A case of prolonged atrial pacing latency.
Ontology highlight
ABSTRACT:
SUBMITTER: Tanabe J
PROVIDER: S-EPMC7501926 | biostudies-literature | 2020 Aug
REPOSITORIES: biostudies-literature
Publications
A case of prolonged atrial pacing latency.
Tanabe Junya J Fujita Sayuri S Watanabe Nobuhide N Tanabe Kazuaki K
European heart journal. Case reports 20200728 4
Similar Datasets
Project description:Sustained atrial tachycardia leads to multiple molecular and cellular effects collectively defined as atrial tachycardia remodeling (ATR). ATR is thought to play a major role in the self-perpetuating nature of atrial fibrillation (AF) and has been a subject of intense research in large mammalian models of AF. Recently, rodents are increasingly used to gain insight on the pathophysiology AF. However, little is known regarding the effects of rapid pacing on the atria of rats and mice mainly due to technical challenges in electrophysiological studies of unanesthetized rodents. Using an implantable device for electrophysiological studies in unanesthetized rodents we examine, on a daily basis, the effects of continuous rapid atrial pacing (RAP) for at least 4 consecutive days on the developed AF substrate of Sprague-Dawley rats and C57BL6 mice. AF induction protocol consisted 10 aggressive bursts (20 seconds, double diastolic threshold, 10 ms cycle length [CL]). This protocol failed to induce AF at baseline in both species, but repeatedly induced AF episodes in rats following 2 days of sustained RAP. Microarray study of left atrial tissue from rats exposed for 2 days to RAP (70 ms CL) vs control pacing (140 ms CL) identified 304 differentially expressed genes (155 upregulated and 149 downregulated). Real-time qt-PCR confirmed the validity of the microarray. Enrichment analysis and comparison with a dataset of atrial tissue from AF patients revealed indications of increased carbohydrate metabolism, and changes in pathways that are thought to have critical role in human AF including TGF-beta and IL-6 signaling. Among 19 commonly affected genes in comparison with human AF, downregulation of FOXP1 and upregulation of the KCNK2 gene encoding the Kir2.1 potassium channel were conspicuous finding suggesting NFAT activation. Further results in line with NFAT activation included reduced expression of MIR-26, MIR-101, which were linked to upregulation of the KCNK2 in human AF. Our results demonstrate electrophysiological evidence for AF promoting effects of RAP in rats and some important molecular similarities between the effects of RAP in large and small mammalian models. The effects of atrial tachypacing are well documented in large mammals but very little is know regarding the effects of tacypacing on the rodent atria.
2019-08-01 | GSE126711 | GEO
Project description:BackgroundAtrial fibrillation (AF) is a common arrhythmia in patients with hypertrophic cardiomyopathy (HCM) and can deteriorate haemodynamic status.Case summaryWe report a case of a 77-year-old woman with cardiogenic shock due to paroxysmal AF, complicated with HCM and aortic stenosis. Atrial fibrillation was successfully managed with temporary atrial pacing and administration of nifekalant hydrochloride without invasive mechanical circulatory support until surgery. Septal myectomy, aortic valve replacement, and pulmonary vein isolation were performed.DiscussionThis case suggests that atrial pacing and nifekalant may be safe and effective for rhythm control.
| S-EPMC7319856 | biostudies-literature
Project description: Not available
| S-EPMC1767518 | biostudies-literature
Project description:BackgroundIt is unknown whether atrial fibrillation (AF) burden varies by pacing site in patients with reactive atrial antitachycardia pacing (rATP). We aimed to compare AF burden in patients with high atrial septal pacing (HASp) via delivery catheter and right atrial appendage pacing (RAAp) in patients with sick sinus syndrome (SSS).MethodsWe retrospectively identified 109 patients with a history of paroxysmal AF and SSS who had received dual-chamber pacemaker implantation between January 2017 and December 2019, of whom 39 and 70 patients had HASp and RAAp, respectively. rATP was initiated after a 1-month post-implantation run-in period.ResultsPatients with HASp had a significantly shorter P-wave duration during atrial pacing than those with RAAp (99.3 ± 10.4 vs. 116.0 ± 14.3 ms, p < .001). During the 3-year follow-up period, the incidence of an AF lasting longer than 1 or 7 days was significantly lower (hazard ratio [HR], 0.45; p = .016; HR, 0.24; p = .004) than in those with RAAp. The median time of AF/AT per day in the follow-up periods was significantly shorter in the HASp group than in the RAAp group (10 vs. 18 min/day, p = .018). Atrial lead division did not occur in the HASp group during the follow-up period.ConclusionsHASp via delivery catheter is as safe as RAAp, and HASp combined with rATP is effective for reducing AF burden in patients with SSS and paroxysmal AF.
| S-EPMC10407182 | biostudies-literature
Project description:BackgroundReactive atrial-based antitachycardia pacing (rATP) aims to terminate atrial tachyarrhythmia/atrial fibrillation (AT/AF) episodes when they spontaneously organize to atrial flutter or atrial tachycardia; however, its effectiveness in the real-world has not been studied. We used a large device database (Medtronic CareLink, Medtronic, Minneapolis, MN, USA) to evaluate the effects of rATP at reducing AT/AF.MethodsPacemaker, defibrillator, and resynchronization device transmission data were analyzed. Eligible patients had device detected AT/AF during a baseline period but were not in persistent AT/AF immediately preceding first transmission. Note that 1:1 individual matching between groups was conducted using age, sex, device type, pacing mode, AT/AF, and percent ventricular pacing at baseline. Risks of AT/AF events were compared between patients with rATP-enabled versus control patients with rATP-disabled or not available in the device. For matched patients, AT/AF event rates at 2 years were estimated by Kaplan-Meier method, and hazard ratios (HRs) were calculated by Cox proportional hazard models.ResultsOf 43,440 qualifying patients, 4,203 had rATP on. Matching resulted in 4,016 pairs, totaling 8,032 patients for analysis. The rATP group experienced significantly lower risks of AT/AF events lasting ≥1 day (HR 0.81), ≥7 days (HR 0.64), and ≥30 days (HR 0.56) compared to control (P < 0.0001 for all). In subgroup analysis, rATP was associated with reduced risks of AT/AF events across age, sex, device type, baseline AT/AF, and preventive atrial pacing.ConclusionsAmong real-world patients from a large device database, rATP therapy was significantly associated with a reduced risk of AT/AF. This association was independent of whether the patient had a pacemaker, defibrillator, or resynchronization device.
| S-EPMC6850031 | biostudies-literature
Project description:Left atrial tissue of rats exposed to rapid atrial pacing
| PRJNA523021 | ENA
Project description:AimThe self-perpetuating nature of atrial fibrillation (AF) has been a subject of intense research in large mammalian models exposed to rapid atrial pacing (RAP). Recently, rodents are increasingly used to gain insight into the pathophysiology of AF. However, little is known regarding the effects of RAP on the atria of rats and mice. Using an implantable device for electrophysiological studies in rodents, we examined on a daily basis, the effects of continuous RAP on the developed AF substrate of unanesthetized rats and mice.Methods and resultsAggressive burst pacing did not induce AF at baseline in the large majority of rodents, but repeatedly induced AF episodes in rats exposed to RAP for more than 2 days. A microarray study of left atrial tissue from rats exposed to RAP for 2 days vs. control pacing identified 304 differentially expressed genes. Enrichment analysis and comparison with a dataset of atrial tissue from AF patients revealed indications of increased carbohydrate metabolism and changes in pathways that are thought to play critical roles in human AF, including TGF-beta and IL-6 signaling. Among 19 commonly affected genes in comparison with human AF, downregulation of FOXP1 and upregulation of the KCNK2 gene encoding the Kir2.1 potassium channel were conspicuous findings, suggesting NFAT activation. Further results included reduced expression of MIR-26 and MIR-101, which is in line with NFAT activation.ConclusionOur results demonstrate electrophysiological evidence for AF promoting effects of RAP in rats and several molecular similarities between the effects of RAP in large and small mammalian models.
| S-EPMC6763969 | biostudies-literature
Project description:BackgroundThe use of transvenous pacing leads is associated with the risk of developing tricuspid valve (TV) dysfunction. This develops through several mechanisms including the failure of leaflet coaptation or direct damage to the TV or to its sub-valvular apparatus and can result in significant tricuspid regurgitation (TR). Multiple approaches to pacemaker implantation after transvenous lead extraction (TLE) or surgical TV repair have been described. Placement of pacing leads across the TV is generally avoided in such circumstances.Case summaryA 66-year-old woman presented with a year-long history of exertional dyspnoea, peripheral oedema, and postural neck pulsations. Her medical history included a dual-chamber pacemaker implantation for sinus node dysfunction 14 years ago. Echocardiography revealed severe lead-related TR. Her case was discussed in our multi-disciplinary team meeting. A decision was made to perform a TLE and implant a leadless pacemaker in an attempt to avoid open-heart surgery if possible. This was reserved as an option in the event of persistent severe TR. Transvenous extraction of the right ventricular lead was performed. The atrial lead was preserved and connected to and AAI device. A Micra AV was implanted allowing for atrioventricular (AV) synchronous pacing.DiscussionWe present the first case of successful implementation of AV sequential pacing using a dual-pacemaker approach involving the use of an AAI pacemaker and a Micra AV device. This was performed after TLE for severe lead-related TR.
| S-EPMC8343438 | biostudies-literature
Project description:ObjectiveIonic remodeling has a close correlation with the occurrence of atrial fibrillation (AF). Atrial tachypacing remodeling is associated with characteristic ionic remodeling. The purpose of this study was to assess the efficacy of cilostazol, an oral phosphodiesterase 3 inhibitor, for preventing atrial ionic remodeling in long-term rapid atrial pacing (RAP) dogs.MethodsWe use the methods of patch-clamp and molecular biology to investigate the effect of cilostazol on ion channel and channel gene expression in long-term RAP dogs. Twenty-one dogs were randomly assigned to sham, control paced, and paced+cilostazol (5 mg/kg/d, cilo) groups, with 7 dogs in each group. The sham group was instrumented with a pacemaker but without pacing. RAP at 500 beats/min was maintained for 2 weeks in the paced and cilo groups. During the pacing, cilostazol was given orally in the cilo group. Whole-cell patch-clamp technique was used to record atrial L-type Ca2+ (ICaL) and fast sodium channel (INa) ionic currents. Western blot and RT-PCR were applied to estimate the gene expression of the ICaLα) 1C (Cav1.2) and INav1.5α) Nav1.5α) subunits. Statistical analysis was performed using SPSS 13.0.ResultsThe density of ICaL and INa currents (pA/pF) was significantly reduced in the paced group (ICaL: -6.55±1.42 vs. -4.46±0.59 pA/pF; INa: -48.24±10.54 vs. -30.48±5.20 pA/pF, p<0.01). The paced+cilo group could not increase the density of ICaL currents (ICaL: -4.37±1.25 pA/pF, p>0.05), while the INa currents were recovered (-44.54±12.65 pA/pF, p<0.01) compared with the paced group. The mRNA and protein expression levels of Cav1.2 and Nav1.5α were apparently down-regulated in the paced group (p<0.01), but after cilostazol treatment, both of these subunits were up-regulated significantly (p<0.01).ConclusionCilostazol may have protective effects on RAP-induced atrial ionic remodeling.
| S-EPMC5368467 | biostudies-literature
Project description:BackgroundThe mouse is the most widely used mammal in experimental biology. Although many clinically relevant in vivo cardiac stressors are used, one that has eluded translation is long-term cardiac pacing. Here, we present the first method to chronically simulate and simultaneously record cardiac electrical activity in conscious mobile mice. We then apply it to study right ventricular pacing induced electromechanical dyssynchrony and its reversal (resynchronization).Methods and resultsThe method includes a custom implantable bipolar stimulation and recording lead and flexible external conduit and electrical micro-commutator linked to a pulse generator/recorder. This achieved continuous pacing for at least 1 month in 77% of implants. Mice were then subjected to cardiac ischemia/reperfusion injury to depress heart function, followed by 4 weeks pacing at the right ventricle (dyssynchrony), right atrium (synchrony), or for 2 weeks right ventricle and then 2 weeks normal sinus (resynchronization). Right ventricular pacing-induced dyssynchrony substantially reduced heart and myocyte function compared with the other groups, increased gene expression heterogeneity (>10 fold) comparing septum to lateral walls, and enhanced growth and metabolic kinase activity in the late-contracting lateral wall. This was ameliorated by restoring contractile synchronization.ConclusionsThe new method to chronically pace conscious mice yields stable atrial and ventricular capture and a means to dissect basic mechanisms of electromechanical physiology and therapy. The data on dyssynchrony and resynchronization in ischemia/reperfusion hearts is the most comprehensive to date in ischemic heart disease, and its similarities to nonischemic canine results support the translational utility of the mouse.
| S-EPMC6513021 | biostudies-literature