Clinical application of pacemakers in atrial tachyarrhythmias

The diagnostic programmes of modern pacemakers have increased our knowledge of atrial tachyarrhythmias (ATAs) in chronically paced patients. These programmes also support the evaluation of the effects of pharmacological treatment of ATAs. The success of interruption and/or prevention of ATAs with pacemakers depends strongly on the diagnostic accuracy and the properties of the pacing algorithms, their individual programming and the site and configuration of the pacing leads. Atrial septum pacing can be beneficial in patients with paroxysmal atrial fibrillation and prolonged P wave duration. Recent large-scale studies on preventive and interruptive atrial pacing of ATAs show modestly positive or no results. Therefore, atrial pacing therapy for ATAs should be considered cautiously, serving as an adjuvant to pharmacological treatment rather than as a primary intervention. This also applies for pacing interventions for ATAs in cardiac resynchronisation therapy. The pacemaker algorithms for the detection of ATAs and atrial lead configuration are crucial for the success of pacemaker-mediated prevention or interruption of ATAs. The success of these interventions is dependant on future improvements of pacemaker technology. (Neth Heart J 2008;16 (suppl 1): S20-S24.)     

Percutaneous left atrial appendage closure for stroke prevention in atrial fibrillation

Background

Percutaneous left atrial appendage (LAA) closure can be an alternative to coumadin treatment in patients with atrial fibrillation (AF) at high risk for thromboembolic events and/or bleeding complications. We report the initial experience with this new technique.

Methods

Patients were eligible if they had AF with a high stroke risk (CHADS₂ score >1), and/or contraindication for coumadin therapy. The procedure was performed under general anaesthesia, using biplane fluoroscopy and (3D) transoesophageal echocardiography (TEE) guidance. Patients were discharged on coumadin until a TEE was repeated at 45 days after closure to evaluate LAA occlusion. If LAA occlusion was achieved, oral anticoagulation was discontinued and aspirin started.

Results

Percutaneous LAA closure was performed in 10 patients (50% male, age 61.6 ± 9.6 years). The median CHADS₂ score was 3 (range 2–4), median CHA₂DS₂-VASc score 3.5 (range 2–6) and HAS-BLED score 1.5 (range 1–4). Nine patients had a history of stroke and 2 patients had a history of major bleeding while on coumadin. Concomitant pulmonary vein isolation was performed in 9 patients. The device was successfully placed in all patients within a median of 56 min (38–137 min). Asymptomatic catheter thrombus occurred in one patient. At 45-day follow-up, no thromboembolic events occurred, TEE showed minimal residual flow in the LAA in three patients. In one patient the LAA device was dislocated, requiring successful percutaneous retrieval.

Conclusion

Device closure of the LAA may provide an alternative strategy to chronic coumadin therapy in patients with AF and high risk of stroke and/or bleeding complications using coumadin.     

Diagnostic tools for atrial tachyarrhythmias in implantable pacemakers: a review of technical options and pitfalls

Background. Correct pacemaker (PM) diagnosis of paroxysmal atrial tachyarrhythmias is crucial for their prevention and intervention with specific atrial pacing programmes. The PM mode switch to only ventricular pacing after detection of atrial tachyarrhythmias is often used as the parameter to quantify the ‘burden’ of atrial tachyarrhythmias. Objectives. This review addresses potential errors in the detection and diagnosis of atrial tachyarrhythmias, sometimes resulting in incorrect mode switches. The interpretation of PM-stored data of patients with atrial tachyarrhythmias and the results of trials of pace prevention and intervention can be better appreciated with more insight into the technical options and pitfalls. Results. Literature and clinical experience demonstrate that the correctness of PM-derived diagnosis of atrial tachyarrhythmias depends on 1) the sensitivity setting to detect the onset and perpetuation of atrial tachyarrhythmias frequently characterised by variable and low-voltage signals, 2) the rejection of far-field R wave sensing by the atrial sense amplifier, 3) the facility for verification of mode switches by a high-quality intracardiac registration of the nonmodified atrial electrogram. The configuration of the atrial lead also contributes to the diagnostic performance of the PM. Conclusion. Not only pacing algorithms and diverse technical PM features but also the atrial lead configuration are currently the limiting factors to the fully reliable, automated detection and diagnosis of atrial tachyarrhythmias. If these technical shortcomings can be improved, better signal processing will result. Then atrial pacing to prevent or suppress atrial tachyarrhythmias will be more justified. (Neth Heart J 2008;16:201-10.)     

Spinal cord stimulation suppresses bradycardias and atrial tachyarrhythmias induced by mediastinal nerve stimulation in dogs

Spinal cord stimulation (SCS) applied to the dorsal aspect of the cranial thoracic cord imparts cardioprotection under conditions of neuronally dependent cardiac stress. This study investigated whether neuronally induced atrial arrhythmias can be modulated by SCS. In 16 anesthetized dogs with intact stellate ganglia and in five with bilateral stellectomy, trains of five electrical stimuli were delivered during the atrial refractory period to right- or left-sided mediastinal nerves for up to 20 s before and after SCS (20 min). Recordings were obtained from 191 biatrial epicardial sites. Before SCS (11 animals), mediastinal nerve stimulation initiated bradycardia alone (12 nerve sites), bradycardia followed by tachyarrhythmia/fibrillation (50 sites), as well as tachyarrhythmia/fibrillation without a preceding bradycardia (21 sites). After SCS, the number of responsive sites inducing bradycardia was reduced by 25% (62 to 47 sites), and the cycle length prolongation in residual bradycardias was reduced. The number of responsive sites inducing tachyarrhythmia was reduced by 60% (71 to 29 sites). Once elicited, residual tachyarrhythmias arose from similar epicardial foci, displaying similar dynamics (cycle length) as in control states. In the absence of SCS, bradycardias and tachyarrhythmias induced by repeat nerve stimulation were reproducible (five additional animals). After bilateral stellectomy, SCS no longer influenced neuronal induction of bradycardia and atrial tachyarrhythmias. These data indicate that SCS obtunds the induction of atrial arrhythmias resulting from excessive activation of intrinsic cardiac neurons and that such protective effects depend on the integrity of nerves coursing via the subclavian ansae and stellate ganglia.     

Unprovoked atrial tachyarrhythmias in aging spontaneously hypertensive rats: the role of the autonomic nervous system

Experimental models of unprovoked atrial tachyarrhythmias (AT) in conscious, ambulatory animals are lacking. We hypothesized that the aging, spontaneously hypertensive rat (SHR) may provide such a model. Baseline ECG recordings were acquired with radiotelemetry in eight young (14-wk-old) and eight aging (55-wk-old) SHRs and in two groups of four age-matched Wistar-Kyoto (WKY) rats. Quantification of AT and heart rate variability (HRV) analysis were performed based on 24-h ECG recordings in unrestrained rats. All animals were submitted to an emotional stress protocol (air-jet). In SHRs, carbamylcholine injections were also performed. Spontaneous AT episodes were observed in all eight aging SHRs (median, 91.5; range, 4-444 episodes/24 h), but not in young SHRs or WKY rats. HRV analysis demonstrated significantly decreased low frequency components in aging SHRs compared with age-matched WKY rats (P < 0.01) and decreased low/high frequency ratios in both young (P < 0.01) and aging (P = 0.01) SHRs compared with normotensive controls. In aging SHRs, emotional stress significantly reduced the number of arrhythmic events, whereas carbamylcholine triggered AT and significantly increased atrial electrical instability. This study reports the occurrence of unprovoked episodes of atrial arrhythmia in hypertensive rats, and their increased incidence with aging. Our results suggest that autonomic imbalance with relative vagal hyperactivity may be responsible for the increased atrial arrhythmogenicity observed in this model. We also provide evidence that, in this model, the sympatho-vagal imbalance preceded the occurrence of arrhythmia. These results indicate that aging SHRs may provide valuable insight into the understanding of atrial arrhythmias.     

Improving stroke prevention therapy for patients with atrial fibrillation in primary care: protocol for a pragmatic,cluster-randomized trial

Background

The prevalence of atrial fibrillation (AF) is growing as the population ages, and at least 15% of ischemic strokes are attributed to AF. However, many high-risk AF patients are not offered guideline-recommended stroke prevention therapy due to a variety of system, provider, and patient-level barriers.

Methods

We will conduct a pragmatic, cluster-randomized controlled trial randomizing primary care clinics to test a “toolkit” of quality improvement interventions in primary care. In keeping with the recommendations of the chronic care model to simultaneously activate patients and facilitate proactive care by providers, the toolkit includes provider-focused strategies (education, audit and feedback, electronic decision support, and reminders) plus patient-directed strategies (educational letters and reminders). The trial will include two feedback cycles at baseline and approximately 6 months and a final data collection at approximately 12 months. The study will be powered to show a difference of 10% in the primary outcome of proportion of patients receiving guideline-recommended stroke prevention therapy. Analysis will follow the intention-to-treat principle and will be blind to treatment allocation. Unit of analysis will be the patient; models will use generalized estimating equations to account for clustering at the clinical level.

Discussion

Stroke prevention therapy using anticoagulation in patients with AF is known to reduce strokes by two thirds or more in clinical trials, but most studies indicate under-use of this treatment in real-world practice. If the toolkit successfully improves care for patients with AF, stakeholders will be engaged to facilitate broader application to maximize the potential to improve patient outcomes. The intervention toolkit tested in this project could also provide a model to improve quality of care for other chronic cardiovascular conditions managed in primary care.

Trial registration

ClinicalTrials.gov (NCT01927445). Registered August 14, 2014 at https://clinicaltrials.gov/.

     

Catheter ablation of atrial incisional tachycardia mistaken for atrial flutter

Incisional sustained tachycardias are frequent in patients who have undergone a surgical repair of interatrial defect. A 43-year-old woman with drug refractory, highly symptomatic, persistent atrial tachycardia in the last year, was referred to our unit for catheter ablation. The patient had undergone a cardiac operation for repairing interatrial secundum ostium type defect with a patch five years before. A previous radiofrequency ablation procedure had been performed for common atrial flutter. We describe a case of incisional atrial tachycardia ablation guided by the new EnSite NavX system equipped with a new electroanatomic mapping system.     

Cost effectiveness of primary stroke prevention in atrial fibrillation: Swedish national perspective.

OBJECTIVE--To assess the potential effects of primary prevention with anticoagulants or aspirin in atrial fibrillation on Swedish population. DESIGN--Analysis of cost effectiveness based on the following assumptions: about 83,000 people have atrial fibrillation in Sweden, of whom 22,000 would be potential candidates for treatment with anticoagulants and 55,000 for aspirin treatment; the annual 5% stroke rate is reduced by 64% (with anticoagulants) and 25% (with aspirin); incidence of intracranial haemorrhage of 0.3%, 1.3%, or 2.0% per year; direct and indirect costs of a stroke of Kr180,000 and Kr90,000; estimated annual cost of treatment is Kr5030 for anticoagulants and Kr100 for aspirin. SETTING--Total Swedish population. MAIN OUTCOME MEASURES--Direct and indirect costs of stroke saved, number of strokes prevented, and cost of preventive treatment. RESULTS--Depending on the rate of haemorrhagic complications 34 to 83 patients would need to be treated annually with anticoagulants to prevent one stroke; 83 patients would need to be treated with aspirin. Giving anticoagulant treatment only would reduce costs by Kr60 million if the incidence of intracranial haemorrhage were 0.3% but would imply a net expense if the complication rate exceeded 1.3%. The total savings from giving anticoagulant (22,000 patients) and aspirin (55,000 patients) treatment would be Kr175 million per year corresponding to 2 million pounds per million inhabitants each year. CONCLUSIONS--Treatment with anticoagulants and, if contraindications exist, with aspirin is cost effective provided that the risk of serious haemorrhage complications due to anticoagulants is kept low.