Pacing to prevent atrial fibrillation.

PURPOSE OF REVIEW: Pacemakers are frequently implanted in patients with atrial fibrillation. Many patients with pacemakers also develop atrial fibrillation. Over a period of time, through many studies on different pacing modes, sites, and algorithms, significant insights have been gained in the field of treatment and prevention of atrial fibrillation. The purpose of this review is to discuss some aspects of the scientific basis, current standards and possible future research related to cardiac pacing for prevention of atrial fibrillation. RECENT FINDINGS: Trials involving pacing at the alternative pacing site per se or in combination with specific algorithms for prevention of atrial fibrillation have not shown consistent results. Recently, a new generation of antitachycardia pacing therapies has brought on a new optimism with promising outcome data of reduction in permanent atrial fibrillation, cardiovascular hospitalizations, and mortality. SUMMARY: Multiple trials and clinical observational studies of different pacing methods and algorithms, with the exception of newer therapies in conjunction with atrial pacing algorithms, have not been shown to prevent atrial fibrillation. Hence, while permanent pacing is indicated for sinus node dysfunction and conduction abnormalities in patients with or without atrial fibrillation, the prevailing data in the literature does not support implantation of a permanent pacemaker for prevention of atrial fibrillation per se.

Early repolarisation and J wave syndromes.

J wave syndrome has emerged as a significant cause of Idiopathic ventricular fibrillation (IVF) responsible for sudden cardiac death. A large body of data is now available on genesis, genetics and ionic mechanisms of J wave syndromes. Two of these viz., Early repolarization syndrome (ER) and Brugada syndrome (BrS) are fairly well characterized enabling correct diagnosis in most patients. The first part of repolarization of ventricular myocardium is governed by Ito current i.e., rapid outward potassium current. The proposed mechanism of ventricular fibrillation (VF) and ventricular tachycardia (VT) storms is the faster Ito current in the epicardium than in the endocardium results in electrical gradient that forms the substrate for phase 2 reentry. Prevention of Ito current with quinidine supports this mechanism. Majority of ER patterns in young patients are benign. The key issue is to identify those at increased risk of sudden cardiac death. Association of both ER syndrome and Brugada syndrome with other disease states like coronary artery disease has also been reported. Individuals resuscitated from VF definitely need an implantable cardiac defibrillator (ICD) but in others there is no consensus regarding therapy. Role of electrophysiology study to provoke ventricular tachycardia or fibrillation is not yet well defined. Radiofrequency ablation of epicardial substrate in right ventricle in Brugada syndrome is also under critical evaluation. In this review we shall discuss historical features, epidemiology, electrocardiographic features, ionic pathogenesis, clinical features and current status of proposed treatment of ER and BrS.

J Wave Syndrome: Clinical Diagnosis, Risk Stratification and Treatment.

J wave syndrome has emerged from a benign electrocardiographic abnormality to a proarrythmic state and a significant cause of idiopathic ventricular fibrillation responsible for sudden cardiac death. Electrical genesis, genetics and ionic mechanisms of J wave syndromes are active areas of research. Typically two of these viz., Early repolarization syndrome (ER) and Brugada syndrome (BrS) are fairly well characterized enabling correct diagnosis in most patients. In early repolarization syndrome, J waves are seen in inferior (2,3, avF) or lateral leads (V4, V5, V6), while in Brugada syndrome they are best seen in right precordial leads (V1-V3). The first part of repolarization of ventricular myocardium is governed by Ito current i.e., rapid outward potassium current. The proposed mechanism of ventricular fibrillation (VF) and ventricular tachycardia (VT) storms is faster Ito current in the epicardium than in the endocardium resulting in electrical gradient that forms the substrate for phase 2 re-entry. Prevention of Ito current with quinidine supports this mechanism. Morphological features of benign variety of J wave syndrome and malignant/ proarrythmic variety have now been fairly well characterized. J waves are very common in young, athletes and blacks; risk stratification for VF/sudden cardiac death (SCD) is not easy. Association of both ER syndrome and Brugada syndrome with other disease states like coronary artery disease is being reported frequently. Those with ECG abnormality as the only manifestation are difficult to manage. Certain ECG patterns are more proarrythmic. Individuals resuscitated from VF definitely need an implantable cardiac defibrillator (ICD) but in others there is no consensus regarding therapy. Role of electrophysiology study to provoke ventricular tachycardia or fibrillation is not yet well defined. Radiofrequency ablation of epicardial substrate in right ventricle in Brugada syndrome is reported and is also under critical evaluation. In this review we shall discuss some interesting historical features, epidemiology, electrocardiographic features, and ionic mechanisms on pathogenesis, clinical features, risk stratification and treatment issues in J wave syndromes. Brugada syndrome is not discussed in this review.

Atrial fibrillation: current concepts.

Atrial fibrillation (AF) is the most common arrhythmia which is a focus of newer modalities of treatment, especially ablation techniques using innovative mapping techniques. Its incidence and prevalence increases with aging and presence of structural heart disease, the latter being less than 1% prior to age 40, rising to 8% at age 80. Concomittant morbidity and excessive mortality is related to the increased incidence of stroke and congestive heart failure. Once developed in a clinical setting, it tends to either persist or recur. Pharmacotherapy to control rate or rhythm tends to have a secondary failure, and therefore there is a growing interest in ablation techniques. The use of anticoagulation is also associated with bleeding risks and therefore the management of AF needs to be individualized in every patient. In this article, we shall be discussing clinical types of AF, etiology, the mechanism of genesis, symptoms, complications and approach to treatment in various clinical scenarios.