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Can we count on echocardiography to identify different types of cardiac amyloidosis?
Session:
Posters (Sessão 6 - Écran 5) - Imagem 4 - Ecocardiografia 2
Speaker:
Miguel Azaredo Raposo
Congress:
CPC 2022
Topic:
B. Imaging
Theme:
03. Imaging
Subtheme:
03.1 Echocardiography
Session Type:
Pósters Electrónicos
FP Number:
---
Authors:
Miguel Azaredo Raposo; Pedro Silvério António; Sara Couto Pereira; Joana Brito; Beatriz Valente Silva; Pedro Alves da Silva; Ana Beatriz Garcia; Ana Margarida Martins; Catarina Simões de Oliveira; João Santos Fonseca; Catarina Gregório; Ana Abrantes; João Agostinho; Fausto j. Pinto; Dulce Brito
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><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">: Cardiac amyloidosis (CA) is a heterogeneous disease with diverse phenotypes</span></span></span><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#444444"><span style="background-color:#ffffff">. </span></span></span></span><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">Most cases are caused by one of two misfolded proteins: immunoglobulin light-chain (AL) or amyloid transthyretin (ATTR). Target therapies may influence ATTR amyloidosis prognosis and so an early diagnosis is critical. Selected echocardiographic parameters have been suggested to distinguish AL-CA from ATTR-CA.</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>Aim</strong></span></span></span><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">: To compare the diagnostic accuracy of various conventional and deformation echo parameters in differentiating AL-CA from ATTR-CA.</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><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">: Single-center retrospective study in a reference center of hereditary ATTR-CA patients (pts) with cardiac amyloidosis. At baseline, laboratory, electrocardiography (ECG), 2D echocardiography and DPD-scintigraphy were performed in all pts. Some pts performed cardiac magnetic resonance imaging. Quantifiable conventional morphological and functional parameters along with</span></span></span><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><strong> </strong></span></span></span><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">strain analyses of left and right ventricle were analyzed.</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>Results: </strong></span></span></span><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">We included 84 pts with CA, 18 pts with AL-CA and 66 pts with ATTR-CA - 24 with hereditary (h) ATTR-CA and 42 ATTR-wt CA. ATTR pts were 65±9 year-old and 83.3% were male while AL pts 71±12 year-old and 61.1% were male. Pts with ATTR-wt CA presented more LV hypertrophy, predominantly of IVS (17.6±2.9mm vs 15.3±3.9mm h-ATTR-CA vs 15.6±2.9mm AL-CA), reduced LVEF (46±16%vs59±8% in h-ATTR-CA vs 55±10% in AL-CA) and more RV hypertrophy (5.7±3.3mm vs 5±2.1mm in h-ATTR-CA vs 4.4±2.7mm in AL-CA), with no statistically significant differences. </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">When comparing only ATTR amyloidosis types, pts with ATTR-wt CA had higher grade of LV hypertrophy, reduced biventricular function (LVEF, TAPSE) and higher grades of LV diastolic dysfunction, with statistically significance – table 1. Moreover, pts with ATTR-CA tend to present with pericardial effusion at diagnosis (p=0.44). Strain analysis was reduced in all pts, with statistically differences between ATTR-wt CA pts and hATTR-CA (LV GLS: 9.5±4.3% vs 13.9%±3.1, p<0.001; RV 4 chamber strain: 11±3.8%vs15.9%±4.3, p=0.001), but with no differences between AL-CA and ATTR-CA – Table 2. Other echocardiographic variables were very similar between different types.</span></span></span></p> <p><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><strong>Conclusions</strong></span></span></span><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">: Our study showed that in pts with CA, cardiac involvement could be more expressive in ATTR-wt, which probably relates to late diagnosis and absence of modifier therapeutic in these pts when compared to h-ATTR. Despite that, no echo parameters were able to accurately differentiate between h-ATTR and AL-CA.</span></span></span></p>
Slides
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