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12-Month effect of tafamidis on the clinical progression of cardiac amyloidosis in a single centre cohort
Session:
Sessão de Posters 14 - Amiloidose Cardíaca
Speaker:
Ricardo Carvalheiro
Congress:
CPC 2024
Topic:
F. Valvular, Myocardial, Pericardial, Pulmonary, Congenital Heart Disease
Theme:
17. Myocardial Disease
Subtheme:
17.4 Myocardial Disease – Treatment
Session Type:
Cartazes
FP Number:
---
Authors:
Ricardo Da Silva Carvalheiro; Isabel Cardoso; Miguel Antunes; André Ferreira; José Viegas; Pedro Brás; Inês Almeida; Sílvia Aguiar Rosa; Rui Cruz Ferreira
Abstract
<p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><strong>Introduction</strong>: Transthyretin cardiac amyloidosis (ATTR – CA) is a progressive disease with significant morbidity and mortality. Tafamidis, a drug that binds to transthyretin, stabilizing the tetramer and avoiding the dissociation and the subsequent formation of amyloid, has shown promise in improving outcomes and slowing disease progression, offering hope for a better prognosis in affected individuals.</span></span></p> <p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><strong>Objectives: </strong>To assess the 12-month effect of tafamidis on clinical, echocardiographic, laboratory and functional parameters in a population with ATTR – CA.</span></span></p> <p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><strong>Methods:</strong> We prospectively evaluated a cohort of patients with ATTR-CA treated with tafamidis in a single-centre.</span></span></p> <p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><strong>Results: </strong>A total of 34<strong> </strong>patients (79.4% male) were included, with a mean age of 79 ± 9.1 years at the start of treatment and a median follow up of 15 months. Most patients presented wild-type ATTR-CA, as 9 pts (26.5%) had TTR mutation. At the start of treatment, 73.5% of pts presented NYHA class II sypmtoms and 23.5% presented NYHA class III. Mean furosemide dose was of 59 ± 39 mg, and 15 pts (44.1%) had previous hospitalizations for heart failure (with a total of 21 hospitalizations). Mean left ventricle ejection fraction (LVEF) was <span style="color:black">54 ± 2.5 %, GLS -10.9 ± 4.4 %, indexed left atrium volume (LAVi) 49 ± 15.4 ml/m2 and median E/e' ratio 18 (8). Pts walked a mean of 292 ± 103.6 m on the 6-minute walk test (6MWT). Regarding laboratory parameters, mean glomerular filtration rate (GFR) was of 50 ± 22.9 mL/min/1.73, mean high-sensitivity (hs) troponin was 190 ± 85 ng/L and median NTproBNP was 2031 (3357) pg/mL. At 12 months follow up, our analysis showed no statistically significant worsening of LVEF (p=0.542), GLS (p=0.197), LAVi (p=0.420) or E/e’ ratio (p=0.300). There was no statistically significant difference on the 6MWT (302 ± 96.7, p=0.650). We found no statistically significant differences in GFR (p=0.248) or NTproBNP (p=0.848) at 12 months, but a significant reduction in troponin (104 ± 77 [p=0.020]). 4 pts (13.3%) were hospitalized in the 12 months after tafamidis initiation, representing a significant decrease when compared with previous hospitalizations (Z= -2.336, p=0,019).</span></span></span></p> <p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><strong><span style="color:black">Conclusions: </span></strong><span style="color:black">In our cohort of patients, there was no statistically significant deterioration of echocardiographic parameters, 6 minutes walking test distance and NT pro BNP after 12 months of treatment with tafamidis. There was a decrease in troponin values and number of hospitalizations after treatment.</span></span></span></p>
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