Scenario: A 25-year-old man was referred from a cardiology clinic for an acute exacerbation of supraventricular tachycardia (SVT) during an exercise stress echocardiogram. He has a history of dilated cardiomyopathy (50% left ventricular ejection fraction [LVEF]), wall motion abnormalities, and long QT syndrome. In the clinic before admission, an SVT event was captured during an electrocardiogram (ECG) recording and resolved with a carotid sinus massage. The patient was fully conscious during the event. A few days later, he underwent an electrophysiology (EP) study with radio frequency ablation for atrioventricular reentrant tachycardia (AVRT). He was transferred to the cardiac step-down unit after the EP procedure, and his blood pressure was 94/56 mm Hg, heart rate 87/min, respiratory rate 21/min (regular), oxygen saturation 94% via room air, and body temperature 37 °C (99 °F). The 12-lead ECG below was taken 6 hours after admission to the unit.Normal sinus rhythm, frequent premature ventricular complexes (PVCs) in a quadrigeminy pattern, prolonged QTc interval.Generally, wide QRS complexes (>120 milliseconds) represent electrical activity that originates from the ventricles. Exceptions are aberrantly conducted supraventricular beats, preexcitation associated with an accessory pathway, bundle branch block, and electrolyte imbalance. Given the AVRT diagnosis with recent ablation treatment, these PVCs may be mistaken for preexcitations associated with an accessory pathway, especially as the PVC QRSs appear slurred (ie, “pseudo” delta wave), a characteristic associated with an accessory pathway. However, some features support PVC as the cause. First, the wide QRS complexes are premature, albeit only slightly at first glance. However, if calipers are used, or even on careful visual inspection, one can appreciate that these beats are indeed premature. In this case, the P waves fall just before the PVC but should not be confused with a delta wave. Furthermore, there is a complete compensatory pause after the PVCs because the timing of the sinus node is not interrupted. In contrast, a supraventricular beat (eg, aberrancy, premature atrial complex) would typically have a P wave before the QRS complex, and one would see an incomplete pause because these beats usually enter the sinus node and reset its timing.PVCs can be monomorphic, as in this case, or polymorphic (multiple QRS morphologies). Interestingly, the morphology of the PVC can be used to determine the ventricle of origin (ie, left or right) by examining lead V1. In this example, the morphology resembles a left bundle branch block (ie, negative wide QRS complex). This pattern indicates that the ectopic impulse is moving away from lead V1 and travels toward the left ventricle (ie, deep S wave). The QRS complex is wide because the ventricular impulse travels slowly from the right ventricle, outside the normal conduction system, to the left ventricle, slowing depolarization.Premature beats, including PVCs, can trigger reentrant tachyarrhythmias when an accessory pathway is present. Although PVCs were not documented as the source of the AVRT events in this patient, they are a likely source. This patient’s history of cardiomyopathy may be contributing to the occurrence of PVCs, which may also need to be treated with ablation. Considering that this patient has a prolonged QTc and other significant risk factors (postablation, AVRT, cardiomyopathy, and reduced EF), medications that prolong the QT/QTc should be closely reviewed and adjusted if necessary to prevent torsades de pointes. This patient was discharged home and was followed up by outpatient cardiology.