Several Boston Scientific pacemaker models have a known issue with intermittent oversensing of the minute ventilation sensor when paired with non-Boston Scientific leads. Several of our patients with these hybrid systems have had transient out of range impedances and oversensing after safety switching which we suspected may be related. A retrospective analysis of 395 patients who had pacemakers implanted between 2015-2017 found that transient out of range impedances with safety switching was present in 9% of Boston Scientific pacemakers paired with Abbott or Medtronic leads compared with 0% in other device-lead combinations (P = 0.0089).We postulate that the root cause of the minute ventilation oversensing and transient high impedance issue is the same, a header-lead interaction from low-level incompatibility. Recognizing this issue is critical to prevent unnecessary lead revisions or extractions as it can be prevented with a simple reprogramming of lead pace/sense configuration.

Background: The Nanostim {trade mark, serif} Leadless Cardiac Pacemaker (LCP) has been shown to be safe and effective in human clinical trials. Since there is little information on the effect of implant location on LCP performance, the aim of this study was to determine whether anatomic position affects the long-term pacing performance of the LCP. Methods: Patients who enrolled in the Leadless II IDE Clinical Trial and had finished 6 months follow up (n = 479) were selected for the study. The implanting investigators determined the LCP final position under fluoroscope, which was categorized into three groups: RV apex (RVA, n = 174), RV apical septum (RVAS, n = 101), and RV septum (RVS, n = 204) (Figure 1). Data on capture threshold (at a 0.4 ms pulse width), R-wave amplitude and impedance were analyzed at implant, hospital discharge and 2 weeks, 6 weeks, 3 months and 6 months post-implant. Results: At implant, the mean capture thresholds in the RVA, RVAS and RVS were 0.77 ± 0.45, 0.81 ± 0.61 and 0.78 ± 0.59 volts, respectively. R-wave amplitudes were 8.0 ± 3.0 mV, 7.7 ± 2.9 mV and 7.6 ± 2.9 mV, respectively. Impedance values were 727 ± 311, 765 ± 333, and 677 ± 227 respectively. There were no differences among the 3 implant locations in capture threshold or R-wave amplitudes at 6 months (P > 0.06); however, all 3 performance parameters significantly improved over time (P < 0.001). Conclusions: The LCP implant location does not affect capture thresholds or R-wave amplitudes at 6 months, and there is little effect on impedance. Although implant location does not appear to be a predictor of electrical performance, additional long-term data will help guide optimal implant location.

INTRODUCTION: Coronary artery aneurysms (CAAs) are rare (<1%) and are commonly associated with obstructive atherosclerotic disease. Giant CAAs are defined as dilatation of the coronary artery exceeding 20 mm in diameter. CAAs are associated with complications such as myocardial infarction, arrhythmia or sudden cardiac death. 1 CASE PRESENTATION: A 61 year-old Albanian male with a history of hypertension presented following an episode of syncope associated with lightheadedness, diaphoresis and nausea following a bowel movement. Upon presentation, vital signs were stable and physical exam was unremarkable. Initial laboratory testing showed eosinophilia and an elevated sedimentation rate. A transthoracic echocardiogram revealed an extracardiac thick-walled loculated cyst-like structure with partial compression of the left atrium and ventricle without hemodynamic compromise (EF of 55-60%). A CT of the chest revealed three well-circumscribed vascular masses with central vascular enhancement. The largest mass (5.3cm x 5.7cm x 10cm) was noted adjacent to the left atrium and ventricle in the course of the left circumflex artery (LCx). Cardiac catheterization showed three CAAs with possible arterio-venous fistulas. Cardiac MRI showed partially thrombosed LCx and RCA aneurysms and extensive mediastinal lymphadenopathy without any RV dysplasia noted. Given the loculated structure and eosinophilia, cardiac echinococcus was considered but the echinococcus antibody was negative. Rheumatological workup including ANA, p-ANCA and c-ANCA were negative. Surgical resection and repair of the LCx and RCA aneurysm along with quadruple coronary artery bypass grafting (CABG) was performed. Mediastinal lymph node biopsy was also performed but was negative for acid-fast bacilli or fungi or histo-pathological abnormality. Two post-operative incidents of sustained monomorphic ventricular tachycardiac (VT) were noted. Subsequently, an electro-physiology study performed which revealed inducible monomorphic VT. An implantable cardioverter defibrillator was placed for secondary prevention. DISCUSSION: Giant CAAs involving all three coronary arteries are extremely rare and have only been reported in one case report previously 1. The natural course of giant CAAs is unknown given the rarity of this pathology. Size of the aneurysm is usually not an indication for surgery. However, surgical correction is often performed due to the risk of lethal complications, as these aneurysms are often thrombosed. Surgical correction may include reconstruction or arterial ligation and CABG 1. Reconstruction was not feasible in this case given the markedly increased luminal diameters. CONCLUSIONS: Giant CAAs are often discovered incidentally on routine cardiac imaging. Cardiac catheterization and MRI are crucial in guiding the pre-surgical evaluation and planning.