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PubMed2006

Kv1.5 channelopathy due to KCNA5 loss-of-function mutation causes human atrial fibrillation.

Atrial fibrillation is a rhythm disorder characterized by chaotic electrical activity of cardiac atria. Predisposing to stroke and heart failure, this common condition is increasingly recognized as a heritable disorder. To identify genetic defects conferring disease susceptibility, patients with idiopathic atrial fibrillation, lacking traditional risk factors, were evaluated. Genomic DNA scanning revealed a nonsense mutation in KCNA5 that encodes Kv1.5, a voltage-gated potassium channel expressed in human atria. The heterozygous E375X mutation, present in a familial case of atrial fibrillation and absent in 540 unrelated control individuals, introduced a premature stop codon disrupting the Kv1.5 channel protein. The truncation eliminated the S4-S6 voltage sensor, pore region and C-terminus, preserving the N-terminus and S1-S3 transmembrane domains that secure tetrameric subunit assembly. Heterologously expressed recombinant E375X mutant failed to generate the ultrarapid delayed rectifier current I(Kur) vital for atrial repolarization and exerted a dominant-negative effect on wild-type current. Loss of channel function translated into action potential prolongation and early after-depolarization in human atrial myocytes, increasing vulnerability to stress-provoked triggered activity. The pathogenic link between compromised Kv1.5 function and susceptibility to atrial fibrillation was verified, at the organism level, in a murine model. Rescue of the genetic defect was achieved by aminoglycoside-induced translational read-through of the E375X premature stop codon, restoring channel function. This first report of Kv1.5 loss-of-function channelopathy establishes KCNA5 mutation as a novel risk factor for repolarization deficiency and atrial fibrillation.

Animals↗

PubMed2005

Ximelagatran for stroke prevention in atrial fibrillation.

Atrial fibrillation is the most common sustained cardiac arrhythmia and the most frequently encountered cause of embolic stroke. Vitamin K antagonists (such as warfarin) have represented the cornerstone of anticoagulation practice for the last 60 years. Although highly effective in preventing thromboembolic events among patients with atrial fibrillation, warfarin therapy is limited by a multitude of potential problems. Hence, warfarin is significantly underused in clinical practice, with only half of warfarin-treated patients actually achieving therapeutic anticoagulation in routine clinical practice. Consequently, there is an overwhelming need for an alternative oral anticoagulant for patients with atrial fibrillation that is safer, more practical and effective. Ximelagatran (Exanta, AstraZeneca) is a novel oral direct thrombin inhibitor that is rapidly converted to the active compound melagatran after oral absorption. It has a low potential for drug interactions, anticoagulation monitoring is not required, and it is administered at a fixed twice-daily dose. The Stroke Prevention using the ORal Thrombin Inhibitor in patients with nonvalvular atrial Fibrillation (SPORTIF) III and V trials have together demonstrated the noninferiority of ximelagatran relative to warfarin for the prevention of stroke and embolic events in atrial fibrillation. Unfortunately, initial optimism has been tempered by serious concerns over its safety data in view of its propensity to cause elevation in liver enzymes.

Anticoagulants↗

PubMed2006

Catheter ablation of atrial fibrillation: ongoing atrial fibrillation inside a single pulmonary vein after successful electrical disconnection and restoration of sinus rhythm in both atria.

Explore the source record for details and available documents.

Aged↗

PubMed2005

[Non-channel drugs to prevent atrial fibrillation].

Atrial fibrillation is the most prevalent sustained cardiac arrhythmia. To terminate or prevent atrial fibrillation, conventional "channel-blocking antiarrhythmics" are generally administered, which directly inhibit current flows through transmembrane sodium, calcium and/or potassium channels that give rise to the atrial action potential. However, prospective, randomized clinical trials have demonstrated that cardiomyocyte ion channel blocking antiarrhythmic drugs have limited long-term-efficacy for preventing recurrences of atrial fibrillation, their safety is far from ideal (because of the high incidence of proarrhythmic and extracardiac side-effects), and do not reduce mortality. Researchers during the last 10 years have revealed that the pathogenetic basis of the recurrence, persistence or permanence of atrial fibrillation is electrical and structural remodelling established by profound alterations in the electrophysiological, contractile and (ultra)structural properties of the myocardium (atrial remodelling). Accordingly, recent interest has shifted from ion channel blockers to the development of drugs that target underlying arrhythmogenic substrates by interference with receptors and specific signal transduction pathways involved in electrical and structural remodelling (non-channel drugs). They include antifibrotic angiotensin-converting enzyme inhibitors, angiotensin II AT1 receptor and aldosterone antagonists, beta-adrenergic blockers, anti-inflammatory statins and glucocorticoids, and a series of new atrioselective antifibrillatory agents that are currently undergoing clinical trials.

Adrenergic beta-Antagonists↗

PubMed2004

Oesophageal electrical cardioversion of atrial fibrillation.

Atrial fibrillation is the most common cardiac arrhythmia and the most frequent cause of hospitalization and utilization expense among all heart diseases. Taking into account persistent atrial fibrillation we know that, in order to cardiovert persistent atrial fibrillation, external direct current cardioversion is the method most frequently used to restore sinus rhythm. But external cardioversion has also some limitations: it requires high energy direct current shocks so that patients have to be anaesthetised, which means a dedicated apparatus and place to adequately assist the patients. The oesophageal cardioversion is an alternative method to restore sinus rhythm, which could obviate some of these limitations of external cardioversion. Compared to external cardioversion oesophageal one has lower defibrillation impedance and requires lower energies to restore sinus rhythm, increasing for the same energy level, success rate. Using low energy shocks, a mild sedation is sufficient to make the procedure well tolerated by most of patients. Other 2 important advantages coming from low energy shocks are the safety in patients with pacemaker or implantable cardioverter-defibrillator and the availability of a back up atrial pacing. Oesophageal cardioversion is not indeed a new technique. Looking at literature, studies in animals and in humans have been performed since the 60s, assessing feasibility, effectiveness and safety of such a procedure. The oesophageal-precordial cardioversion is usually performed on an outpatient regimen, resulting in a very cost-effective method to cardiovert patients with persistent atrial fibrillation, which may definitely represent a real alternative technique to external cardioversion.

Ambulatory Care↗

PubMed1981

Nature of cardiac arrhythmias and electrolyte disturbances. Role of potassium in atrial fibrillation.

Atrial fibrillation is highly favoured by an accelerated atrial muscle repolarization. In hyperthyroidism, this occurs without changes in resting membrane potential level of the atrial muscle cells and without changes in the ionic composition of the cell. In patients prone to atrial fibrillation but without signs of hyperthyroidism, accelerated atrial repolarization can also be demonstrated. In such patients, a decreased atrial muscle potassium content seems responsible for the electrophysiological changes that highly favours the occurrence of atrial fibrillation.

Action Potentials↗

PubMed2003

An update on electrical cardioversion of atrial fibrillation.

Atrial fibrillation is the most frequently encountered sustained arrhythmia in clinical practice. Electrical cardioversion of atrial fibrillation using damped sine wave shocks has been a mainstay of therapy for nearly 4 decades; its limitation remains a failure rate that approaches 20%. Although several alternatives have been proposed, including delivering 720 J shocks using dual monophasic defibrillators, ibutilide pretreatment and internal cardioversion, each of these approaches has significant limitations, which preclude its routine use. Recent data demonstrate that routine use of biphasic shocks for cardioversion of atrial fibrillation is associated with a marked improvement in cardioversion efficacy and suggest that biphasic shocks may be the preferred method for the transthoracic electrical cardioversion of atrial fibrillation.

Anti-Arrhythmia Agents↗

PubMed1997

Preventing stroke in atrial fibrillation.

Atrial fibrillation, a common cardiac arrhythmia, is now recognized as a powerful risk factor for stroke. Previously, atrial fibrillation was thought to predispose persons to stroke only in the presence of rheumatic heart disease with mitral stenosis. The significant impact of nonvalvular atrial fibrillation on stroke incidence, recurrence and mortality was not fully appreciated. A series of clinical trials have confirmed that a five-fold increase in stroke incidence occurs in patients with atrial fibrillation, and that warfarin anticoagulation is efficacious in stroke prevention. This anticoagulation benefit was achieved with an acceptably low risk of serious hemorrhage.

Aged↗

PubMed1998

Cardiac troponin T does not increase after electrical cardioversion for atrial fibrillation or atrial flutter.

OBJECTIVE: To determine whether cardiac troponin T increases after electrical cardioversion in patients with atrial fibrillation or atrial flutter. DESIGN: Serum creatine kinase (CK), creatine kinase-MB (CKMB), and cardiac troponin T were measured before, 24 hours, and 48 hours after cardioversion in 15 patients with atrial fibrillation or atrial flutter. RESULTS: 12 of the 15 patients (80%) were successfully cardioverted to sinus rhythm. The median number of shocks was three (range one to six), the median cumulative energy 710 J (50 to 1430 J), and the median peak energy 300 J (50 to 360 J). Total CK increased from a baseline median concentration of 92 (45 to 259) to 1324 (96 to 6660) U/l at 24 hours and 1529 (120 to 4774) U/l at 48 hours after cardioversion. There was a small increase in CKMB but the ratio of CKMB to CK did not increase. There was no increase in cardiac troponin T in any patient. CONCLUSIONS: Following electrical cardioversion of atrial fibrillation or atrial flutter, cardiac troponin T remains unchanged despite a large rise in total CK, indicating that the CK is derived from skeletal muscle and that myocardial injury does not occur. If cardiac troponin T is increased after cardioversion for atrial arrhythmias then other causes of myocardial damage should be sought.

Aged↗

PubMed1992

Pharmacokinetics and pharmacodynamics of intravenous diltiazem in patients with atrial fibrillation or atrial flutter.

BACKGROUND: Diltiazem, a calcium channel blocker, has been shown to be safe and effective in the treatment of patients in atrial fibrillation and/or atrial flutter. However, there have been no pharmacokinetic/pharmacodynamic studies of diltiazem in these patients. METHODS AND RESULTS: The pharmacokinetics and pharmacodynamics of intravenous diltiazem were determined in 32 patients with atrial fibrillation or atrial flutter (mean +/- SD age, 66 +/- 7 years; mean baseline heart rate, 131 +/- 10 beats per minute) after 20 mg or 20 mg followed by 25-mg bolus doses and a 10 and 15 mg/hr infusion for 24 hours. After the 10 and 15 mg/hr infusions of diltiazem, mean +/- SD elimination half-life was 6.8 +/- 1.8 and 6.9 +/- 1.5 hours, volume of distribution was 411 +/- 151.8 and 299 +/- 70.8 I, and systemic clearance was 42 +/- 12.4 and 31 +/- 8.3 l/hr, respectively. Percentages of the plasma concentrations of the principal metabolites desacetyldiltiazem and N-desmethyldiltiazem to diltiazem were < 15% and < 10%, respectively. Thirty of 32 patients maintained response throughout the 24-hour infusion of diltiazem. Using a sigmoidal Emax pharmacodynamic model, a strong relation (mean +/- SD r2, 0.78 +/- 0.2) was observed between plasma diltiazem concentration and percent heart rate reduction. Mean +/- SD Emax (maximum percent reduction in heart rate from baseline) and EC50 (plasma diltiazem concentration that achieves half Emax) were 52 +/- 17% and 110 +/- 84 ng/ml, respectively. The model predicts that mean plasma diltiazem concentration of 79, 172, and 294 ng/ml are required to produce a 20%, 30%, and 40% reduction in heart rate, respectively. A relation between plasma diltiazem concentration and percent change in systolic blood pressure (SBP) or diastolic blood pressure (DBP) from baseline was not observed (mean +/- SD r2, SBP/DBP: 0.35 +/- 0.24/0.36 +/- 0.2). There were no untoward side effects observed. CONCLUSIONS: First, the pharmacokinetics of diltiazem in patients with atrial fibrillation or atrial flutter is nonlinear with an apparent dose-dependent decrease in systemic clearance with increasing infusion rate. Second, using a sigmoidal Emax model, there is a strong relation between plasma diltiazem concentration and percent heart rate reduction. Third, the plasma concentrations of the principal metabolites desacetyldiltiazem and N-desmethyldiltiazem are low and are not expected to contribute significantly to the pharmacodynamics of intravenous diltiazem in these patients.

Aged↗

PubMed2006

High dose of amiodarone in a short-term period reduces the incidence of postoperative atrial fibrillation and atrial flutter.

OBJECTIVE: To investigate whether oral amiodarone administered before surgery for a short period in high dose would reduce the incidence of postoperative atrial fibrillation or atrial flutter and reduces the length of hospital stay. METHODS: In the double-blind, randomized study, 93 patients were given either oral amiodarone (46 patients) or placebo (47 patients). Therapy consisted of 600 mg of amiodarone three times a day, started at minimum 30 hours and at maximum 56 hours before surgery. RESULTS: Postoperative atrial fibrillation or atrial flutter occurred in 8 of 46 patients in the amiodarone group (17.4%) and 19 of the 47 patients in the placebo group (40.4%) (p=0.027). The mean dose of amiodarone was 2.8 g. Patients in the amiodarone group were hospitalized for 8.9+/-3.1 days and patients in the placebo group were hospitalized for 11.4+/-8.7 days (p=0.07). The hospital length were significantly prolonged in patients who developed atrial arrhythmias after surgery, despite the treatment received.(p<0.001). CONCLUSION: This new alternative way of using amiodarone in high dose and in a short-term period before surgery reduce the incidence of postoperative atrial fibrillation or atrial flutter in coronary artery bypass graft surgery.

Amiodarone↗

PubMed1999

Maintenance of sinus rhythm with oral d,l-sotalol therapy in patients with symptomatic atrial fibrillation and/or atrial flutter. d,l-Sotalol Atrial Fibrillation/Flutter Study Group.

Currently d,l-sotalol is widely used to prevent recurrence of atrial fibrillation and/or atrial flutter, although a randomized dose-response study has not previously been conducted to guide therapy for this indication. This study summarizes findings of a double-blind, placebo-controlled, multicenter, randomized trial evaluating the efficacy, safety, and dose-response relation of 3 fixed doses of d,l-sotalol (80, 120, and 160 mg twice daily) for the maintenance of sinus rhythm in 253 patients with atrial fibrillation and/or atrial flutter. All patients were in sinus rhythm at randomization. Treatment (69 patients on placebo, 59 on 80 mg, 63 on 120 mg, and 62 on 160 mg given twice daily) was continued for 12 months or until documented recurrence of symptomatic atrial fibrillation and/or flutter. Transtelephonic electrocardiographic monitoring was used to detect symptomatic recurrences. Demographic characteristics were not different in the 4 groups. Structural heart disease was present in 57% of patients. Patients with a history of heart failure were excluded. The time from randomization to symptomatic arrhythmia recurrence was significantly longer in the 2 higher d,l-sotalol dose groups than in the placebo group. The median times to recurrence were 27, 106, 229, and 175 days for the placebo, 80, 120, and 160 mg groups, respectively. There were no deaths or cases of torsade de pointes, sustained ventricular tachycardia, or ventricular fibrillation reported. Thus, d,l-sotalol appeared to be both safe and effective in maintaining sinus rhythm in patients with symptomatic atrial fibrillation and/or flutter. Further, the 120-mg twice daily dose appeared to provide the most favorable benefit and/or risk.

Anti-Arrhythmia Agents↗

PubMed1999

Catheter-ablative techniques for the treatment of atrial fibrillation.

Atrial fibrillation is the most commonly encountered arrhythmia in clinical practice and is associated with significant morbidity and mortality. Pharmacologic therapy, although useful for rate control, has proven much less effective in the long term maintenance of sinus rhythm. The utility of implantable atrial defibrillators or pacing to prevent atrial fibrillation remains largely untested. This article describes four catheter-based therapies for atrial fibrillation: His ablation, atrioventricular nodal modification, the Maze procedure, and the ablation of pulmonary vein foci which initiate the arrhythmia. Whereas the first two procedures are largely palliative and recommended for patients with symptomatic, drug-refractory atrial fibrillation, the latter two offer the potential for a curative intervention.

Atrial Fibrillation↗

PubMed2005

Will this be the end of the anticoagulation clinic for patients with atrial fibrillation?

Atrial fibrillation is the most common clinical arrhythmia and with an ageing population, it is an increasing cause of hospital admissions, morbidity and mortality. The most feared complication of atrial fibrillation is stroke. A number of studies have demonstrated that warfarin is at least moderately effective at reducing thromboembolic risk in stroke yet its use in both the community and in secondary care is suboptimal. Concerns about drug interactions, frequent blood monitoring and the risks of over and under coagulation have led to under prescription. Direct thrombin inhibitors are under investigation as an alternative to warfarin for thromboembolic prophylaxis in atrial fibrillation. Two large studies (SPORTIF III and SPORTIF V) have recently been published examining the effectiveness of the direct thrombin inhibitor ximelagatran at reducing thromboembolic risk. Ximelagatran was shown to be non-inferior to warfarin for the prevention of thromboembolic complications. Concerns however have arisen about long-term safety, particularly the possible effects on hepatic function. This review examines the data and discusses whether the introduction of these drugs could result in the end of the anticoagulation clinic for patients with atrial fibrillation.

Anticoagulants↗

PubMed2000

Cost-effective strategies in the acute management of atrial fibrillation.

Atrial fibrillation is the most common sustained arrhythmia likely to be encountered in clinical practice. It is associated with significant morbidity and mortality. The treatment of patients with atrial fibrillation can be complex and costly, especially when patients are hospitalized for acute management of this arrhythmia. In this review, we summarize current approaches to the acute management of atrial fibrillation with an emphasis on the most cost-effective approaches. We review acute methods of heart rate control and cardioversion, including pharmacologic and other minimally invasive strategies. We believe that the most cost-effective approaches may require the use of standardized clinical pathways. This may help to ensure that patients with acute atrial fibrillation receive the most effective and efficient care.

Anti-Arrhythmia Agents↗

PubMed2004

Comparing the guidelines: anticoagulation therapy to optimize stroke prevention in patients with atrial fibrillation.

Atrial fibrillation (AF) is an important risk factor for stroke. According to a pooled analysis of controlled clinical trials with warfarin, anticoagulation therapy reduces stroke risk by 62%. However, clinicians must decide whether the benefit of long-term anticoagulation therapy with available agents outweighs the risk of bleeding for individual patients. Guidelines issued by the American College of Chest Physicians and by the joint American College of Cardiology, American Heart Association, and the European Society of Cardiology task force recommend antithrombotic therapy to protect AF patients from stroke based on risk-stratification algorithms. Risk factors for stroke AF patients include age > or =75 years; hypertension; thyrotoxicosis; diabetes; cardiovascular disease; congestive heart failure; and history of stroke, transient ischemic attack, or thromboembolism. Patients at high risk for stroke experience greater absolute benefit from anticoagulation therapy than patients at low risk. The guidelines are consistent in recommendations for high-risk patients (warfarin therapy, international normalized ratio 2.0 to 3.0) and low-risk patients (aspirin 325 mg), but differ for intermediate-risk patients with diabetes or heart disease. The guidelines continue to evolve, and future guidelines are likely to incorporate new clinical data, including the CHADS(2) algorithm for determining risk and the results of the Atrial Fibrillation Follow-up Investigation of Rhythm Management trial, the Rate Control versus Electrical Cardioversion for Persistent Atrial Fibrillation study, and the Stroke Prevention Using an Oral Thrombin Inhibitor in Atrial Fibrillation II to V trials.

Algorithms↗

PubMed1997

[Esophageal echocardiography in patients with cerebrovascular stroke and atrial fibrillation].

Atrial fibrillation is an important risk factor of embolization into the CNS. Thus affected patients should receive permanent anticoagulant therapy. Oesophageal echocardiography (TEE) can help our decision in patients with relative contraindications of anticoagulant therapy. TEE was performed in 52 patients with atrial fibrillation and cerebrovascular attack (CMP) with an ischaemic aetiology. Transthoracic echocardiography did not reveal the source of embolization. In 10% patients a thrombus was found in the appendage of the left atrium, in another 9% patients a spontaneous echocontrast was found in the left atrium (prethrombotic condition) and in 5% patients an open foramen ovale. The results indicate the highly probable etiology of embolization in patients with cerebrovascular attacks and atrial fibrillation. This supports the recommendation of absolute indication of anticoagulant treatment in patients with cerebrovascular attacks and atrial fibrillation.

Adult↗

PubMed2003

New antiarrhythmic agents for atrial fibrillation and atrial flutter: United States drug market response as an indicator of acceptance.

OBJECTIVE: To determine how well dofetilide and Betapace AF (sotalol, approved solely for atrial fibrillation and atrial flutter), with their detailed dosing and monitoring guidelines for safety, were accepted into clinical practice during the 2 calendar years after their introduction. METHODS AND RESULTS: We reviewed the number of new, refill, and total prescriptions of all antiarrhythmic agents in the United States from April 2000-December 2001 to assess use of dofetilide and Betapace AF in the drug market. Both were prescribed very infrequently throughout the study period. In addition, the infrequent reported use of these drugs for patients with atrial fibrillation and flutter indicated poor acceptance of these agents by prescribing physicians. We speculated that the restricted distribution and required educational program for dofetilide, as well as the availability of generic sotalol products, may have discouraged physicians from prescribing both dofetilide and Betapace AE CONCLUSION: A common goal for both the dofetilide risk-management program and the creation of a sotalol product indicated solely for atrial fibrillation and atrial flutter was to provide safer treatment for patients with these arrhythmias. Unfortunately, limited penetration of dofetilide and Betapace AF into the U.S. market suggests that drugs without a risk-management program or detailed dosing guidelines were more likely than dofetilide or Betapace AF to be selected for treatment of atrial fibrillation and atrial flutter.

Anti-Arrhythmia Agents↗