SPC365

SGLT2 inhibitors in wild-type transthyretin amyloid cardiomyopathy: what to expect?

Session: Sessão de Posters 14 - Amiloidose Cardíaca
Speaker: Luísa Pinheiro

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: Luísa Pinheiro; Mariana Tinoco; Margarida Castro; Tamara Pereira; Olga Azevedo; António Lourenço
<p><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><strong>INTRODUCTION: </strong>Wild-type t<span style="background-color:white"><span style="color:black">ransthyretin&nbsp;amyloid cardiomyopathy&nbsp;(wtATTR-CM) is an increasingly recognized etiology of heart failure (HF). Several drug classes used on traditional HF treatment have not shown benefit in patients with wtATTR-CM. </span></span><span style="background-color:white"><span style="color:black">Sodium-Glucose Co-Transporter 2 Inhibitors (SGLT2i) are a well-established treatment for HF patients, but its impact specifically in wtATTR-CM patients has not been assessed. </span></span></span></span></p>

<p><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><strong>PURPOSE:</strong><span style="background-color:white"><span style="color:black"> To evaluate the efficacy of SGLT2i in wtATTR-CM patients.</span></span></span></span></p>

<p><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><strong><span style="font-family:&quot;Calibri&quot;,sans-serif">METHODS: </span></strong><span style="font-family:&quot;Calibri&quot;,sans-serif">Retrospective, single-center study of</span><strong><span style="font-family:&quot;Calibri&quot;,sans-serif"> </span></strong><span style="background-color:white"><span style="color:black">patients with diagnosis of wtATTR-CM between 2014 and 2023. </span></span><span style="background-color:white"><span style="color:black">The primary endpoint was the composite endpoint of hospitalization due to HF or death from any cause. SGLT2i use and other clinical, laboratory, electrocardiographic and echocardiographic parameters at baseline were compared between patients who achieved vs. did not achieve the primary endpoint. Regression analyses were used to determine the independent predictors of the primary endpoint.</span></span></span></span></p>

<p><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><strong>RESULTS: </strong>A total of 90 patients were included in the study (72% males; mean age 81&plusmn;5 years; baseline left ventricular ejection fraction (LVEF) 54% &plusmn; 14). Median follow-up was 21 [IQR 13-38] months. In this study, 36 (40%) patients were treated with <span style="background-color:white"><span style="color:black">SGLT2i</span></span>, 9 <span style="background-color:white"><span style="color:black">achieved the primary endpoint</span></span> </span></span></p>

<p><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif">Patients who achieved vs. did not achieve the primary endpoint did not present significant differences at baseline regarding gender, diabetes, conduction disturbances, and LVEF. SGLT2i use was associated with more patients free of the primary endpoint (75% vs. 37%; p&lt;0.001), the same association was observed with renin-angiotensin-system-inhibitors (RASI) (70% vs. 34%; p&lt;0.001), non-use of beta-blockers (64% vs. 42%; p=0.032), absence of atrial fibrillation (72% vs. 37%; p=0.001), levels of pro-B-type natriuretic peptide (proBNP) (7583<span style="color:black">&plusmn;8675pg/mL</span> vs. 2549<span style="color:black">&plusmn;2437pg/mL</span>; p=0.001), estimated glomerular filtration rate (eGFR) (69.7<span style="color:black">&plusmn;25.6mL/min vs 57.1&plusmn;22.7; p=0.016), interventricular septal thickness (</span>17.5<span style="color:black">&plusmn;2.8</span>mm<span style="color:black"> vs 19.1&plusmn;3.9; p=0.031), and left ventricular mass index (</span>160.4<span style="color:black">&plusmn;40.8g/m<sup>2</sup> vs 185.7&plusmn;50.9g/m<sup>2</sup>; p=0.013).</span></span></span></p>

<p><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif">On <span style="color:black">multivariate regression analysis, </span>SGLT2i use was a protective factor against the occurrence of the primary endpoint (HR 0.124, 95% CI 0.026-0.593, p=0.009). RASI use was also a protective factor (HR 0.058, 95% CI 0.011-0.293, p&lt;0.001). Accordingly, patients without SGLT2i had a significantly higher frequency of increase in HF hospitalizations and total mortality (p=0.022; p&lt;0.001, respectively), which were reflected in the Kaplan-Meier survival curves (p=0.046; p&lt;0.001, respectively).</span></span></p>

<p><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><strong>CONCLUSIONS:</strong> <span style="background-color:white"><span style="color:black">SGLT2i</span></span> use showed to be a protective factor against the occurrence of the combined endpoint of HF <span style="background-color:white"><span style="color:black">hospitalization</span></span> and total mortality in patients with wtATTR-CM, suggesting a therapeutic benefit of these drugs in this disease. However, further randomized prospective studies on this subject are needed.</span></span></p>