Late-Onset Infection in a Leadless Pacemaker

Abstract

Infection of leadless pacemakers (LPM) is rare, even in patients at high risk for infections. Only 3 cases of LPM infection have been documented in the literature, all occurring within 1 month of device implantation. We report the first case, to our knowledge, of late-onset LPM infection, developing almost 2 years after implantation. (Level of Difficulty: Beginner.).

Keywords: ECG, electrocardiogram; LPM, leadless pacemaker; RBB, right bundle branch; cardiac implantable electronic device; infection; leadless pacemaker.

Graphical abstract

Figure 1

Comparative Images Showing the Anatomic Location of the Leadless Pacemaker and a Large Vegetation Attached to It (A) A right anterior oblique fluoroscopic view shows that the leadless pacemaker was implanted along the septomarginal trabeculation, at the base of the moderator band; white dots delineate the right ventricle and pulmonary root. (B) A transesophageal echocardiographic view of the corresponding sectional plane shows a large vegetation (1.4 × 0.8 cm) attached to the mid to distal part of the leadless pacemaker and extending toward the pulmonary valve. (C) An anatomic image shows the corresponding sagittal plane of the right ventricular outflow tract. (Illustration courtesy of UCLA Cardiac Arrhythmia Center, Wallace A. McAlpine MD Collection.)

Figure 2

The 12-Lead Electrocardiogram Before and After Leadless Pacemaker Infection, Suggesting Right Bundle Branch Injury Although the change is minor, the appearance of a positive notch within the QRS complex of V₁, indicative of a delay in right ventricular depolarization, may be caused by an infectious involvement of the right bundle branch in the setting of right ventricular septal pacing near the base of the moderator band. An alternative explanation for the notch would be that it represents a myocardial scar or anisotropic conduction in the setting of chronic or acute hemodynamic shifts, given that the V₁ voltage dropped from 14 mV to 10 mV and the P-wave developed a deeper negative deflection suggestive of a P-mitrale pattern. The electrocardiograms were recorded 9 months apart and, for the low- and high-pass filters, were set at 150 Hz and 0.05 Hz, respectively. Of note, the shift in precordial transition (V₅ preinfection vs V₄ during infection) seems to reflect only changes in the position of the leads, as this shift was not consistent across serial electrocardiograms.