Complicated Pocket Infection in Patients Undergoing Lead Extraction: Characteristics and Outcomes.

Cardiac implantable electronic device (CIED) infection can present with pocket or systemic manifestations, both necessitating complete device removal and pathogen-directed antimicrobial therapy. Here, we aim to characterize those presenting with both pocket and systemic infection. A retrospective analysis of CIED extraction procedures included 300 patients divided into isolated pocket (n = 104, 34.7%), complicated pocket (n = 54, 18%), and systemic infection (n = 142, 47.3%) groups. The systemic and complicated pocket groups frequently presented with leukocytosis and fever > 37.8, as opposed to the isolated pocket group. Staphylococcus aureus was the most common pathogen in the systemic and complicated pocket groups (43.7% and 31.5%, respectively), while Coagulase-negative staphylococci (CONS) predominated (31.7%) in the isolated pocket group (10.6%, p < 0.001). No differences were observed in procedural success or complications rates. Kaplan-Meier survival analysis found that at three years of follow-up, the rate of all-cause mortality was significantly higher among patients with systemic infection compared to both pocket groups (p < 0.001), with the curves diverging at thirty days. In this study, we characterize a new entity of complicated pocket infection. Despite the systemic pattern of infection, their prognosis is similar to isolated pocket infection. We suggest that this special category be presented separately in future publications of CIED infections.

Occluded vein as a predictor for complications in non-infectious transvenous lead extraction.

Background: The use of cardiovascular implantable electronic device (CIED) is steadily increasing, and complications include venous occlusion and fractured leads. Transvenous lead extraction (TLE) can facilitate the re-implantation of new leads. Aims: This study aims to explore predictors and complications of non-infectious TLE. Methods: This study involves a retrospective analysis and comparison of characteristics, complications, and outcomes of patients with and without occluded veins (OVs) undergoing TLE at our center. Results: In total, eighty-eight patients underwent TLE for non-infectious reasons. Indications for TLE were lead malfunction (62; 70.5%) and need for CIED upgrade (22; 25%). Fourteen patients referred due to lead malfunction had an OV observed during venography. The OV group (36 patients) were significantly older (65.7 ± 14.1 vs. 53.8 ± 15.9, p = 0.001) and had more comorbidities. Ejection fraction (EF) was significantly lower for the OV group (27.5 vs. 57.5%, p = 0.001) and had a longer lead dwelling time (3,226 ± 2,324 vs. 2,191 ± 1,355 days, p = 0.012). Major complications were exclusive for the OV group (5.5% vs. none, p = 0.17), and most minor complications occurred in the OV group as well (33.3 vs. 4.1%, p < 0.001). Laser sheath and mechanical tools for TLE were frequently used for OV as compared to the non-occluded group (94.4 vs. 73.5%, respectively, p = 0.012). Procedure success was higher in the non-occluded group compared to the OV group (98 vs. 83.3%, respectively, p = 0.047). Despite these results, periprocedural mortality was similar between groups. Conclusion: Among the TLE for non-infectious reasons, vein occlusion appears as a major predictor of complex TLE tool use, complications, and procedural success. Venography should be considered prior to non-infectious TLE to identify high-risk patients.

Publisher Correction: Pyroglutamic acidosis as a cause for high anion gap metabolic acidosis: a prospective study.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Predictors of short-term mortality in patients undergoing a successful uncomplicated extraction procedure.

BACKGROUND: The prognosis of patients with untreated cardiac implantable electronic device (CIED) infection is poor. Whether removal of all leads by a successful transvenous lead extraction (TLE) procedure changes the prognosis is unclear. OBJECTIVE: To identify predictors of mortality in patients with CIED infection despite successful TLE. METHODS: Retrospective single-center analysis of prospectively collected database from consecutive patients undergoing TLE at our center. Predictors for mortality were identified and a score predicting high mortality rate was calculated. RESULTS: A total of 371 consecutive patients underwent TLE, of whom 337 (90.8%) had complete hardware removal. Most were extracted due to infectious causes (81.3%). Approximately one-third (35%) died during a mean follow-up of 1056 ± 868 days. There was significantly higher mortality observed in the infectious group. Multivariate logistic regression models for infectious group only identified creatinine and albumin measurements as risk markers for 30 days mortality (odds ratio [OR], 1.68; 95% confidence interval [CI], 1.19-2.38; P = .003 and OR, 0.4; 95% CI, 0.16-0.97; P = .039, respectively). A risk score was created based on cutoff values of creatinine ≥2md/dL (1 point) and albumin ≤3.5 g/dL (1 point). A value of 2 points predicted a 50% chance of 30-day mortality and a 75% chance of 1-year mortality (P < .0001 for both). CONCLUSIONS: Creatinine and albumin can be used as a combined risk score to successfully identify patients at risk of death despite undergoing a successful TLE procedure for infectious reasons. This score could help decision making when contemplating on conservative antibiotic treatment vs TLE.

Pyroglutamic acidosis as a cause for high anion gap metabolic acidosis: a prospective study.

5-oxoprolinemia (pyroglutamic acid, PGA) in the absence of acetaminophen use has been rarely reported as a cause for high anion gap metabolic acidosis. We investigated the prevalence and risk factors for elevated PGA concentrations among hospitalized patients with high anion gap metabolic acidosis: We prospectively enrolled patients with high anion gap metabolic acidosis hospitalized in the department of medicine. For each patient we collected the main diagnosis, concurrent medications and laboratory parameters. Spot urine samples were tested for PGA concentration. Levels ≥63 µmol/mmol creatinine were considered elevated. Overall, forty patients were prospectively followed. Mean age was 66.9 (17.9) years. Four (6.3%) patients had a high urine PGA level and demonstrated also lower blood pH (7.2 vs 7.3, p = 0.05) and lower serum lactate concentration (17.5 mg/dl vs 23.0 mg/dl, p = 0.04). Additionally, the high PGA level group consisted of more patients with septic shock [2/4 (50%) vs 3/36 (8.3%)] with a trend towards significance (p = 0.07). In conclusion, PGA might have a role in patients with septic shock and acidosis. Being a treatable condition, PGA should be taken into consideration particularly when no other cause for high anion gap is identified.

De novo and inherited SCN8A epilepsy mutations detected by gene panel analysis.

OBJECTIVES: To determine the incidence of pathogenic SCN8A variants in a cohort of epilepsy patients referred for clinical genetic testing. We also investigated the contribution of SCN8A to autism spectrum disorder, intellectual disability, and neuromuscular disorders in individuals referred for clinical genetic testing at the same testing laboratory. METHODS: Sequence data from 275 epilepsy panels screened by Emory Genetics Laboratory were reviewed for variants in SCN8A. Two additional cases with variants in SCN8A were ascertained from other testing laboratories. Parental samples were tested for variant segregation and clinical histories were examined. SCN8A variants detected from gene panel analyses for autism spectrum disorder, intellectual disability, and neuromuscular disorders were also examined. RESULTS: Five variants in SCN8A were identified in five individuals with epilepsy. Three variants were de novo, one was inherited from an affected parent, and one was inherited from an unaffected parent. Four of the individuals have epilepsy and developmental delay/intellectual disability. The remaining individual has a milder epilepsy presentation without cognitive impairment. We also identified an amino acid substitution at an evolutionarily conserved SCN8A residue in a patient who was screened on the autism spectrum disorder panel. Additionally, we examined the distribution of pathogenic SCN8A variants across the Nav1.6 channel and identified four distinct clusters of variants. These clusters are primarily located in regions of the channel that are important for the kinetics of channel inactivation. CONCLUSIONS: Variants in SCN8A may be responsible for a spectrum of epilepsies as well as other neurodevelopmental disorders without seizures. The predominant pathogenic mechanism appears to involve disruption of channel inactivation, leading to gain-of-function effects.