No abstract

As the number and complexity of cardiovascular implantable electronic devices has increased, so too has the incidence of device-related infections. Such a rise requires that the focus be directed toward developing universal standards for infected lead removal. To date, no consensus currently exists regarding the optimal management of patients with large vegetations (diameter > 2 cm). In these individuals, medical therapy is universally ineffective and they are often too ill for surgical extraction; furthermore, transvenous lead extraction (TLE) carries with it a risk of large septic pulmonary emboli. We present a series of five cases in which the AngioVac thrombectomy system (AngioDynamics Inc., Latham, NY, USA) was used as an adjunct to TLE. Debridement of infected leads prior to percutaneous lead extraction was accomplished as either a bridge to or as concomitant therapy with laser lead removal at our institution. This study included three males and two females with an average age of 52 years. The sizes of vegetations removed from leads ranged from 1.5 cm to 3.9 cm in the largest dimension and the average diameter was 2.65 cm ± 1.1 cm. The vegetations were successfully debulked in all five patients. This suggests that TLE performed with assistance from the AngioVac system (AngioDynamics Inc., Latham, NY, USA) is a safe and effective alternative to open surgical lead removal in patients with large lead vegetations.

In a diverse community-based population free of CVD and compared with normal rotation, clockwise rotation was associated with increased risk of all-cause and CVD mortality while counterclockwise rotation was associated with lower risk of all-cause mortality and non-significant association with CVD mortality. These findings call for attention to these often neglected ECG markers, and probably call for revising the current definition of normal rotation.

Background It is unclear if the location of implantation of the leadless pacemaker (LP) makes a difference in the incidence of pacing‐induced cardiomyopathy (PICM). Aim The aim of this study was to compare the incidence of PICM based on the location of implantation of LP. Methods A total of 358 consecutive patients [women: 171 (48%), mean age: 73 ± 15 years] with left ventricular ejection fraction (EF) > 50%, who received an LP (Micra) between January 2017 and June 2022, formed the study cohort. Micra‐AV and Micra‐VR were implanted in 122 (34%) and 236 (66%) patients, respectively. Fluoroscopically, the location of implantation of LP in the interventricular septum (IS) was divided into two equal halves (apex/apical septum [AS] and mid/high septum [HS]). During follow‐up, PICM was defined as an EF drop of ≥10%. Results LP was implanted in 109 (34%) and 249 (66%) patients at AS and HS locations, respectively. During a mean 18 ± 8 months follow‐up, 28 patients (7.8%) developed PICM. Among the 249 patients with HS placement of LP, 10 (4%) developed PICM, whereas among the 109 patients with AS placement of LP, 18 (16.5%) developed PICM (p = .002). AS location was associated with a higher risk of PICM compared to HS locations (adjusted hazard ratio: 4.42, p < .001). Conclusion AS location of LP was associated with a higher risk of PICM compared to HS placement. Larger randomized studies are needed to confirm our findings.

Ventricular tachycardia storm is associated with high mortality rates and is often refractory to treatment. Historically, few options for treatment have existed in cases when antiarrhythmic drugs fail. We report the case of a patient with incessant ventricular fibrillation (VF) in the postinfarction period that was triggered by premature ventricular contractions (PVCs) that persisted despite normal electrolytes, exclusion of ongoing ischemia, infusions of antiarrhythmic drugs, general anesthesia, full circulatory support with extracorporeal membranous oxygenation, and cardiac sympathetic denervation. Given that the VF appeared to be triggered consistently by a unifocal, short-coupled PVC (consistent with Purkinje fiber–mediated VF), we performed catheter ablation, after which point, the patient experienced no further PVCs or ventricular arrhythmia. This case serves as a reminder of three key teaching points. First, not all VF is created equal, with some cases being chiefly the result of a vulnerable substrate and others being best accounted for by frequent triggers. Second, examining the available electrocardiographic data and appropriately interpreting them can guide the selection of therapies up to and including catheter ablation for treatment-refractory VF. Third, full circulatory support greatly facilitates successful electroanatomic mapping and catheter ablation of unstable ventricular arrhythmias.