LAUSR

Pacing ‐ induced cardiomyopathy (PICM), or development of left ventricular systolic dysfunction secondary to right ventricular (RV) pacing, is increasingly recognized as an important cause of heart failure. 1 PICM is most commonly defined as a decrease in left ventricular ejection fraction (LVEF) of ≥ 10% resulting in LVEF < 50% following pacemaker implantation in the absence of an alternative cause. 1 PICM is thought to arise from electrical and mechanical dyssynchrony secondary to nonphysiologic ventricular activation. For unclear reasons, PICM affects only a minority of individuals exposed to a critical threshold of RV pacing (roughly ≥ 20%), 2,3 with an overall PICM incidence of 10% – 20% at 5 – 10 years. 1,4 Prior studies have identified risk factors for PICM including older age, male sex, wider native QRS duration, wider paced QRS duration, RV pacing burden, and lower preimplant LVEF (even within the normal range). 1 Early work suggested that an apical transvenous RV lead position may be associated with greater PICM risk versus a septal lead position, 5 although this finding was subsequently refuted by multiple studies. 2,6,7 Recently, leadless pacemakers (LP) have emerged as an alternative to transvenous devices, offering lower complication rates for patients who do not require atrial pacing, such as those with long ‐ standing persistent atrial fibrillation (AF). 8 Limited data exist regarding risk of PICM after LP, although one small study suggests PICM incidence may be lower. 9 Furthermore, it is unclear whether anatomic location of LP implant may affect PICM incidence.