Ventricular Arrhythmias in a Patient With Mitral Valve Prolapse: Role of Cardiac Mri in Risk Stratification

Background Mitral valve prolapse (MVP), historically regarded as a benign valvular condition, has progressively gained attention for its potential arrhythmic implications. A subset of patients exhibits ventricular ectopy or complex arrhythmias, sometimes in the absence of significant valvular dysfunction. In this context, cardiac magnetic resonance (CMR) has become essential for identifying myocardial fibrosis, an established substrate for malignant ventricular arrhythmias. Case Summary A 34–year–old woman with no prior cardiovascular disease underwent gastroscopy for persistent dyspeptic symptoms. During the procedure, the anesthetist incidentally noted frequent ventricular ectopic beats, prompting referral for cardiologic evaluation. Twenty–four–hour Holter monitoring captured 4,362 premature ventricular beats, including ventricular couplets and periods of bigeminy, although no sustained or repetitive ventricular arrhythmias were recorded. To further investigate the ectopic burden, an exercise stress test was performed. During peak exertion, the ECG demonstrated horizontal ST–segment depression in precordial leads, although the patient remained entirely asymptomatic. Sporadic ventricular ectopy reappeared during recovery, reinforcing the suspicion of an underlying structural abnormality. Transthoracic echocardiography revealed a bileaflet MVP, with marked myxomatous thickening of the posterior leaflet and mild mitral regurgitation. The characteristic systolic curling of the mitral annulus and subtle inferobasal myocardial “tugging” suggested increased mechanical stress—features associated with the so–called arrhythmogenic MVP phenotype.Given these findings, CMR was undertaken to refine risk stratification and confirmed bileaflet prolapse with normal biventricular volumes and preserved systolic function. Importantly, there was no late gadolinium enhancement, ruling out focal myocardial fibrosis and significantly reducing the probability of malignant arrhythmogenic substrate. Discussion This case illustrates how an incidental finding during a non–cardiac procedure can uncover a potentially arrhythmogenic MVP phenotype. This case highlights the crucial value of multimodality imaging in preventing overtreatment while ensuring vigilant monitoring of patients at possible arrhythmic risk.In the absence of myocardial fibrosis, conservative management with structured follow–up was deemed appropriate.