Outflow tract ventricular arrhythmias: When and how to treat?

Abstract

In the 1970s, many studies demonstrated that premature ventricular contractions (PVCs) were associated with up to a 3-fold increase in mortality in patients with prior myocardial infarction [1,2]. In subsequent decades, several large series also demonstrated that even in apparently healthy people, this association is still present [3]. When more detailed analysis focuses on specific characteristics of PVCs, the association becomes more nuanced. A study of exerciseinduced PVCs demonstrated that patients with RBBB or multiple-morphology PVCs had increased mortality, but patients with an LBBB morphology alone had unchanged mortality [4]. In this issue of Trends in Cardiovascular Medicine, Lerman [5] reviews the current understanding of outflow tract (OT) arrhythmias. Much of this information has come from his own elegant work. As he notes in his review, OT PVCs have often been considered benign: as these idiopathic arrhythmias usually have a LBBB morphology, this may account for the more benign implications of LBBB PVCs. However, OT arrhythmias may cause significant morbidity. When patients present with OT arrhythmias, their symptoms, PVC burden, and left ventricular function should drive decisions about therapy. Patients may have palpitations from isolated ectopy or more sustained episodes. Fatigue or exercise intolerance may also occur due to relative bradycardia: premature ventricular “contractions” often result in very little actual contraction of the ventricle, and patients in bigeminy may have an effective pulse rate that is half the electrical heart rate. Sustained arrhythmias can result in presyncope or syncope. In this setting, the patient should be carefully evaluated for more malignant episodes. OT PVCs can rarely serve as triggers for polymorphic VT and VF, and PVC suppression can prevent recurrent episodes [6].