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Real-World Predictors of Adverse Outcomes in HCM: Who Is Really at Risk?
Session:
Sessão de Posters 18 - Miocardiopatia hipertrófica: genética, fenótipo e desfechos
Speaker:
Rita Figueiredo
Congress:
CPC 2026
Topic:
F. Valvular, Myocardial, Pericardial, Pulmonary, Congenital Heart Disease
Theme:
17. Myocardial Disease
Subtheme:
17.2 Myocardial Disease – Epidemiology, Prognosis, Outcome
Session Type:
Posters Eletrónicos
FP Number:
---
Authors:
Ana Rita M. Figueiredo; Diogo Ferreira; Marta Vilela; João Cravo; Daniel Inácico Cazeiro; Catarina Gregório; Beatriz Garcia; Oana Moldovan; Hugo Madeira; Fausto J. Pinto; Dulce Brito
Abstract
<p style="text-align:justify"><strong>Introduction</strong>:</p> <p style="text-align:justify">Risk prediction in hypertrophic cardiomyopathy (HCM) remains challenging in clinical practice. Although several prognostic markers have been proposed, real-world patients often show substantial phenotypic variability and evolving disease expression, which may limit the performance of conventional risk models. Identifying which clinical features truly reflect long-term vulnerability to adverse events is therefore essential for optimising management. This study aimed to identify predictors of adverse outcomes in a real-world HCM cohort.</p> <p style="text-align:justify"><strong>Methods: </strong></p> <p style="text-align:justify">We conducted a single-centre observational study including consecutive patients diagnosed with HCM according to ESC criteria between 2000 and 2024. All patients underwent genetic testing using a large Next-generation sequencing (NGS) panel. The ESC HCM-Risk-SCD score was calculated at baseline. The primary endpoint was a composite of appropriate ICD therapies, cardiovascular hospitalisation (CVH), and cardiovascular death (CVD). Survival analyses were performed using Kaplan-Meier curves with log-rank testing, and predictors of the composite outcome were assessed using Cox regression.</p> <p style="text-align:justify"><strong>Results</strong>:</p> <p style="text-align:justify">A total of 153 patients were included (mean age 49±2 years; 49% male). Sarcomeric variants were identified in 141 (90%), with pathogenic/likely pathogenic mutations mainly in <em>MYH7</em> (36%) and <em>MYBPC3</em> (35%) genes. Baseline left ventricular ejection fraction (LVEF) was 62±0.8%, maximal wall thickness 18 ± 0.4 mm; 15% had obstructive physiology, and 13% were classified as high-risk by ESC HCM-Risk-SCD score.<br /> Over a mean follow-up of 10±0.9 years, 34 (22%) patients underwent ICD implantation, 14 (9%) had septal reduction therapy, and 48 (31%) developed new-onset atrial fibrillation. The composite endpoint occurred in 43 patients (28%), including 9 (5%) appropriate ICD therapies, 32 (21%) CVH and 17 (11%) CVD. </p> <p style="text-align:justify">Patients with events had larger left atrial diameter (49±2 vs 42±1 mm; p=0.03), higher ESC HCM-Risk-SCD scores (3.9±0.5 vs 2.8±0.2; p=0.04) and higher follow-up NT-proBNP (1582 [438–3916] vs 564 [134–1458] pg/mL; p=0.002). Kaplan–Meier analysis (Fig.1) showed significantly higher event rates in patients with moderate–high ESC HCM-Risk-SCD scores, with early and sustained separation of survival curves. In Cox regression, a moderate–high ESC risk category independently predicted the composite endpoint, conferring an approximately three-fold increased hazard compared with low-risk patients (HR 2.7; 95% CI 1.3–5.2; p=0.01).</p> <p style="text-align:justify"><strong>Conclusion</strong>:</p> <p style="text-align:justify">In this real-world HCM cohort, larger left atrial size, higher NT-proBNP levels, and a moderate–high ESC HCM-Risk-SCD category were associated with a greater burden of adverse cardiovascular outcomes. The ESC HCM-Risk-SCD score independently predicted the composite endpoint, supporting its prognostic relevance beyond sudden cardiac death.</p>
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