Atrial premature beats (APBs), also referred to as atrial or supraventricular extrasystoles, represent premature atrial depolarization occurring earlier than the next expected regular sinoatrial activation, usually from a site outside the sinus node. Premature depolarizations originating from the atrioventricular node or His bundle are termed atrioventricular junctional premature beats. In general, APBs occur in adults of any age, with or without structural heart disease. Increased atrial volume and/or pressure, or increased sympathetic tone are associated with increased frequency of APBs, while in individuals without structural heart disease APBs often originate from the pulmonary veins and may precipitate atrial fibrillation. Patients with APBs are often asymptomatic, or experience palpitations, dizziness, or even presyncope. Significant haemodynamic compromise due to APBs is uncommon. Physical examination may reveal pulse irregularity, and surface electrocardiograms (ECGs) usually show premature P waves which differ from the sinus P morphology, followed by a normal, shortened, or prolonged PR interval (depending on the APB site of origin) and narrow QRS complex. Ambulatory ECG (Holter) monitoring helps to establish the diagnosis when symptoms are sporadic or to quantify the frequency of APBs. Counselling and reassurance would suffice in most minimally symptomatic or asymptomatic patients with APBs, but any underlying cardiovascular disorder must be treated. Beta blockers or class III antiarrhythmic drugs (or class IC in patients without significant structural heart disease) can be used to attenuate symptoms or suppress the APBs facilitating other tachyarrhythmias. Catheter ablation could be considered in selected patients.
Ventricular tachycardia ablation in structural heart disease: Impact of ablation strategy and non-inducibility as an end-point on long term outcome
