Long-term tafamidis therapy reduced the extent of cardiac worsening in patients with ATTR-CM. The study, published in Clinical Research in Cardiology, analyzed 56 patients who underwent serial multi-parametric cardiovascular magnetic resonance (CMR) imaging over a mean follow-up of 27 ± 6 months. Tafamidis 61 mg once daily was initiated in 39 patients (95% male), while 17 (76% male) remained untreated.

Clinical and imaging parameters deteriorated in both groups, but progression was significantly less in tafamidis-treated patients. Left ventricular ejection fraction declined from 54% to 48% with tafamidis versus 56% to 46% without treatment (Δp = 0.008). Global longitudinal strain worsened less in the treated group (−7.4 to −5.3 vs −8.8 to −4.8; Δp = 0.003). LV wall thickness increased modestly with tafamidis (18.5 mm to 19.2 mm) compared with a larger rise in untreated patients (18.2 mm to 21.1 mm; Δp < 0.001).

Serum N-terminal pro–B-type natriuretic peptide (NT-proBNP) levels rose in both groups but to a greater extent without tafamidis (p = 0.014). Both native T1 and extracellular volume (ECV) values increased significantly, although the ECV rise was smaller in the tafamidis group (51% to 57%) compared with untreated patients (50% to 67%; Δp < 0.001).

Although disease progression persisted, tafamidis therapy substantially reduced the magnitude of myocardial, biomarker, and functional deterioration. These findings highlight its sustained benefit in moderating long-term cardiac decline in ATTR-CM.