Shockwave Intravascular Lithotripsy Facilitated Transvenous Lead Extraction.

BACKGROUND: Dense calcifications encasing pacing leads with long dwell times are common and increase the difficulty of and risks associated with transvenous lead extraction procedures (TLE). Shockwave intravascular lithotripsy (IVL) focuses sound waves to fracture calcified tissue within a narrow radius to the catheter. OBJECTIVES: This study sought to assess the impact of Shockwave IVL pretreatment during extraction of long dwell time pacemaker and defibrillator leads. METHODS: Data were compiled retrospectively from patients undergoing TLE at Essentia Health in Duluth, Minnesota, from October 2019 to April 2023. IVL pretreatment was performed using currently available 7- and 8-mm balloons with ≤300 pulses delivered in close proximity to the leads via a retrograde approach, after which the procedure was completed as usual. RESULTS: Of the 120 patients undergoing TLE procedures, 55 were excluded from the study because the leads were freely mobile. Among the remaining 65 patients, 14 received IVL pretreatment. The median patient ages were similar at 67 (IQR: 63-76) years, with a lead dwell time of 10.7 (IQR: 6.9-14.9) years. The frequencies of diabetes, stroke, prior sternotomy, and lead types were not significantly different between the IVL and conventional groups. IVL pretreatment resulted in an average of 25 (IQR: 9-42) fewer minutes actively extracting leads (P = 0.007). CONCLUSIONS: These data represent the first known cases using Shockwave IVL as an adjunctive measure during extraction of high-risk and high-complexity leads, with a resulting significant reduction in the amount of time spent engaging in the highest-risk phase of the procedure.

Searching for NF-kappaB-based treatments of ischemia reperfusion injury.

When a tissue becomes ischemic, a host of changes occur at the cellular level that lead to a shift in transcriptional activity of many inflammatory and cytoprotective compounds, a process which is extensively controlled through a family of transcription factors known as nuclear factor kappa-B (NF-kappaB). This shift in activity paradoxically results in both a cytoprotective effect at the cellular level and upon reperfusion, a generally destructive inflammatory response, a phenomenon referred to as ischemia reperfusion (IR) injury. To date, a number of methods of modifying the activity of NF-kappaB through either physiologic or pharmacologic manipulation have been developed and studied in animal models of IR injury and in some cases in human clinical trials. Nearly every method of NF-kappaB antagonism has demonstrated a discrete protective effect allowing investigators to reduce myocardial infarct sizes by 60% and cerebral infarct sizes by 57% relative to untreated control animals. The problem of IR injury is all too common and represents a discrete threat not only to the tissues directly involved in the ischemic event, but also to distal sites as well as is seen in the evolution of acute respiratory distress and severe inflammatory response syndromes. In the course of this review, the nature of NF-kappaB and its involvement in IR injury is examined along with the efficacy of the various NF-kappaB-based investigational treatment developed to date.