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Tracking the Fall: Serum Transthyretin Decline as a Harbinger of Heart Failure in hATTR-CM
Session:
Sessão de Posters 15 - Prognóstico, estratificação de risco e comorbilidades na amiloidose cardíaca
Speaker:
João Mendes Cravo
Congress:
CPC 2026
Topic:
F. Valvular, Myocardial, Pericardial, Pulmonary, Congenital Heart Disease
Theme:
17. Myocardial Disease
Subtheme:
17.3 Myocardial Disease – Diagnostic Methods
Session Type:
Posters Eletrónicos
FP Number:
---
Authors:
João Cravo; Daniel Inácio Cazeiro; Marta Vilela; Catarina Campos; Isabel Conceição; Fausto Pinto; Dulce Brito; João Agostinho
Abstract
<p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><strong>Introduction:</strong></span></span></span></p> <p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">Transthyretin cardiac amyloidosis (ATTR-CM) is a progressive infiltrative cardiomyopathy arising from transthyretin protein misfolding leading to myocardial amyloid deposition. Nowadays, a few biomarker-based prognostic models for ATTR-CM have been proposed. Serum transthyretin levels (sTTR) may serve as a surrogate of disease burden and amyloid deposition. Despite its potential, the prognostic value of sTTR remains uncertain.</span></span></span></p> <p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><strong>Aims:</strong></span></span></span></p> <p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">To evaluate the prognostic value of sTTR in patients with hereditary transthyretin cardiac amyloidosis (hATTR-CM).</span></span></span></p> <p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><strong>Methods:</strong></span></span></span></p> <p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">Single-center retrospective observational study including patients diagnosed with </span></span></span><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="background-color:#ffffff">hATTR-CM between 2022-2025. Diagnosis was established according to int</span></span></span></span><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">ernational criteria, including genetic testing. Clinical, laboratory, </span></span></span><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><sup>99m</sup></span></span></span><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">TC-DPD scintigraphy and echocardiographic data were systematically collected at baseline and during follow-up. sTTR levels (measured as pre-albumin) were collected at baseline and serially during follow-up and correlated with disease severity and prognostic events. </span></span></span></p> <p><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><strong>Results:</strong></span></span></span></p> <p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">A total of 51 patients with hATTR-CM were included (median age at diagnosis 57 years [IQR 47–67]; 40 [78%] male). The majority carried the Val30Met variant (44 [86%]), followed by V122</span></span></span><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="background-color:#ffffff">I (6 [12%]) and G89L (1 [2%]). Hypertension was present in 40 (78%) and atrial fibrillation in 11 (22%). 40 were treated with tafamidis 61mg and 9 with vutrisiran. Median sTTR at diagnosis was 20 mg/dL (IQR 12–24).</span></span></span></span></p> <p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="background-color:#ffffff">Lower sTTR levels were observed in patients with greater functional impairment requiring diuretics, (23 [IQR 16–26] vs 27 [IQR 22–33]; p=0.047), and in those with interventricular septum thickness >15 mm (21 ± 3 vs 26 ± 1 mm; p=0.049). A non-significant trend towards lower sTTR levels was seen in patients with a Perugini score 3 on </span></span></span></span><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="background-color:#ffffff"><sup>99m</sup></span></span></span></span><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="background-color:#ffffff">TC-DPD scintigraphy (22.5 ± 2 vs 26 ± 2 mg/dL; p=0.20).</span></span></span></span></p> <p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">During a mean follow-up of 35 ± 3 months, 11 heart-failure (HF) decompensations requiring diuretic uptitration occurred. Patients who experienced HF events had significantly lower sTTR at diagnosis (17.7 ± 3 vs 26 ± 1 mg/dL; p=0.010). A decline in sTTR from baseline was strongly associated with cardiovascular events (−1.3 ± 0.6 vs +6 ± 1 mg/dL in those without events; p=0.010).</span></span></span></p> <p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">Patients with sTTR <25 mg/dL had significantly shorter event-free survival compared with those ≥25 mg/dL (log-rank χ²=4.48; p=0.034). In Cox regression analysis, low sTTR was associated with a seven-fold higher risk of events (HR 7.06; 95% CI 0.85–58.7; p=0.071).</span></span></span></p> <p><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><strong>Conclusion:</strong></span></span></span></p> <p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">Lower serum transthyretin levels at diagnosis were associated with more advanced cardiac involvement, impaired functional status, and a higher risk of subsequent heart failure decompensation. sTTR may represent a practical and clinically relevant biomarker for disease severity and short-term prognosis in hATTR-CM, serving as a complementary tool alongside established markers such as NT-proBNP.</span></span></span></p>
Slides
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