Impact of Leadless Pacemaker Therapy on Cardiac and Atrioventricular Valve Function Through 12 Months of Follow-Up

Endocardial pacemaker leads and right ventricular (RV) pacing are well-known causes of tricuspid valve, mitral valve, and cardiac dysfunction. Lead-related adverse consequences can potentially be mitigated by leadless pacemaker (LP) therapy by eliminating the presence of a transvalvular lead. This study assessed the impact of LP placement on cardiac and valvular structure and function.

Echocardiographic studies before and 12±1 months after LP implantation were performed between January 2013 and May 2018 at our center and compared with age- and sex-matched controls of dual-chamber transvenous pacemaker recipients.

A total of 53 patients receiving an LP were included, of whom 28 were implanted with a Nanostim and 25 with a Micra LP device. Tricuspid valve regurgitation was graded as being more severe in 23 (43%) patients at 12±1 months compared with baseline ( P<0.001). Compared with an apical position, an RV septal position of the LP was associated with increased tricuspid valve incompetence (odds ratio, 5.20; P=0.03). An increase in mitral valve regurgitation was observed in 38% of patients ( P=0.006). LP implantation resulted in a reduction of RV function, according to a lower tricuspid annular plane systolic excursion ( P=0.003) and RV tricuspid lateral annular systolic velocity ( P=0.02), and a higher RV Tei index ( P=0.04). LP implantation was further associated with a reduction of left ventricular ejection fraction ( P=0.03) and elevated left ventricular Tei index ( P=0.003). The changes in tricuspid valve regurgitation in the LP group were similar to the changes in the dual-chamber transvenous pacemaker control group (43% versus 38%, respectively; P=0.39).

LP therapy is associated with an increase in tricuspid valve dysfunction through 12 months of follow-up; yet it was comparable to dual-chamber transvenous pacemaker systems. Furthermore, LP therapy seems to adversely impact mitral valve and biventricular function.