### Learning objectives Premature ventricular complexes (PVCs) are the most common arrhythmias in daily practice. At the cellular level, ventricular myocytes spontaneously depolarise to create an extrasystole ‘out of sync’ with the cardiac cycle.1 The prevalence depends on the characteristics and comorbidities of the population, the method by which the population is studied and the duration of observation. PVCs have been described in 1% of clinically normal people on standard electrocardiography (EKG) and 40%–75% of healthy people assessed by short-term ambulatory monitoring.2 Atherosclerosis Risk in Communities, a large population-based study of 15 792 Americans aged 45–65 years, demonstrated a higher prevalence of PVCs with age, structural heart disease (SHD), hypertension, African–American ethnicity, male sex and lower education.3 PVCs are generally benign in patients without SHD.4 5 However, PVCs can be a trigger for life-threating arrhythmias such as ventricular tachycardia (VT) and ventricular fibrillation (VF) causing sudden cardiac death (SCD), especially in patients post-myocardial infarction (MI). Risk stratification for PVCs varies in specific populations with underlying cardiac disease, family history, genetic variants and sometimes coupling interval. The differing implications with these variables is the basis of this review. The symptoms of PVCs are variable. Patients often have palpitations described as fluttering, pounding, skipping beats or often a strange sensation in the neck. Others may have fatigue, shortness of breath or change of stamina and endurance. The increased stroke volume of the post-PVC beat may cause chest discomfort. Non-sustained or sustained episodes of VT may be associated with presyncope or syncope. In contrast, many patients are …