P37 MULTIMODALITY DIAGNOSTIC APPROACH TO A JUVENILE CASE OF SUSTAINED VENTRICULAR TACHYCARDIA

Abstract

Abstract Clinical case 31–year–old male subject, former competitive athlete, with family history of coronary artery disease and no further cardiovascular risk factors or previous cardiac events. Previous SARS–CoV2–related paucisymptomatic infection (January 2022) and subsequent episode of fever (August 2022) with negative SARS–CoV2 nasal swab. In September 2022 he reported sudden onset of palpitations after hearty meal. Because of such symptoms, the patient underwent Holter ECG showing 90 episodes of ventricular tachycardia (VT) and one episode of sustained VT. Based on such evidence, the patient went to the emergency room (ER). During the ER stay, blood exams (blood count, high–sensitivity troponin, BNP, CRP, D–dimer) and ECG were normal and SARS–CoV2 test was negative. The patient was then hospitalized in cardiac ICU. The echocardiogram showed left ventricle with normal dimension, thickness and wall motion (EF: 65%, mean GLS: –20%), trivial mitral and aortic regurgitation, no pericardial effusion. Subsequently, a cardiac coronary CT scan was performed showing absence of atherosclerotic lesions and myocardial bridge of the middle segment of LAD artery. The diagnostic pathway went on with cardiac magnetic resonance (CMR) demonstrating focal hypokinesia and wall thickness reduction of the anteroseptal–anterior junctional wall at middle–distal level (minimum thickness: 3 mm) where a millimetric area of late gadolinium enhancement with transmural distribution was described; absence of myocardial oedema. In addition, an EPS was performed with electroanatomical high–density/definition mapping of the left ventricle showing normal volumes, signals and activation and absence of LAVA/LV. Taking into account such findings, a subcutaneous defibrillator was implanted for primary prevention and a control CMR was scheduled in the follow–up period. Conclusions This case underlines the central role of CMR in identifying areas of myocardial fibrosis that can represent the electroanatomical substrate for triggering ventricular arrhythmias. In this case, the arrhythmic events are associated with a focal area of transmural fibrosis and wall thinning, usually indicating ischaemic damage, nonetheless in the presence of normal coronary arteries.