Abstract 2971: Managed Ventricular Pacing In Pediatric Patients And Patients With Congenital Heart Disease

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Jonathan R Kaltman ◽  
Pamela Ro ◽  
Frank Zimmerman ◽  
Jeffrey P Moak ◽  
Michael Epstein ◽  
...  

Introduction: Ventricular dyssynchrony induced by ventricular pacing (VP) may predispose patients (pts) to congestive heart failure. The detrimental effects of VP are directly related to the cumulative percentage of VP (Cum%VP). Managed ventricular pacing (MVP, Medtronic) is a novel pacing algorithm developed to minimize unnecessary VP by uncoupling atrial pacing from VP. The use, efficacy, and safety of MVP in pediatrics pts and pts with congenital heart disease (CHD) have not been described. Methods: A multicenter review evaluated all pediatric pts < 22 years old and older pts with CHD that had an implanted device using an MVP algorithm. Primary outcome variables were Cum%VP and adverse events. A subgroup analysis evaluated pts that had a DDD/R pacemaker prior to MVP device with similar low pacing rate and compared Cum%VP before and after initiation of MVP, using Wilcoxon signed-rank test. Results: 62 patients from 6 centers were included for the review (see table ). Mean age at MVP device implant was 21.5 ± 9.6 years (range 7–51). 63% of pts had CHD. With MVP device, mean Cum%VP was 4.3 ± 14.6% (range 0 – 83.7). By pacing indication, Cum%VP was 2.9 ± 6.5% in pts with sinus node dysfunction (n = 24), 34.8 ± 41.3% in pts with atrioventricular (AV) block (n = 5), and 0.6 ± 1.0% in pts with an ICD (n = 33). 11 patients were eligible for subgroup analysis. With DDD/R pacing, mean low rate was 64 ppm and mean paced/sensed AV intervals were 251 and 241 ms. With MVP, mean low rate was 63 ppm and mean paced/sensed AV intervals were 193 and 166 ms. Compared to DDD/R, Cum%VP significantly decreased with MVP (67.1 ± 29.4 vs. 9.2 ± 24.8%; p < 0.005). One MVP-related adverse event occurred: a pt with intermittent AV block had symptoms with nonconducted atrial beats and was reprogrammed to DDD. Conclusions: MVP can be used safely and can significantly reduce unnecessary ventricular pacing in pediatric pts and pts with CHD. MVP should be considered when choosing a pacing mode for this pt population.

2005 ◽  
Vol 289 (6) ◽  
pp. H2387-H2391 ◽  
Author(s):  
Ferdinando Iellamo ◽  
Alberto Galante ◽  
Jacopo M. Legramante ◽  
Maria Enrichetta Lippi ◽  
Claudia Condoluci ◽  
...  

We tested the hypothesis that individuals with Down syndrome, but without congenital heart disease, exhibit altered autonomic cardiac regulation. Ten subjects with Down syndrome (DS) and ten gender-and age-matched healthy control subjects were studied at rest and during active orthostatism, which induces reciprocal changes in sympathetic and parasympathetic traffic to the heart. Autoregressive power spectral analysis was used to investigate R-R interval variability. Baroreflex modulation of sinus node was assessed by the spontaneous baroreflex sequences method. No significant differences between DS and control subjects were observed in arterial blood pressure at rest or in response to standing. Also, R-R interval did not differ at rest. R-R interval decreased significantly less during standing in DS vs. control subjects. Low-frequency (LFNU) and high-frequency (HFNU) (both expressed in normalized units) components of R-R interval variability did not differ between DS and control subjects at rest. During standing, significant increase in LFNU and decrease in HFNU were observed in control subjects but not in DS subjects. Baroreflex sensitivity (BRS) did not differ between DS and control subjects at rest and underwent significant decrease on going from supine to upright in both groups. However, BRS was greater in DS vs. control subjects during standing. These data indicate that subjects with DS exhibit reduced HR response to orthostatic stress associated with blunted sympathetic activation and vagal withdrawal and with a lesser reduction in BRS in response to active orthostatism. These findings suggest overall impairment in autonomic cardiac regulation in DS and may help to explain the chronotropic incompetence typically reported during exercise in subjects with DS without congenital heart disease.


1999 ◽  
Vol 10 (3) ◽  
pp. 351-357 ◽  
Author(s):  
CHRISTOPHER L. JOHNSRUDE ◽  
CARL L. BACKER ◽  
BARBARA J. DEAL ◽  
JANETTE F. STRASBURGER ◽  
CONSTANTINE MAVROUDIS

Open Heart ◽  
2020 ◽  
Vol 7 (2) ◽  
pp. e001374
Author(s):  
Benjamin M Moore ◽  
Caroline Medi ◽  
Mark A McGuire ◽  
David S Celermajer ◽  
Rachael L Cordina

ObjectivesLong-term single-site ventricular pacing may adversely affect ventricular function, due to dyssynchronous systemic ventricular contraction. We sought to determine the incidence, predictors and outcomes of pacing-associated cardiomyopathy (PACM) in an adult congenital heart disease (ACHD) cohort.MethodsWe retrospectively identified all patients in our database with a permanent pacemaker from 2000 to 2019. Patients were followed for the primary endpoint of unexplained decline in systemic ventricular function (PACM) and the secondary endpoint of heart failure admission.ResultsOf 2073 patients in our database, 106 had undergone pacemaker implantation. Over a median follow-up of 9.4 years, 25 patients (24%) developed PACM, but only in those with ventricular pacing percentage (VP%) ≥70%; PACM occurred in 0% of those with VP <70% and 47% of those with VP ≥70% (p<0.001). High-burden ventricular pacing (≥70%) remained predictive of PACM in transposition of the great arteries, tetralogy of Fallot and complex biventricular repair subgroups, but not in Fontan patients. Those with PACM were more likely to be admitted with heart failure (44% vs 15%, p=0.002). Cardiac resynchronisation therapy (CRT) upgrade was performed in 11 patients, with 9 responders (82%).ConclusionsIn a cohort of patients with ACHD followed long-term post-pacing, 24% developed cardiomyopathy that was significantly associated with a higher burden of ventricular pacing (VP ≥70%). Given promising response rates to CRT, patients with ACHD expected to pace in the ventricle should be closely monitored for systemic ventricular decline.


2018 ◽  
Author(s):  
Min Zhang ◽  
Yue Gu ◽  
Mu Su ◽  
Shumei Zhang ◽  
Chuangeng Chen ◽  
...  

AbstractVentricular septal defect (VSD) is one of the most common types of congenital heart disease. To find more and more molecular alteration is conducive to explore the mechanism and biomarker in VSD. Herein we devised a predictive strategy to uncover novel lncRNA of VSD integrating DNA methylation, gene expression and lncRNA expression of early embryo and VSD by profiles from GEO database. In totally, 175 lncRNAs, 7290 genes and 3002 DNA methylation genes were obtained by logistic regression analysis associated with embryonic development. Moreover, 7304 DMGs were significant differential methylated by Wilcoxon rank test and Student’s test in VSD. We constructed the lncRNA-mRNA co-expression network in embryo (LMCNe). Then, a reconstructed co-expression weighted network (RCWN) was built integrated LMCNe and the DNA methylation associated network (DMAN) based on the correlation of the DNA methylation level and protein interaction network between embryonic development and VSD. We extracted top 10 lncRNAs with higher score performing DRaWR from the weight network, which as potential VSD related lncRNAs. Six lncRNAs showed a high level of expression in the heart tissue recorded in the NONOCOND database. Furthermore, associated lncRNA genes DCAF8L1, NIT1, SH2D7 and DOCK9-AS2 in validated samples showed a prominently association with VSD. These outcomes provide a reference for lncRNA involved in VSD initialization and a new insight for studies of VSD-associated lncRNAs.Author SummaryVentricular septal defect (VSD) is one of the most common types of congenital heart disease and has a high mortality rate in infants. Many molecular markers have proved effective as biomarker in VSD like DNA methylation and lncRNA. lncRNA is a type of non-coding RNA which has important effect in regulation gene expression and disease occurrence. VSD is an embryonic stage developmental disease. Therefore we hypothesized that lncRNA which was associated with DNA methylation and mRNA in early embryonic development may also affect the occurrence of VSD. So in this work, from the perspective of embryonic development, we devised a predictive strategy to uncovering novel lncRNA of VSD. In our result, four lncRNA associated genes were found differential expressed in VSD and normal samples by qPCR validation. The identification of lncRNA associated with ventricular septal defect is beneficial to further study the mechanism of VSD from the molecular level and also provides a good molecular marker for clinical therapeutic and diagnosis. At the same time, it also provides a new insight for the researches of lncRNA associated with VSD.


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