosis, 12 months of tafamidis therapy stabilized echocardiographic parameters, suggesting attenuation of structural and functional cardiac progression.
Supports disease modification with tafamidis in ATTR-CA; leaves open translation to clinical outcomes in randomized trials.
Background Transthyretin cardiac amyloidosis (ATTR-CA) is characterized by progressive myocardial infiltration leading to structural remodeling and functional impairment. Tafamidis has demonstrated clinical benefit in ATTR-CA; however, real-world data regarding longitudinal echocardiographic evolution during therapy remain limited. Methods We conducted a single-center observational study that included 158 consecutive patients with ATTR-CA receiving tafamidis therapy. Clinical and echocardiographic parameters were assessed at treatment initiation and after 12 months. Continuous variables are presented as median (interquartile range). Paired comparisons between baseline and 12-month measurements were performed using the Wilcoxon signed-rank test. Results The cohort’s median age was 82 years (IQR 77–85), and 131 patients (82.9%) were males. After 12 months of tafamidis therapy, no statistically significant changes were observed in key echocardiographic parameters. Global longitudinal strain remained stable (baseline −11.4% [−14 to −9.1] vs 12 months −12.6% [−15.8 to −10.1], p=0.476). Left ventricular ejection fraction showed no significant variation (50% [42–55] vs 55% [48–55], p=0.773). Similarly, interventricular septal thickness (15 mm [13–16] vs 14 mm [14–15], p=0.855) and posterior wall thickness (14 mm [12–15] vs 14 mm [12.5–14], p=0.740) remained unchanged over follow-up. Conclusions In this real-world cohort of ATTR-CA patients treated with tafamidis, echocardiographic parameters remained stable during the first year of therapy. These findings suggest that treatment with tafamidis has a disease-modifying effect of reflected by attenuation of structural and functional cardiac progression.
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Alifragki et al. (2026) conducted a cohort in Transthyretin cardiac amyloidosis (ATTR-CA) (n=158). Tafamidis vs. Baseline (pre-treatment) was evaluated on 12-month evolution of echocardiographic parameters (global longitudinal strain, LVEF, interventricular septal thickness, posterior wall thickness) (p=0.476). Tafamidis therapy maintained stable echocardiographic parameters over 12 months in ATTR-CA, including global longitudinal strain (-11.4% vs -12.6%, p=0.476) and LVEF (50% vs 55%, p=0.773).
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