Atrial pacing for rhythm control of atrial fibrillation

After atrial fibrillation (AF) develops, the first step is to search for and treat underlying (heart) s. Thereafter, AF should be treated. This includes prevention of cardiovascular morbidity and mortality, especially vascular events, and reduction of symptoms.1 The latter may be obtained by two treatment strategies: rhythm-control and/or rate-control treatment. Recent randomised trials have shown that rate control is not inferior to rhythm control with regard to cardiovascular morbidity and mortality.2 In these studies, predominantly elderly patients with underlying heart s (especially hypertension) were included. Patients with (severely) symptomatic AF and advanced heart failure were excluded. Since then, rate-control treatment has been adopted more frequently, even as first-choice therapy, especially in the elderly.     

Atrial pacing, the forgotten pacing mode

In patients with sick sinus syndrome and normal atrioventricular conduction, physiological pacing can be accomplished with either a single chamber atrial pacemaker AAI/R or a dual chamber pacemaker DDD/R. The single chamber device has the advantages of simpler implantation and lower initial costs, while the dual chamber device offers protection in case atrioventricular conduction disturbances develop in the future. When rigorous attention is paid to the pre-implantation selection criteria, the incidence of reported second- or third-degree atrioventricular block varied between 0.4 and 1.8% per annum. Medical practice, however, has shifted to predominant implantation of DDD/R pacemakers in more than 95% of patients with sick sinus syndrome. Recent publications have reported an increase in left atrial diameter, decrease in left ventricular fractional shortening and increased incidence of atrial fibrillation in patients with DDD/R pacing as compared with patients with single chamber atrial devices. These changes were proportional to the percentage of ventricular paced beats. New algorithms in dual chamber devices have been developed in order to minimise ventricular stimulation. These are being evaluated at present. In my opinion there is still a place for atrial pacing in selected patients with sick sinus syndrome with a minimum risk of developing complete atrioventricular block. (Neth Heart J 2008;16(suppl 1): S25-S27.)     

Atrial fibrillation and hyperthyroidism

Atrial fibrillation occurs in 10 - 15% of patients with hyperthyroidism. Low serum thyrotropin concentration is an independent risk factor for atrial fibrillation. Thyroid hormone contributes to arrythmogenic activity by altering the electrophysiological characteristics of atrial myocytes by shortening the action potential duration, enhancing automaticity and triggered activity in the pulmonary vein cardio myocytes. Hyperthyroidism results in excess mortality from increased incidence of circulatory diseases and dysrhythmias. Incidence of cerebral embolism is more in hyperthyroid patients with atrial fibrillation, especially in the elderly and anti-coagulation is indicated in them. Treatment of hyperthyroidism results in conversion to sinus rhythm in up to two-third of patients. Beta-blockers reduce left ventricular hypertrophy and atrial and ventricular arrhythmias in patients with hyperthyroidism. Treatment of sub clinical hyperthyroidism is controversial. Optimizing dose of thyroxine treatment in those with replacement therapy and beta-blockers is useful in exogenous subclinical hyperthyroidism.     

Atrial fibrillation and delayed gastric emptying

Background

Atrial fibrillation and delayed gastric emptying (DGE) are common after pancreaticoduodenectomy. Our aim was to investigate a potential relationship between atrial fibrillation and DGE, which we defined as failure to tolerate a regular diet by the 7^th postoperative day.

Methods

We performed a retrospective chart review of 249 patients who underwent pancreaticoduodenectomy at our institution between 2000 and 2009. Data was analyzed with Fisher exact test for categorical variables and Mann-Whitney U or unpaired T-test for continuous variables.

Results

Approximately 5% of the 249 patients included in the analysis experienced at least one episode of postoperative atrial fibrillation. Median age of patients with atrial fibrillation was 74 years, compared with 66 years in patients without atrial fibrillation (p = 0.0005). Patients with atrial fibrillation were more likely to have a history of atrial fibrillation (p = 0.03). 92% of the patients with atrial fibrillation suffered from DGE, compared to 46% of patients without atrial fibrillation (p = 0.0007). This association held true when controlling for age.

Conclusion

Patients with postoperative atrial fibrillation are more likely to experience delayed gastric emptying. Interventions to manage delayed gastric function might be prudent in patients at high risk for postoperative atrial fibrillation.     

Atrial fibrillation in the elderly

Atrial fibrillation (AF) is prevalent in the elderly (affecting 5% of persons aged >or= 65 years and around 10% of those aged >or= 80 years old) and is associated with stroke, heart failure and poor quality of life. The symptoms of AF are palpitations, fatigue, reduced exercise capacity, dyspnea or dizziness. AF is associated with comorbidity, mainly hypertension in outpatients, and ischaemic heart disease and heart failure in hospitalized patients. Two therapeutic strategies are available to treat arrhythmia: rhythm control or frequency control. In many elderly patients with AF, frequency control is an effective option, particularly when there is heart failure, contraindications to antiarrhythmic agents or when cardioversion is not indicated. Anticoagulation is the main measure to reduce stroke risk. If anticoagulation is not appropriate for a patient, antiaggregants can be used, but the benefit is clearly lower than that provided by anticoagulation.     

Atrial fibrillation pacing decreases intravascular shear stress in a New Zealand white rabbit model: implications in endothelial function

Atrial fibrillation (AF) is characterized by multiple rapid and irregular atrial depolarization, leading to rapid ventricular responses exceeding 100 beats per minute (bpm). We hypothesized that rapid and irregular pacing reduced intravascular shear stress (ISS) with implication to modulating endothelial responses. To simulate AF, we paced the left atrial appendage of New Zealand White rabbits (n = 4) at rapid and irregular intervals. Surface electrical cardiograms were recorded for atrial and ventricular rhythm, and intravascular convective heat transfer was measured by microthermal sensors, from which ISS was inferred. Rapid and irregular pacing decreased arterial systolic and diastolic pressures (baseline, 99/75 mmHg; rapid regular pacing, 92/73; rapid irregular pacing, 90/68; p < 0.001, n = 4), temporal gradients ( ${\partial\tau/\partial t}$ from 1,275 ± 80 to 1,056 ± 180 dyne/cm² s), and reduced ISS (from baseline at 32.0 ± 2.4 to 22.7 ± 3.5 dyne/cm²). Computational fluid dynamics code demonstrated that experimentally inferred ISS provided a close approximation to the computed wall shear stress at a given catheter to vessel diameter ratio, shear stress range, and catheter position. In an in vitro flow system in which time-averaged shear stress was maintained at ${{\tau_{\rm avg}} = 23 \pm 4\, {\rm dyn}\, {\rm cm}^{-2} {\rm s}^{-1}}$ , we further demonstrated that rapid pulse rates at 150 bpm down-regulated endothelial nitric oxide, promoted superoxide (O ₂ ^.? ) production, and increased monocyte binding to endothelial cells. These findings suggest that rapid pacing reduces ISS and ${\partial\tau/\partial t}$ , and rapid pulse rates modulate endothelial responses.     

Mechanisms of disease: Atrial fibrillation

ATRIAL FIBRILLATION (AF) is the most common sustained dysrhythmia in adults. It is ironic, then, that although mechanisms and effective treatments for most other supraventricular tachyarrhythmias have been discovered, AF remains incompletely understood and poorly treated. Nonetheless, our understanding of the pathophysiology of AF has improved in the last half-century, including some groundbreaking observations made in the last 10 years. Indeed, for some patients, the potential for cure now appears to be available. Because no unifying mechanism of AF has been proven, the aim of this review is to describe some of the common and important concepts behind current mechanistic theories of AF and how they contribute to our clinical understanding of AF.     

Atrial fibrillation: an unusual cause

A 28-year-old male presenting with atrial fibrillation (AF) underwent successful electrical cardioversion to restore sinus rhythm. He had no prior history of AF or other cardiac disease. However, transthoracic echocardiography (TTE), performed to exclude structural abnormalities as a cause of AF, demonstrated a large mass in the left atrium (LA). For further analysis the patient was referred to our centre, and echocardiography, multislice detector computed tomography (MDCT) and cardiovascular magnetic resonance imaging (CMR) were performed for further noninvasive diagnostic work-up.     

Atrial remodeling in atrial fibrillation and association between microRNA network and atrial fibrillation

Atrial fibrillation (AF) remains one of the leading causes of morbidity and mortality in the world which are related to palpitations, fainting, congestive heart failure or stroke. The mechanism for atrial fibrillation has been identified as electrical remodeling, structure remodeling and intracellular calcium handling remodeling. microRNAs (miRNAs) have recently emerged as one of the important factors in regulating gene expression. So far, thousands of miRNA genes have been found in diverse animals with the function of regulating cell death, cell proliferation, haematopoiesis and even participate in the processing of cardiovascular disease. In this review, we summarize the mechanism of AF and the association of microRNAs network with AF. We provide a potential perspective of miRNAs as the therapeutic target for AF.     

Atrial fibrillation precipitated by acute hypovolaemia.

Six patients with varying degrees of acute cardiorespiratory failure were seen. All patients deteriorated noticeably when rapid atrial fibrillation developed. In all patients intravenous digitalis failed to slow the ventricular response, and in three patients misguided attempts at electrical cardioversion failed. Haemodynamic monitoring showed a normal or low pulmonary artery occlusion pressure in all patients. Controlled expansion of plasma volume was associated with an immediate slowing of the heart rate in all patients, and the heart rate in all patients returned to sinus rhythm within 30 minutes of transfusion. It is suggested that hypovolaemia in critically ill patients may contribute to the development of atrial fibrillation.