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ICE-guided pulmonary vein antrum isolation seems to prevent cerebrovascular accidents in patients with symptomatic drug-refractory AF who are not receiving anticoagulation therapy. ICE-guided pulmonary vein antrum isolation is an effective and safe treatment for AF.

Atrial flutter (AFL) is an arrhythmia which occurs frequently. Epidemiological data show an incidence of 88/100 000 new cases per year in the general population in USA, with 200 000 new cases every year [1]. The main predictors of this arrhythmia are heart failure and chronic obstructive pulmonary disease. It often coexists with atrial fibrillation (AF); moreover, it is not unusual that patients undergoing antiarrhythmic treatment with class IC drugs or amiodarone for the treatment of AF develop episodes of AFL. Often AFL is poorly tolerated due to the high ventricular response. This happens even in patients with good control of ventricular rate at rest, who do not tolerate AFL during effort, since ventricular rate increases suddenly.

Recently many studies have reported that the left atrium has a central role in the initiation and maintenance of atrial fibrillation (AF); the most arrhythmogenic areas of the left atrium are in the pulmonary veins, atriovenous junctions, and contiguous atrial regions [1–3]. Electrical isolation of the pulmonary veins seems to be the most effective ablation technique for patients with AF [4,5].

Pulmonary vein isolation is becoming the treatment of choice for symptomatic atrial fibrillation (AF) that is refractory to drugs [1–3]. However, thromboembolic complications are an important limitation of this approach [4], occurring in up to 2.8% of the patients. Alternative energy sources such as cryoablation and ultrasound have the potential to improve the safety of the procedure by preventing disruption of the endothelial surface during energy delivery [5,6].

Atrial fibrillation (AF) is the most common cardiac arrhythmia, with a prevalence of between 2% and 4% in the general population over 60 years old and an increasing incidence with age [1]. Its presence causes a rise in morbidity and mortality rates due to the increase of embolic risk and loss of atrial function with a consequent decrease in cardiac performance. Very often AF is associated with disabling symptoms-such as palpitations, exercise intolerance, and fatigue-that can influence the quality of life significantly. In patients affected by persistent or permanent AF with rapid ventricular response, the persistent high rate may produce a tachycardiomyopathy that can be reversible when sinus rhythm is restored or the ventricular rate is controlled. This arrhythmia is also a significant social financial burden. In the USA, AF causes more hospital admissions than any other arrhythmia, accounting for a nearly 1 million hospital days per year [2].

Atrial fibrillation (AF) is the most common cardiac arrhythmia in the general population. Its prevalence ranges from 0.5% to 9% between the ages of 50 and 80 years. It may occur in the clinical history of any patient with cardiopathy and even in apparently healthy people or those with minor structural anomalies of the heart [1]. Its presence causes a rise in morbidity and mortality due to the loss of atrial function and the consequent decrease in heart performance and increase in embolic risk. Very often AF is associated with disabling symptoms such as palpitations, which alone can significantly influence quality of life. Moreover, literature data [2] suggest that the incidence of this arrhythmia increases dramatically in patients with heart failure. In those with asymptomatic or symptomatic left ventricular systolic dysfunction it is independently associated with an increased risk of all-cause mortality. Persistently elevated ventricular rate during AF can produce dilated ventricular cardiomyopathy. Heart failure may thus be a consequence of rather than the cause of AF in clinical practice. For this reason, recovery and maintenance of sinus rhythm is one of the main objectives of treatment. However, antiarrhythmic drug therapy of AF is often unsatisfactory because recurrences frequently occur. Only 60% of patients remain in sinus rhythm after 6 months [2]. Moreover, antiarrhythmic therapy with class I drugs in patients with heart failure leads to an increase in mortality, so that the only efficient and safe drug therapy is amiodarone.

Atrial fibrillation is the most common cardiac arrhythmia, with a prevalence ranging from 2% to 4% in the general population over 60 years old and an incidence that increases with age.

Radiofrequency ablation of either the fast or the slow pathway in AV nodal reentrant tachycardia was introduced in the early 1990s [1–4]. Both methods have a high success rate and low complications. As the procedures require the delivery of energy close to the AVN and the bundle of His, a possible complication is second or third degree AV block.

Atrial fibrillation is the most frequent arrhythmia in clinical practice. Its prevalence varies from 0.5% to 9% [1] of the general population between 50 and 80 years of age. It may appear in the clinical history of every patient with cardiopathy and even in appearently healthy persons or those with minor structural anomalies of the heart. Its presence causes a rise in morbidity and mortality rates due to the loss of atrial function and the consequent decrease in heart performance and increase in embolic risk. For this reason recovery and maintenance of sinus rhythm is one of the main objectives of treatment.

Atrial fibrillation (AF) is one of the commonest types of arrhythmia, occurring in up to 4% of patients over 60 years of age [1–3]. Cardioversion is performed in patients with AF in an effort to improve cardiac function, relieve symptoms, and decrease the risk of thrombus formation. Successful cardioversion is associated with a 5%-7% incidence of embolism among patients who have not received adequate anticoagulation therapy [4–9]. The cardioversion of AF to sinus rhythm is associated with transient mechanical dysfunction of the left atrium (LA) and left atrial appendage (LAA) and the development of spontaneous echocardiographic contrast. This phenomenon has been termed “stunning” and is considered an important factor for thromboembolic stroke following cardioversion of AF to sinus rhythm [10–15].

The goal of ICD therapy is to prevent premature sudden cardiac death (SCD) in patients who would otherwise have a long-term survival expectancy. The major challenge is to detect the greatest number of patients who might benefit from an ICD [1]. For instance, prevention of SCD in the general, unselected adult population requires an intervention in many individuals to prevent a few SCDs. On the other hand, to consider only very high-risk subgroups is much more efficient but the impact on the total number of SCDs is low. Heart failure patients and those with ventricular dysfunction and low left ventricular ejection fraction (LVEF) represent an intermediate but growing subgroup with an high incidence of SCD per year, in which a potentially effective intervention would be efficient; while the contribution of SCDs in congestive heart failure (CHF) patients to the total number of SCDs is high enough to predict a significant impact if an effective intervention could be applied. In this context, another important matter relating to CHF patients, in this era of implantable devices is the emerging data on the novel use of biventricular pacing to improve functional status and quality of life in such patients [2,3].

Low-energy internal atrial defibrillation has recently been introduced into clinical practice as an effective and safe method of restoring sinus rhythm in patients with atrial fibrillation [1–5]. The technique has proved to be particularly useful in patients with long-standing atrial fibrillation or a very enlarged left atrium [1, 2, 6]. However, these patients are considered to be at very high risk of early recurrence of atrial fibrillation. Thus, it seems justified to ask the question: how many patients maintain sinus rhythm after successful internal atrial defibrillation, and for how long?

Vasovagal events, like many other autonomic nervous system disturbances, have a cyclic and unpredictable course with usually brief periods of symptom recrudescence (so-called “clusters”) alternating with sometimes very long periods of quiescience and asymptomatic status [1, 2]. Thus, chronic therapy with drugs does not appear indicated in the majority of cases and is often associated with serious or intolerable side effects as well as poor patient compliance, especially in young people [3]. Moreover, when events occur, prevention of vasovagal reaction usually requires high drug plasma levels which are difficult to attain through chronic oral administration [4]. Indeed, only occasionally have oral drugs proved to be effective in the few double-blind, randomized, placebo-controlled trials performed to date [5–9]. It is also noteworthy that electrical treatment with a pacemaker, even when useful, rarely leads to complete elimination of symptoms [10, 11], because of the hypotensive effects of the vasodepressor reflex that is practically present in all subjects, generally precedes cardioinhibition and bradycardia [12] and is not amenable to correction or reversal by cardiac pacing. For all these reasons, it seems logical and desirable to develop an implantable drug delivery system for treatment of vasovagal syncope [3]. Such a device would allow the automatic “on demand” delivery of a bolus of a vasoactive or a cardioactive drug, previously recognized to be effective and safe in preventing tilt-induced syncope, possibly together with the activation of sequential cardiac pacing.

Atrial fibrillation (AF) is the most common arrhythmia in clinical practice for which patients are hospitalized, engendering high human and economic costs [1, 2]. The limited efficacy and the side effects of drugs used both to maintain sinus rhythm and to control the heart rate have increased interest in the development of non-pharmacological therapy for AF [3]. The implantable atrial defibrillator (IAD) is one such therapeutic tool.

Slow pathway ablation is currently used to cure common and uncommon A-V node reentrant tachycardia (AVN RT). The technique has a success rate of about 100% and a 0.5%–2% risk of inadvertent complete AV block [1–4]. Although the risk of block is low, it is difficult to tolerate in patients with a benign arrhythmia, especially when they are young.

Controlling ventricular rate in patients with intermittent or chronic atrial fibrillation (AF), in whom it is not possible to maintain sinus rhythm through drug therapy, is often a problem. Control of ventricular rate is necessary because of invalidating palpitations and/or occurrence of hemodynamic impairment [1].

Transesophageal atrial pacing was first attempted by Shafiroff and Linder in 1957 (1). However, it could not be employed because of its low tolerance due to the high intensity necessary for the stimulation.This limitation was overcome by Gallagher in 1982 (2), who lengthened the distance between the electrodes while giving a longer electric pulse duration.

Atrioventricular (AV) node reentrant tachycardia (AVNRT) is the most common cause of paroxysmal supraventricular tachycardia (1). Many electrophysiologic data suggest that the reentry circuit in AVNRT contains, as its critical components, a “fast” AV nodal pathway connecting the atrium to the His bundle and a “slow” pathway with a longer conduction time (1, 2). In the common variety (slow-fast), AVNRT the slow pathway provides the anterograde limb of the circuit and the fast pathway the retrograde limb. In the uncommon variety (fast-slow) the fast pathway provides the anterograde limb of the circuit and the slow pathway the retrograde limb.