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Silent Danger on the Pitch: The Hidden Battle of Left-Dominant Arrhythmogenic Cardiomyopathy
Session:
CASOS CLÍNICOS DE ARRITMOLOGIA
Speaker:
Sofia Esteves
Congress:
CPC 2025
Topic:
C. Arrhythmias and Device Therapy
Theme:
04. Arrhythmias, General
Subtheme:
04.6 Arrhythmias, General – Clinical
Session Type:
Sessão de Casos Clínicos
FP Number:
---
Authors:
Sofia Esteves; Daniel Inácio Cazeiro; Miguel Azaredo Raposo; Catarina Gregório; Ana Abrantes; Diogo Rosa Ferreira; Marta Miguez Vilela; Oana Moldovan; Tatiana Guimarães; João R. Agostinho; Fausto J. Pinto; Rui Plácido
Abstract
<p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Aptos,sans-serif"><strong><span style="font-size:13.5pt"><span style="font-family:"Calibri",sans-serif"><span style="color:black">Introduction:</span></span></span></strong></span></span></p> <p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Aptos,sans-serif"><span style="font-size:13.5pt"><span style="font-family:"Calibri",sans-serif"><span style="color:black">Arrhythmogenic cardiomyopathy (ACM) is a genetic heart disorder marked by structural changes, arrhythmias and a high risk of sudden cardiac death (SCD). Left-dominant arrhythmogenic cardiomyopathy (LDACM), an emerging subtype, is less commonly recognized.</span></span></span></span></span></p> <p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Aptos,sans-serif"> </span></span></p> <p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Aptos,sans-serif"><strong><span style="font-size:13.5pt"><span style="font-family:"Calibri",sans-serif"><span style="color:black">Case Report:</span></span></span></strong></span></span></p> <p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Aptos,sans-serif"><span style="font-size:13.5pt"><span style="font-family:"Calibri",sans-serif"><span style="color:black">A 21-year-old soccer player presented to the emergency department with sudden-onset paresthesia in the left upper limb and hemiface. His history included mitral valve prolapse and mild COVID-19, with no significant findings on physical examination. Laboratory tests revealed normal inflammatory markers and NT-proBNP, but markedly elevated high-sensitivity troponin I (hsITrop 4202.1 ng/L). He reported chest discomfort and fatigue two weeks prior and was admitted to the hospital with the diagnosis of acute myocarditis.</span></span></span></span></span></p> <p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Aptos,sans-serif"> </span></span></p> <p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Aptos,sans-serif"><span style="font-size:13.5pt"><span style="font-family:"Calibri",sans-serif"><span style="color:black">Electrocardiogram (ECG) showed sinus bradycardia and biphasic T waves in V1-V3. Transthoracic echocardiography (TTE) revealed left ventricular (LV) dilation (LVEDV 103 mL/m²), concentric hypertrophy, preserved ejection fraction (LVEF 61%), apical lateral hypokinesia, reduced global longitudinal strain (GLS 16.5%) and a mobile apical mass. Brain MRI identified embolic ischemic lesions, prompting initiation of warfarin. Holter monitoring showed sinus rhythm with occasional ectopic beats.</span></span></span></span></span></p> <p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Aptos,sans-serif"> </span></span></p> <p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Aptos,sans-serif"><span style="font-size:13.5pt"><span style="font-family:"Calibri",sans-serif"><span style="color:black">Cardiac MRI confirmed LV dilation, the apical mass, myocardial edema, and late gadolinium enhancement (LGE) in the apical segments without an ischemic pattern. Viral serologies were negative. Thrombophilia screening identified weak lupus anticoagulant. He was discharged with physical activity restrictions.</span></span></span></span></span></p> <p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Aptos,sans-serif"> </span></span></p> <p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Aptos,sans-serif"><span style="font-size:13.5pt"><span style="font-family:"Calibri",sans-serif"><span style="color:black">At a 2.5-month follow-up, TTE showed resolution of the apical mass, persistent LV dilation, slightly reduced GLS and a normal LVEF. hsITrop remained elevated. Repeat cardiac MRI revealed progressive LV dilation (LVEDV 148 mL/m²), reduced LVEF (52%), apical hypokinesia and mid-basal septal LGE. Endomyocardial biopsy demonstrated myocyte architectural disorganization and myocytolysis. Genetic testing identified a heterozygous MYBPC3 newly variant (c.1484G>A, p.(Arg495Gln)).</span></span></span></span></span></p> <p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Aptos,sans-serif"> </span></span></p> <p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Aptos,sans-serif"><span style="font-size:13.5pt"><span style="font-family:"Calibri",sans-serif"><span style="color:black">Despite medical advice, the patient resumed soccer. During a match, he suffered SCD due to ventricular fibrillation but was successfully resuscitated without neurological deficits. TTE post-arrest revealed LVEF of 52%. Coronary CT angiography excluded coronary artery disease, and cardiac MRI findings were consistent with prior results. A subcutaneous implantable cardioverter-defibrillator (ICD) was placed for primary prevention.</span></span></span></span></span></p> <p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Aptos,sans-serif"> </span></span></p> <p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Aptos,sans-serif"><strong><span style="font-size:13.5pt"><span style="font-family:"Calibri",sans-serif"><span style="color:black">Discussion/Conclusion:</span></span></span></strong></span></span></p> <p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Aptos,sans-serif"><span style="font-size:13.5pt"><span style="font-family:"Calibri",sans-serif"><span style="color:black">This case underscores the diagnostic challenge of distinguishing ACM from myocarditis during inflammatory “hot” phases. LDACM presents a unique risk to athletes, requiring precise diagnosis and management. This patient’s presentation highlights the importance of strict activity restrictions and ICD placement to prevent SCD in LDACM. </span></span></span></span></span></p>
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