Wandering permanent pacemaker generators in children: a case series

<p>Abstract</p> <p>Introduction</p> <p>Epicardial permanent pacemaker generators are implanted some times in the abdominal wall in pediatric age groups.</p> <p>Case presentation</p> <p>Three permanent epicardial pacemakers that migrated in an unusual manner producing intraabdominal complications are reported.</p> <p>Conclusion</p> <p>The different clinical presentations of pacemaker migration in the pediatric age groups are highlighted and a few suggestions are made for avoiding such a complication.</p

Failure of epicardial pacing leads in congenital heart disease: not uncommon and difficult to predict

AIMS: We evaluate the incidence of epicardial lead failure and try to identify risk factors in patients with congenital heart disease. METHODS: All patients with a congenital heart defect and an epicardial pacing system, implanted within a timeframe of 25 years, were included in this study. Patients' medical records and lead data were reviewed. Lead failure was defined as the primary endpoint. RESULTS: In total 198 active epicardial leads (atrial 40, ventricular 158) were implanted in 93 patients (median age at implantation 4.4 years (range 0-58.6)). During a total follow-up of 1235 lead-years, 29 lead failures (14.6%, 4 atrial, 25 ventricular) were documented in 22 patients (23.7%). Lead failure occurred at a median time period of 4.8 years (range 1.2-24.1) after implantation. Five-year freedom of lead failure was 88%. The only independent predictor for lead failure was the age at implantation (HR 0.44; 95%CI 0.20-0.97, p = 0.04), other characteristics failed to predict lead failure. Sudden cardiac death occurred in four patients (4.3%), in one a lead failure was documented. CONCLUSION: A high incidence of epicardial lead failures is found in patients with congenital heart disease. Unfortunately, it is difficult to predict this potentially life-threatening complication.status: publishe

Founder mutations in the Netherlands: SCN5a 1795insD, the first described arrhythmia overlap syndrome and one of the largest and best characterised families worldwide*

In this part of a series on founder mutations in the Netherlands, we review a Dutch family carrying the SCN5a 1795insD mutation. We describe the advances in our understanding of the premature sudden cardiac deaths that have accompanied this family in the past centuries. The mutation carriers show a unique overlap of long-QT syndrome (type 3), Brugada syndrome and progressive cardiac conduction defects attributed to a single mutation in the cardiac sodium channel gene SCN5a. It is at present one of the largest and best-described families worldwide and we have learned immensely from the mouse strains with the murine homologue of the SCN5a 1795insD mutation (SCN5a 1798insD). From the studies currently performed we are about to obtain new insights into the phenotypic variability in this monogenic arrhythmia syndrome, and this might also be relevant for other arrhythmia syndromes and the general population. (Neth Heart J 2009;17:422-8.).</p

Neonates born to mothers with preeclampsia exhibit sex-specific alterations in microvascular function

This study aimed to characterize early neonatal microvascular function after preeclamptic pregnancy with respect to infant sex and in utero growth. Peripheral microvascular blood flow was examined prospectively from 6 to 72 h of age using laser Doppler flowmetry in a cohort of term infants of normotensive women and women with late-onset preeclampsia. For male infants, those born to preeclamptic women had greater microvascular blood flow at 6 h (p < 0.05) with no change over time. Male infants of normotensive women exhibited increasing blood flow with time (p = 0.005). Female infants of preeclamptic mothers exhibited similar blood flow at 6 h of age to females of normotensive mothers, followed by significantly greater blood flow by 72 h (p < 0.001). Altered fetal microvascular structure and function in response to maternal preeclampsia may result in sexually dimorphic patterns of fetal growth and account for alterations in neonatal microvascular adaptation after birth