Pacemaker Syndrome: A Narrative Review

ABSTRACT

Since the first pacemaker implantation in 1958, cardiac pacing has transformed the management of bradyarrhythmias and conduction system disease. Despite major technological advances and the widespread use of dual‐chamber and biventricular pacing systems, pacemaker therapy may be complicated by pacemaker syndrome, a clinical entity resulting primarily from atrioventricular (AV) dyssynchrony. Pacemaker syndrome is characterized by a constellation of cardiovascular and neurologic symptoms including fatigue, dyspnea, dizziness, hypotension, palpitations, and neck pulsations. Although initially associated with single‐chamber ventricular pacing, it is now recognized that pacemaker syndrome can occur with any pacing modality when inappropriate timing between atrial and ventricular contractions exists. The underlying pathophysiology involves reduced ventricular preload, loss of atrial contribution to cardiac output, retrograde ventriculoatrial conduction, elevated atrial pressures, and abnormal baroreceptor and neurohormonal responses. These mechanisms lead to impaired hemodynamics and a wide spectrum of clinical manifestations, ranging from mild exercise intolerance to overt heart failure and syncope. The reported incidence varies widely, from 2% to 80%, depending on diagnostic criteria and pacing mode, with higher rates observed in ventricular‐paced systems. Diagnosis is primarily clinical and requires correlation of symptoms with device function and cardiac rhythm through pacemaker interrogation and electrocardiography. Management focuses on restoring AV synchrony by device reprogramming or upgrading to dual‐chamber pacing, along with guideline‐directed therapy for associated ventricular dysfunction. Early recognition and intervention are essential, as untreated pacemaker syndrome may lead to persistent ventricular dysfunction, atrial arrhythmias, reduced quality of life, and increased morbidity.