Objective
Premature ventricular contractions are among the cardiovascular pathologies which are frequently observed in young subjects. Some features of PVCs; frequency, morphology, and etc; may be a predictor of the severity of underlying myocardial disease. Polymorphic PVCs or ventricular tachycardia are generally originated from myocardial disease or genetic ion channel disorders and are associated with higher risk of sudden death.
Methods
Herein we presented a young subject who complained about palpitation. He was previously performed TTE which was reported as normal. Since frequent atrial premature contractions (8000 beats per day) and a NSTV with 5 PVCs were detected on 24 hours rhythm holter monitoring, metoprolol 50 mg/day was initiated to the patient. His palpitation has been reduced but not completely relieved. So he admitted our service and was examined. When we interrogated his symptoms, we learned that he sometimes suffered dizziness and pre-syncope besides the palpitations. Then we planned a new 24 hour rhythm monitoring. We observed that he suffered NSVT with 3-4 PVCs for several times in a day. Additionally single PVCs were developed about 100 beats a day. When we assessed the origin of the PVCs we concluded that the PVCs had been originated from the basal inferior septal segments of right ventricular. Furthermore PVCs either as single or as ventricular run were presenting polymorphism and diversity in QRS morphology. At least four different morphologies of PVCs; either as single or in ventricular run; were observed. Moreover multiple notching of PVCs was remarkably eye-catching (Figure). Thereafter we performed a new TTE focusing on the right ventricle. Indeed the left ventricular dimensions and functions were normal. However we observed that right ventricle (RV) was slightly dilated at the basal level. RV was within normal limits at mid and apical segments with slightly thinned myocardial thickness. Then CMR was planned with the pre-diagnosis of arrhythmogenic right ventricular dysplasia. CMR revealed that the RV myocardium was thin and demonstrating the characteristics of arrhythmogenic RV dysplasia. Additionally basal segments of RV were dyskinetic during the periods of systole and diastole (Figure). Unfortunately, the patient did not accept the electrophysiologic study for stimulation and assessment for ventricular arrhythmia and also probability of intracardiac cardioverter defibrillator implantation.
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