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Effect of mavacamten on the remodelling and microstructural architecture of the myocardium: A Preliminary Mechanistic Study
Session:
SESSÃO DE COMUNICAÇÕES ORAIS 16 – AVANÇOS NO DIAGNÓSTICO E TRATAMENTO DAS MIOCARDIOPATIAS
Speaker:
Sílvia Aguiar Rosa
Congress:
CPC 2025
Topic:
F. Valvular, Myocardial, Pericardial, Pulmonary, Congenital Heart Disease
Theme:
17. Myocardial Disease
Subtheme:
17.4 Myocardial Disease – Treatment
Session Type:
Comunicações Orais
FP Number:
---
Authors:
Sílvia Aguiar Oliveira Rosa; Miguel Marques Antunes; Vera Ferreira; Inês Miranda; Isabel Cardoso; José Viegas; Cláudia Marra; Filipa Gerardo; Rodrigo Brandão; Maria Passos; Rui Cruz Ferreira; João Augusto
Abstract
<p><span style="font-size:11pt"><span style="font-family:Aptos,sans-serif"><strong><span style="font-family:"Calibri",sans-serif">Background: </span></strong><span style="font-family:"Calibri",sans-serif">Mavacamten is an allosteric inhibitor of cardiac myosin, capable of modifying </span></span></span><span style="font-size:11pt"><span style="font-family:Aptos,sans-serif"><span style="font-family:"Calibri",sans-serif">myosin mechanochemistry leading to a reduction in sarcomere force generation, myocardial hypercontractility, and left ventricular outflow tract obstruction in patients with hypertrophic cardiomyopathy (HCM).</span></span></span></p> <p> </p> <p><span style="font-size:11pt"><span style="font-family:Aptos,sans-serif"><strong><span style="background-color:white"><span style="font-family:"Calibri",sans-serif"><span style="color:black">Objective</span></span></span></strong><span style="background-color:white"><span style="font-family:"Calibri",sans-serif"><span style="color:black">: To study the effect of mavacamten in ventricular remodeling, microvascular dysfunction, left ventricular (LV) strain and interstitial and replacement fibrosis, assessed by cardiovascular magnetic resonance (CMR). </span></span></span></span></span></p> <p> </p> <p><span style="font-size:11pt"><span style="font-family:Aptos,sans-serif"><strong><span style="font-family:"Calibri",sans-serif">Methods: </span></strong><span style="font-family:"Calibri",sans-serif">We conducted a prospective observational study in HCM patients from two different centers. Eligible patients were required to have left ventricular outflow tract (LVOT) obstruction and were prescribed mavacamten as part of clinical care. All patients were treated with mavacamten for at least 24 weeks, with doses individualized to achieve targeted reductions in LVOT gradients based on echocardiographic assessments. We measured the effect of mavacamten at 24 weeks on microvascular dysfunction assessed by myocardial blood flow after stress perfusion CMR with regadenoson, specifically reporting the proportion (%) of LV hypoperfusion. We additionally obtained other CMR-derived metrics at baseline and follow-up: LV and right ventricle ejection fraction (LVEF, RVEF), LV and RV volumes, LV mass, global longitudinal and radial strains (GLS, GRS), native T1 and T2 mapping, extracellular volume (ECV), and percentage of LV late gadolinium enhancement (LGE). LVOT gradient was meassured on echocardiogram.</span></span></span></p> <p> </p> <p><span style="font-size:11pt"><span style="font-family:Aptos,sans-serif"><strong><span style="font-family:"Calibri",sans-serif">Results: </span></strong><span style="font-family:"Calibri",sans-serif">A total of 8 HCM patients were included, mean age 59.4 ± 9.5 years, 62.5% were male. Mavacamten reduced LVOT obstruction (gradient from 99.0 [80.8-115.3]mmHg to 20 [14.0-44.0]mmHg), reflecting the concomitant reduction in LVEF (baseline 67.9%±6.2%, follow-up 63.0%±4.9%). CMR demonstrated stability in terms of ventricular adverse remodeling (no significant changes in LV and RV volumes or RVEF) and no progression in measures of fibrosis (stable native T1 mapping, ECV and % LGE). Notably, mavacamten decreased LV mass and improved LV systolic performance assessed by ventricular strain. Four patients concluded baseline and follow-up stress perfusion. Mavacamten reduced LV hypoperfusion (from 21.0±15.5% to 15.6±11.9%)(figure 1 and 2). All results are detailed in Table 1.</span></span></span></p> <p> </p> <p><span style="font-size:11pt"><span style="font-family:Aptos,sans-serif"><strong><span style="font-family:"Calibri",sans-serif">Conclusion:</span></strong><span style="font-family:"Calibri",sans-serif"> Mavacamten caused a reverse remodeling of the LV, leading to an improvement in systolic performance assessed by LV strain, and reduced microvascular ischemic burden.</span></span></span></p>
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