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This paper is an executive summary of the full European Heart Rhythm Association (EHRA) consensus document on the management of supraventricular arrhythmias, published in Europace. It summarises developments in the field and provides recommendations for patient management, with particular emphasis on new advances since the previous European Society of Cardiology guidelines. The EHRA consensus document is available to read in full at http://europace.oxfordjournals.org

Clinical electrophysiology has made the traditional classification of rapid atrial rhythms into flutter and tachycardia of little clinical use. Electrophysiological studies have defined multiple mechanisms of tachycardia, both re-entrant and focal, with varying ECG morphologies and rates, authenticated by the results of catheter ablation of the focal triggers or critical isthmuses of re-entry circuits. In patients without a history of heart disease, cardiac surgery or catheter ablation, typical flutter ECG remains predictive of a right atrial re-entry circuit dependent on the inferior vena cava-tricuspid isthmus that can be very effectively treated by ablation, although late incidence of atrial fibrillation remains a problem. Secondary prevention, based on the treatment of associated atrial fibrillation risk factors, is emerging as a therapeutic option. In patients subjected to cardiac surgery or catheter ablation for the treatment of atrial fibrillation or showing atypical ECG patterns, macro-re-entrant and focal tachycardia mechanisms can be very complex and electrophysiological studies are necessary to guide ablation treatment in poorly tolerated cases. Sin financiación 0.760 SJR (2017) Q2, 133/362 Cardiology and Cardiovascular Medicine, 52/102 Physiology (medical) UEM

Impaired interatrial conduction or interatrial block is well documented but is not described as an individual electrocardiographic (ECG) pattern in most of ECG books, although the term atrial abnormalities to encompass both concepts, left atrial enlargement (LAE) and interatrial block, has been coined. In fact, LAE and interatrial block are often associated, similarly to what happens with ventricular enlargement and ventricular block. The interatrial blocks, that is, the presence of delay of conduction between the right and left atria, are the most frequent atrial blocks. These may be of first degree (P-wave duration > 120 milliseconds), third degree (longer P wave with biphasic [+/-] morphology in inferior leads), and second degree when these patterns appear transiently in the same ECG recording (atrial aberrancy). There are evidences that these electrocardiographic P-wave patterns are due to a block because they may (a) appear transiently, (b) be without associated atrial enlargement, and (c) may be reproduced experimentally. The presence of interatrial blocks may be seen in the absence of atrial enlargement but often are present in case of LAE. The most important clinical implications of interatrial block are the following: (a) the first degree interatrial blocks are very common, and their relation with atrial fibrillation and an increased risk for global and cardiovascular mortality has been demonstrated; (b) the third degree interatrial blocks are less frequent but are strong markers of LAE and paroxysmal supraventricular tachyarrhythmias. Their presence has been considered a true arrhythmological syndrome. (C) 2012 Elsevier Inc. All rights reserved.

Genetic background can be difficult to relate to accepted mechanisms of atrial fibrillation (AF). Mutation of genes encoding cardiac structures can be associated to AF risk without clear definition of mechanisms. Full-time, continuous monitoring of 1 ECG lead (average 12 days / 282±55 h / 22±1.5

Atrial fibrillation (AF) is already an endemic disease, and its prevalence is soaring, due to both an increasing incidence of the arrhythmia and an age-related increase in its prevalence. Indeed, 1–2% of the population suffer from AF at present, and the number of affected individuals is expected to double or triple within the next two to three decades both in Europe and in the USA.1–4 Although epidemiological data for other parts of the world are less robust, a similar increase in AF in the community can be assumed in other countries. Atrial fibrillation causes marked morbidity and mortality on a population basis. Epidemiological observations suggest that AF is still associated with a doubling of mortality, even after adjustment for confounders.2,5 This observation from the last millennium appears to continue into current randomized trials in AF patients. Also, AF is the single most important risk factor for ischaemic stroke. Furthermore, strokes associated with AF result more often in death or permanent disability than strokes that occur as a result of other aetiologies.6–9 The presence of AF is also associated with a marked reduction in everyday functioning and quality of life.10–13 The harm associated with AF and the perceived detrimental effects of the arrhythmia on general health contrast with the outcome of six trials that compared a ‘rate control’ therapy strategy, aiming at accepting AF and controlling the ventricular rate, with an antiarrrhythmic drug-based ‘rhythm control’ therapy strategy, aiming at maintenance of the ‘natural’ sinus rhythm. Apart from a slight improvement in 6 min walk test in a small trial14 and post hoc analyses,15 the outcome of patients randomized to rhythm control therapy was not better than patients randomized to rate control therapy,14,16–20 …

This paper is an executive summary of the full European Heart Rhythm Association (EHRA) consensus document on the management of supraventricular arrhythmias, published in Europace. It summarises developments in the field and provides recommendations for patient management, with particular emphasis on new advances since the previous European Society of Cardiology guidelines. The EHRA consensus document is available to read in full at http://europace.oxfordjournals.org

Background and Objective: Electrical defibrillation is very effective in interrupting atrial fibrillation (AF). However, its mechanism is not completely understood. We report our observations in patients subjected to external electriocardioversion (ECV) of atrial fibrillation and contrast them with recent theories about defibrillation mechanism. Methods: In 13 consecutive patients transthoracic electrical cardioversion for AF was performed during an electrophysiological study (11 monophasic -200–360 J- and 9 biphasic shocks -50–150 J-). About 10–16 electrograms were obtained with multipolar catheters recording right atrium, coronary sinus, and right pulmonary artery. AF was defined by interelectrogram intervals and changing sequences among recordings, indicating complete lack of organization. We evaluated the presence of propagated activations immediately (

Atrial fibrillation (AF) is associated with impaired functional capacity and quality of life and significant morbidity and mortality. The current management approach fails to maintain stable sinus rhythm (SR) in the majority of patients. For many years, guidelines have recommended antiarrhythmic treatment of a first AF episode only if the AF is poorly tolerated, a position that has been reinforced by studies showing no mortality or morbidity advantage of rhythm control over rate control. During the last decade, research has shown mechanisms of self-perpetuation of AF based on electrophysiological and structural remodelling induced by AF itself. There is mounting evidence that 'lone' AF is because of a host of factors, some of which may be easily treatable, such as hypertension, sleep apnoea, and obesity, thus allowing secondary prevention at the time of the first episode of AF. According to these concepts, lack of early intervention could be one of the reasons for long-term failure of maintenance of SR. In this position paper, we propose testing the working hypothesis that if an SR maintenance strategy is selected, treatment of AF should commence at the first-detected episode and should be based on a double strategy of SR restoration and aggressive treatment of associated conditions that promote atrial remodelling.

Los estudios electrofisiologicos invasivos han cambiado la perspectiva clinica de los pacientes con fluter auricular. El conocimiento de la estructura del circuito de fluter tipico ha permitido desarrollar tecnicas de ablacion con cateter que eliminan las recidivas en > 90% de los casos. Tambien ha cambiado el concepto global de las taquicardias auriculares, lo que ha hecho obsoletas las clasificaciones basadas en el electrocardiograma. Se han demostrado circuitos reentrantes atipicos basados en cicatrices quirurgicas o en zonas fibroticas en ambas auriculas, que son tambien asequibles a tratamiento por ablacion y que en el electrocardiograma son indistinguibles de una taquicardia focal. La ablacion amplia de la auricula izquierda para el tratamiento de la fibrilacion auricular esta dando lugar a un nuevo tipo de taquicardias reentrantes que puede ser problematico en el futuro. Las tecnicas de mapeo y encarrilamiento de los circuitos descritas inicialmente en el fluter permiten definir estos circuitos. El mapeo electroanatomico, que construye moldes anatomicos virtuales de las auriculas, es de gran ayuda en estos casos. A pesar del exito de la ablacion, el pronostico a largo plazo se ensombrece con frecuencia por la aparicion de fibrilacion auricular, lo que indica que hay un sustrato arritmogenico comun al fluter y la fibrilacion, que la ablacion del istmo cavotricuspideo no cambia. En contraste con la clara definicion electrofisiologica, hay escasa informacion sobre el curso clinico del fluter, ya que tradicionalmente la bibliografia se refiere a grupos de «fluter y fibrilacion auricular» y las complejas relaciones entre ambas arritmias quedan aun por revelar claramente. La prevencion primaria y la prevencion de la aparicion de fibrilacion auricular tras la ablacion son retos pendientes.

Introduction: The high posterolateral right atrium (RA) is considered the “sinus node area,” but we lack information on endocardial atrial activation in sinus rhythm. We studied RA and left atrial (LA) endocardial activation in the electrophysiology laboratory. Methods and Results: Thirty-five patients (21 men) aged 47 ± 16.4 years (mean ± SD) underwent RA mapping (22.2 ± 3.8 points). In 21 patients, LA activation was mapped (11.1 ± 3.9 points) through the coronary sinus (CS), right pulmonary artery, and/or a patent oval foramen. Fourteen patients had atrial arrhythmias, and 3 an ECG pattern of Bachmann's bundle block. Endocardial RA activation preceded P wave in 5 (–14 ± 4.2 ms), coincided in 11, and followed P onset in 18 (16.7 ± 6.6 ms). Location of the zero point varied from the superior vena cava to the low RA and from lateral to paraseptal RA. In 19 patients, activation started simultaneously in 2 to 5 points located ≥1 cm apart. RA activation was descending in most, but in 3 with low onset there was collision in the anterior and septal walls. In 15 of 21 patients, descending LA activation dominated, ending in the mid CS in 12, proximal CS in 1, and simultaneously throughout the CS in 2. In 3 with Bachmann's bundle block, CS activation was ascending and in 2 double potentials were recorded from the LA roof. Conclusion: During stable sinus rhythm, RA activation can start in different areas or simultaneously over large areas resulting in different activation patterns, both in the RA and the LA. LA activation is predominantly descending, but in Bachmann's bundle block it becomes ascending, and double potentials suggest a location of block in the LA roof. (J Cardiovasc Electrophysiol, Vol. 15, pp. 524-531, May 2004)

Sin financiación 1.125 JCR (2016) Q3, 91/155 Medicine, General and Internal UEM

Understanding of typical flutter circuits led the way to the study of other forms of macroreentrant tachycardias of the atria, and to their treatment by catheter ablation. It has become evident that the ECG classification of atrial flutter and atrial tachycardia by a rate cutoff and the presence or absence of isoelectric baselines between atrial deflections is not a valid indicator of tachycardia mechanism. Macroreentrant circuits where activation rotates around large obstacles are the most common arrhythmias found in patients with atypical forms of flutter or atrial tachycardia, especially after surgery for congenital heart disease, however, focal mechanisms can also be found. Large areas of low voltage electrograms, suggestive of severe myocardial damage (fibrosis or infiltration) can be found in many atypical macroreentrant tachycardias at the center of the circuit. Many of these circuits can be mapped precisely, critical isthmuses can be defined, and effective catheter ablation can be performed. The need to match activation maps with anatomy precisely, makes computer assisted, anatomically precise mapping a useful tool. Entrainment techniques have to be used sparingly to avoid tachycardia interruption. In complex cases, ablation can be done in sinus rhythm, after definition of conducting channels between low voltage areas and scars or anatomic obstacles. Long-term prognosis is uncertain and depends on the underlying pathology.

NUNEZ, A., et al.: Severe Mitral Regurgitation with Right Ventricular Pacing, Successfully Treated with Left Ventricular Pacing. A case of severe mitral regurgitation with refractory heart failure, after atrioventricular junction ablation and pacemaker implant, was solved with left ventricular pacing. Mitral regurgitation was related to a change in segmental left ventricular motion during right ventricular pacing.

Atrial fibrillation (AF) is a global health problem. The condition brings an increased risk of stroke, systemic embolism, and heart failure (HF) and is associated with impaired quality of life, frequent hospitalizations, and mortality.[1][1] Observational studies have been the main source of

Atrial fibrillation (AF) is generally considered a progressive disease, typically evolving from paroxysmal through persistent to 'permanent' forms, a process attributed to electrical and structural remodelling related to both the underlying disease and AF itself. Medical treatment has yet to demonstrate clinical efficacy in preventing progression. Large clinical trials performed to date have failed to show benefit of rhythm control compared with rate control, but these trials primarily included patients at late stages in the disease process. One possible explanation is that intervention at only an early stage of progression may improve prognosis. Evolving observations about the progressive nature of AF, along with the occurrences of major complications such as strokes upon AF presentation, led to the notion that earlier and more active approaches to AF detection, rhythm-reversion, and maintenance of sinus rhythm may be a useful strategy in AF management. Approaches to early and sustained rhythm control include measures that prevent development of the AF substrate, earlier catheter ablation, and novel antiarrhythmic drugs. Improved classifications of AF mechanism, pathogenesis, and remodelling may be helpful to enable patient-specific pathophysiological diagnosis and therapy. Potential novel therapeutic options under development include microRNA-modulation, heatshock protein inducers, agents that influence Ca(2+) handling, vagal stimulators, and more aggressive mechanism-based ablation strategies. In this review, of research into the basis and management of AF in acute and early settings, it is proposed that progression from paroxysmal to persistent AF can be interrupted, with potentially favourable prognostic impact.

A special form of macroreentrant atrial tachycardia (MRAT), due to reentrant activation around surgical scars, can occur in patients after cardiac surgery. Scar MRAT occurs usually after correction of congenital defects, such as atrial or ventricular septal defects, and especially after Mustard, Senning or Fontan procedures, but it can occur also after myxoma, valvular or coronary bypass surgery. The simplest form of scar MRAT is reentry around a lateral right atrial surgical scar. A basic mapping array with multiple simultaneous recordings from the anterior and septal right atrium is very useful to make the electrophysiological diagnosis. A line of double electrograms can be mapped in the centre of the circuit and a fragmented electrogram usually marks the pivoting point between the inferior end of the scar and the inferior vena cava (IVC). Extension of the scar toward the closest fixed obstacle, usually the IVC, by means of radiofrequency ablation, can interrupt the tachycardia and make it non-inducible. Typical atrial flutter usually coexists with scar MRAT and flutter isthmus ablation is probably indicated in all cases. In patients having undergone baffle atrial surgery it can be impossible to map the whole circuit and entrainment-mapping is helpful to localize critical isthmuses in the circuit. After the Fontan operation the right atrium can be severely dilated and scarred, and multiple, complex reentry circuits can be found. Left atrial MRAT based on large areas of scar has been described, but there is still too little experience with these to propose general rules for diagnosis and management.

Current nomenclature for atrioventricular junctions derives from a surgically distorted view, placing the valvar rings and the triangle of Koch in a single plane with antero-posterior and right-left lateral coordinates. Within this convention, the aorta is considered to occupy an anterior position, while the mouth of the coronary sinus is shown as being posterior. While this nomenclature has served its purpose for the description and treatment of arrhythmias dependent on accessory pathways and atrioventricular nodal re-entry, it is less than satisfactory for the description of atrial and ventricular mapping. To correct these deficiencies, a consensus document has been prepared by experts from the Working Group of Arrhythmias of the European Society of Cardiology, and the North American Society of Pacing and Electrophysiology. It proposes a new, anatomically sound, nomenclature that will be applicable to all chambers of the heart. In this report, we discuss its value as regards the description of the atrioventricular junctions, establishing the principles of this new nomenclature.

Mechanisms of Flutter Induction. Introduction: Typical flutter is due to reentry around caval veins and terminal crest. In patients with typical flutter, reversed (clockwise) reentry can be induced. We studied mechanisms of typical and reversed flutter induction. Methods and Results: Thirteen patients (11 men) underwent 16 radiofrequency (RF) ablation procedures for typical (12) or reversed flutter (1), High right atrium (RA) stimulation included 1 to 3 extrastimuli over cycle lengths 6(M) to 250 msec, and burst. We recorded simultaneously from three levels of septal and anterior RA. RF was delivered to the inferior vena cava-tricuspid isthmus (CTI). Of 25 inductions, 4 were a result of single, 9 double, and 11 triple extrastimuli, and 1 burst. Clinical basal flutter was induced (7 typical, 1 reversed). After RF, typical flutter was reinduced in 9 cases and reversed flutter in 7, with only typical flutter seen clinically. All flutters were interrupted by ablation or catheter pressure on the CTI. Typical flutter began by low RA septal activation block, preceded by repetitive responses in 12 instances, atypical flutter in 1, and directly from stimuli in 4. Reversed flutter started in 8 instances by low RA block of a stimulated front descending the anterior wall and in 1 by repetitive responses. Conclusion: Septal activation block was the usual mechanism of typical flutter induction by RA extrastimuli. Facilitation of reversed flutter after RF application is probably due to a new area of block in the CTI. Flutter induction without intermediate rhythms confirms the presence of block at the terminal crest at baseline.

Common atrial flutter is due to a macroreentry circuit in the right atrium, but the cranial path of the circuit has not been defined. The objectives of this article are to determine the cranial turning point of flutter activation in relation to a hypothetic obstacle, the superior vena cava opening, by examining the changes in activation sequence produced by entrainment from different points. In 13 cases of common atrial flutter with typical counter-clockwise right atrial circuits confirmed by endocardial mapping the atrium was paced from the high posterior and mid-septal walls. Entrainment was confirmed by simultaneous recordings of 6-7 right atrial electrograms. Changes in sequence of electrograms from high septum and high anterolateral walls was sought. Electrogram sequence and morphology did not change with entrainment at the posterior wall with respect to the basal flutter or mid-septal wall entrainment. Pacing "below" the superior vena cava did not advance the anterior wall electrogram in relation to the septal electrogram. These findings support the concept that common flutter activation turned around (cranial and anterior to) the superior vena cava opening, and not around the free end of a line of block below the superior vena cava in the posterior wall. Common atrial flutter activation rotates cranial (and anterior) to the superior vena cava opening, through the "right atrial roof." The line of functional block should span from inferior to superior vena cava openings.

Endocardial mapping has led to a detailed knowledge of reentry mechanisms in atrial flutter. Multipolar and deflecting tip catheters allow recording local electrograms from multiple areas of the right atrium, and from the coronary sinus. In common flutter, with the typical "sawtooth" pattern, there is circular activation of the right atrium in a "counterclockwise" direction, descending in the anterior and lateral walls, and ascending in the septum and posterior wall. Superior and inferior vena cava, linked by a "line" of functional block in the posterolateral wall, make the central obstacle for circular activation. The cranial and caudal turning points are the atrial "roof," and the isthmus between the inferior vena cava and the tricuspid valve. Complex conduction patterns, probably including slow conduction are detectable in the low septal area, around the coronary sinus. Atypical flutter, without the sharp negative deflections of common flutter, sometimes shows circular activation in the right atrium, rotating in the opposite direction of common flutter (clockwise). Other atypical flutters show no circular right atrial activation, and only partial data from coronary sinus activation, combined with the response to atrial stimulation (entrainment) allow the diagnosis of left atrial reentry, without a precise delimitation of the circuits. In patients having undergone cardiac surgery, atypical flutter may be based on reentry around surgical scars. To our knowledge, the mechanism of type II flutter has not been disclosed in humans.

The electrocardiographic (ECG) P-wave pattern, >120 ms, and bimodal (±) in inferior leads has been attributed to Bachmann's bundle block. We have mapped left atrial (LA) activation in a patient with mild mitral stenosis, displaying this pattern, and with history …

Understanding the configuration of the whole flutter circuit is for us the only valid parameter allowing the design of an ablation strategy. Fragmented or double electrograms may have different meanings in different parts of the circuit, and full activation mapping is the best clue to their interpretation. Correlation of anatomy with activation sequence will mark the best ablation target (isthmus) in each case. Multiple simultaneous recordings from the septum and right atrial anterior wall are very helpful to rapidly diagnose circular activation of the right atrium. In cases without this type of activation, coronary sinus recordings and the study of postentrainment cycles are helpful to localize the reentry circuit.

Permanent Reciprocating Tachycardia and Preexcitation. The substrate of the permanent form of junctional reciprocating tachycardia is an accessory pathway with no spontaneous anterograde conduction, usually located in the posteroseptal area. We report a case of this type of tachycardia with overt anterograde ventricular preexcitation. Electrophysiologic study confirmed that tachycardia was due to an accessory pathway with long retrograde conduction time; electrophysiologic findings suggested longitudinal dissociation of the accessory pathway. Radiofrequency application at the coronary sinus os resulted in disappearance of preexcitation and cure of the tachycardia.

Antiarrhythmic drug (AAD) use in the clinical setting remains an often frustrating empirical exercise, despite significant advances in understanding the effect of AADs on myocardial ion channels and action potential. Not only is efficacy lower than desired, but prediction of antiarrhythmic versus arrhythmogenic effects of AADs in a particular case is nearly impossible. Vaughan Williams classification1 helped to describe and group AADs and to differentiate between AADs mainly acting on the low diastolic polarization cells (sinoatrial and atrioventricular nodes) for their effect on β-adrenergic receptors and Ca2+ channels and those capable of slowing conduction velocity and/or prolonging the action potential duration of the working myocardium and Purkinje cells. Unfortunately, usefulness of the Vaughan Williams classification for clinicians was limited because it provided incomplete links among AAD actions, arrhythmia mechanisms, and therapeutic results. Modern arrhythmology is dominated by the concept of reentry as the bases of most clinical tachyarrhythmias. Reentry has been conceived generally as continuous activation rotating around a central obstacle, be it fixed or functional, and the equilibrium necessary between refractory period, conduction velocity, and circuit circumference to maintain reentry has been nicely synthesized in the wavelength (WL) concept. WL is the circuit length covered by the activation front in the time lapse of refractory period duration (Figure 1) and, obviously, it must be shorter than total circuit length in order to leave an excitable gap; otherwise, activation would be extinguished by meeting a barrier of refractory tissue. In animal experiments, the WL of the initiating premature impulse was related to the type of inducible atrial arrhythmias, atrial fibrillation (AF) being induced with the shortest WL, and flutter with slightly longer WL.2 The concept of a critical WL for reentrant arrhythmias led to the suggestion that AADs effects should be described in terms of their influence …

Endocardial mapping has suggested that common atrial flutter (AF) is based on right atrial reentry surrounding the inferior vena cava (IVC). The isthmus between the IVC and the tricuspid valve (TV) appears essential to close the circuit. To test this hypothesis, radiofrequency was applied to the IVC-TV isthmus, with catheter electrodes, in 9 patients with AF. Mapping confirmed a right atrial circuit surrounding the IVC in all. In 4 patients another type of AF was induced that followed the circuit in the opposite direction. Radiofrequency interrupted AF in all patients. Multiple endocardial recordings showed that interruption was due to activation block at the point of application. Radiofrequency produced very brief or sustained, atrial fibrillation in 2 patients, which resulted in sinus rhythm. AF recurred in 4 patients with the same activation pattern and was interrupted again with radiofrequency in the IVC-TV isthmus in 3. AF was noninducible in 7 patients after 1 to 4 sessions. AF-free periods of 2 to 18 months without drugs were observed after radiofrequency, but 2 patients had paroxysmal atrial fibrillation. These results confirm that the IVC-TV isthmus is an essential part of the AF circuit. Ablation of this area may be of therapeutic value, but technical improvements are needed. Long-term efficacy of the procedure is uncertain.

Aims Bidirectional block of the cavo-tricuspid isthmus (CTI) is a widely accepted endpoint for typical atrial flutter ablation, but its evaluation may be difficult, especially in the postero-anterior (clockwise) direction. The main goal was to evaluate pacing at the septal edge of the ablation line as an indicator of clockwise CTI block and as a predictor for flutter recurrence. Methods and results In 94 patients undergoing flutter ablation, CTI block in the antero-posterior (counterclockwise) direction was determined by differential pacing from several levels of the anterior right atrial (RA). CTI block in the clockwise direction was evaluated by analysing electrograms (EGM) at the ablation line during differential pacing of the septal RA ( differential septal pacing ) or by anterior sequence of RA during pacing septal isthmus, next to the ablation line ( septal CTI pacing ). Ablation produced bidirectional block in 78% of the patients, unidirectional counterclockwise block in 9% and bidirectional conduction persisted in 13%. After follow-up (37 ± 23 months), flutter recurrence occurred in 13% (48% if persistent conduction vs. 3% if bidirectional block, P < 0.001). During differential septal pacing, EGMs were difficult to interpret in 36% of the patients; in these cases, the diagnosis of CTI block or conduction in the clockwise direction was clearly established by using septal CTI pacing. Conclusion Activation sequence of anterior RA during septal CTI pacing, next to the ablation line, is a reliable and simple method to diagnose clockwise CTI block and is associated with a low flutter recurrence.

The clinical electrophysiologic approaches to atrial flutter (F) have been activation mapping and the observation of changes induced by programmed stimulation. Sequential endocardial activation mapping has recently yielded information indicating that common F is produced by a large right atrial (RA) reentry circuit, with counterclockwise rotation in the frontal plane, including the inferior vena cava in its center. Functional block in the crista terminalis and conduction slowing in the approaches to the atrioventricular node seem to be important to support reentry. F inscribing positive deflections in the inferior leads usually follows the same path, but in a clockwise direction. Atypical F may be produced by left atrial circuits. Atrial stimulation during F entrains the circuit, resetting it with each stimulus. Collision between antidromic and orthodromic activation during entrainment produces fusion that can be identified in the surface electrocardiogram. The last paced activation restarts F, unless circuit penetration has been enough to modify it by block or disorganization. Entrainment may result in F acceleration, with changes in activation sequence, suggesting a different type of reentry, possibly based on functional factors.

Atrial fibrillation (AF) causes important mortality and morbidity on a population-level. So far, we do not have the means to prevent AF or AF-related complications adequately. Therefore, over 70 experts on atrial fibrillation convened for the 2nd AFNET/EHRA consensus conference to suggest directions for research to improve management of AF patients (Appendix 1). The group defined three main areas in need for research in AF: 1. better understanding of the mechanisms of AF; 2. Improving rhythm control monitoring and management; and 3. comprehensive cardiovascular risk management in AF patients. The group put forward the hypothesis that successful therapy of AF and its associated complications will require comprehensive therapy. This applies e.g. to the "old" debate of "rate versus rhythm control", since rhythm control is generally added to underlying (continued) rate control therapy, but also to the emerging debate of "antiarrhythmic drugs versus catheter ablation", of which both may be needed in most patients to maintain sinus rhythm, but also to therapy of conditions that predispose to AF and contribute to cardiovascular complications such as stroke, cognitive decline, heart failure, and acute coronary syndromes. We call for research initiatives aiming at a better understanding of the different causes of AF and its complications, and at development and validation of mechanism-based therapies. The future of AF therapy may require a combination of management of underlying and concomitant conditions, early and comprehensive rhythm control therapy, adequate control of ventricular rate and cardiac function, and continuous therapy to prevent AF-associated complications (e.g. antithrombotic therapy). The reasons for these suggestions are detailed in this paper.

Experimental data have suggested a relation between Torsades de Pointes and early post-depolarization (EPD). We have studied the effect of intravenous verapamil in three patients with atrioventricular block (AVB) and Torsades de Pointes (TP), to obtain indirect evidence of slow membrane channel involvement in the TP mechanism. In two cases TP were completely suppressed and in one there was marked, albeit partial, suppression. In two cases verapamil did not shorten QT, while in the third suppression verapamil was related to junctional escape acceleration and QT shortening. In one of the cases where QT was not changed, the abolition of long pauses may have played a role in TP suppression. The affect of verapamil on TP in our patients is consistent with a combination of mechanisms, including direct membrane effects (EPD inhibition) and junctional pacemaker acceleration. Verapamil might be of therapeutic value in this clinical setting.

Figure 1. Panel A shows the end of an entrainment run from the RV. From top to bottom: leads I, II, and V1 and recordings from the RA roof, anterior RA from high (A1) to low (A4), septal RA from low (S4) to high (S1), CS from proximal (CS1) to distal (CS5) and right pulmonary artery (RPA). Panel B shows the effect of an RV extrastimulus with proximal (His P) and distal (His D) His-bundle area recordings. The right lower panel shows the approximate location of the atrial recording catheters. Case Report A 48-year-old man underwent aortic and mitral valve replacement in 1986 for rheumatic valve disease. In 2004 reoperation was needed for prosthetic thrombosis and a transeptal incision was made to access the left atrium. Before reoperation he had episodes of paroxysmal atrial fibrillation but after the new procedure palpitations were

A 70-year-old lady with diabetes and monoclonal gammopathy underwent pacemaker implant for 2:1 atrioventricular block. Within 7 days, a painful, infiltrating, necrotic lesion involved the implant area. Biopsy was compatible with pyoderma gangrenosum and corticosteroid treatment led to healing in 3 weeks.

Invasive electrophysiologic studies have changed the clinical outlook for patients with atrial flutter. Recognition of the reentrant circuit responsible for typical atrial flutter has led to the development of catheter ablation techniques that can prevent recurrence in >90% of cases. In addition, general understanding of atrial tachycardias has changed radically, such that ECG-based classifications are now obsolete. Atypical reentrant circuits associated with surgical scars or fibrotic areas in either atrium, which are indistinguishable from focal tachycardias on ECG, have been identified. These circuits also seem amenable to treatment by ablation. Recently, a new type of reentrant tachycardia that could be problematic in the future has emerged in patients who have undergone extensive left atrial ablation for the treatment of atrial fibrillation. These atypical circuits can be characterized using the mapping and entrainment techniques initially developed for typical flutter. In these cases, electroanatomical mapping, involving the construction of a virtual anatomical model of the atria, is extremely helpful. Despite the success of ablation, long-term prognosis is frequently overshadowed by the appearance of atrial fibrillation, which suggests that flutter and fibrillation share a common arrhythmogenic origin that is not modified by cavotricuspid isthmus ablation. In contrast with our clear electrophysiologic understanding of atrial flutter, little is known about the natural history of the condition because the literature has traditionally grouped patients with flutter and fibrillation together. Consequently, the complex relationship between the two arrhythmias has still to be clearly delineated. Primary prevention and preventing the development of atrial fibrillation after ablation remain outstanding clinical challenges.

n typical atrial flutter, circular activation around the tricusid ring is possible because the terminal crest prevents hort-circuiting on the posterior wall, and the myocardium etween the inferior vena cava (IVC) and the lower rim of he tricuspid ring is the obligatory pathway to close the ircuit in the low right atrium (RA) (Figure 1). This IVC– ricuspid ring isthmus (cavotricuspid isthmus) has become he preferred target for ablation because it is the narrowest oint of the circuit, it is easily accessible, and it is located ar from the AV junction. Variations of the circuit all share he cavotricuspid isthmus as the obligatory path in the low A (Figure 1). Bidirectional block at the cavotricuspid isthmus has become he accepted endpoint of ablation during sinus rhythm.

strate for the arrhythmia. It is perhaps pertinent to note the limitations of the electrocardiogram diagnosis. The term ‘flutter’ is used to describe rapid atrial tachycardias (AT) with an undulating waveform without isoelectric baseline; however, this has been overlooked by many groups reporting left AT that, as in Coffey’s paper, show rather long cycle lengths, around 300 ms, and longer isoelectric baselines between P-waves. Since the term ‘flutter’ is so closely related to typical flutter, depending on the cavotricuspid isthmus, it tends to suggest a macroreentrant mechanism, and the term ‘atrial tachycardia’ would appear more appropriate, as it does not pre-judge the mechanism. 2 In fact, around one-third of the mechanisms described in this study were focal discharges. The mapping technique, leading to ablation of the critical isthmus or the focus responsible for the arrhythmia, is remarkable because it creates excellent activation maps on the virtual atrial anatomy and allows, with some limitations, better understanding of the arrhythmia mechanism. Reduction of pacing manoeuvres to the minimum necessary to confirm the role of critical areas of the circuit minimizes the chances of altering activation sequences, a significant concern in left atrial macroreentrant AT, in which complex combinations of anatomic and functional obstacles can support multiple reentrant circuits and/or focal mechanisms. The average number of AT mechanisms encountered was 1.9 per patient, and 21 patients had three or more AT mechanisms, underlining the importance of this method. Another point of interest is the extremely low voltage recorded at some of the critical isthmuses that would suggest that activation could course over thin epicardial layers of atrial myocardium over endocardial scars. The interpretation of these local electrograms would be very difficult in the absence of the full activation maps supported with critical entrainment runs to confirm participation of adjacent areas in the circuit. The complexity and low amplitude of the electrograms would make quite impossible to reliably measure local post-pacing intervals at these critical isthmuses. Atrial tachycardia mechanisms were based in both atria and one-third were called septal. Two-thirds of the AT had a macroreentrant mechanism, and about one-third were focal. It is not clear from the paper if combinations of focal and macroreentrant mechanisms were found in the same patient and if more than one AT could be localized at distant sites in the same patient, but the report does give the general impression of dealing with severely diseased (remodelled? injured?) atria. The worse performance with ‘septal’ AT raises questions about the ability to precisely locate foci or critical isthmuses in this anatomically complex area. This seems particularly relevant because fragmented electrograms are often recorded from the septal atrial walls 3 and this

Asymptomatic Brugada Syndrome. Typical ECG of that described for Brugada syndrome was elicited in a patient diagnosed with labyrinthopathy during infusion of dimenhydrinate, a first-generation antihistamine usually used to treat motion sickness. Although the patient had no history of syncope or palpitations, and there was no family history of cardiac disease or sudden death, the ECG abnormality was reproduced later with intravenous flecainide, and an asymptomatic Brugada syndrome was diagnosed.

Aims To describe the mechanisms of induction of ventricular fibrillation (VF) by rapid atrial rates in patients with hypertrophic cardiomyopathy (HCM). Methods Electrophysiological studies, management and follow-up in three patients with HCM with VF induced by atrial pacing. Results In one patient, spontaneous sinus tachycardia triggered VF. In another patient, VF occurred after verapamil infusion during rapid atrial fibrillation, and in the remaining patient there was no clinical VF. In all three patients, short runs of atrial pacing (cycle length 272–380 ms) induced VF, and QRS widening preceded fibrillation in all patients. Marked ventricular electrogram fragmentation was documented in one patient during atrial pacing and in another patient during late ventricular extrastimuli. Hypotension was associated with sinus tachycardia in one patient. The two patients developing clinical VF underwent atrioventricular (AV) junctional ablation; a ventricular defibrillator was implanted in one, and a mode-switching dual-chamber pacemaker in the other. No arrhythmic events occurred during 34- and 35-month follow-up, respectively. In the other patient, postatrial fibrillation pauses caused syncope, and he is asymptomatic 52 months after implantation of a dual-chamber pacemaker. Conclusions Rapid atrial rates can trigger VF in some patients with HCM, probably through a combination of electrophysiological and ischaemic mechanisms. AV junctional ablation may prevent VF in selected cases.

This editorial refers to ‘Anatomical variations of the right coronary artery may be a source of difficult block and conduction recurrence in catheter ablation of common-type atrial flutter’ by H.U. Klemm et al., on page 1608 Linear ablation of the inferior vena cava-tricuspid isthmus (CTI) has become the standard treatment for typical atrial flutter (AFL), the most common regular atrial tachycardia in clinical practice. The reasons for making the CTI the ablation target were its position as an obligatory path closing circular activation in the lower right atrium, its relative narrowness, good accessibility, and its safe distance to the atrioventricular junction. The accessibility of the CTI from the femoral vein approach did initially create expectations of an easy ablation procedure; however, 15–20% of cases pose a significant challenge, needing prolonged radiofrequency (RF) applications and long procedure times. Initial ablation procedures were performed during AFL, applying RF with electrodes 4 mm in length, a power limit of 50 W, and using AFL interruption and non-inducibility as the endpoints, and recurrence rates were 30–50%. When a bidirectional, persistent CTI block became the endpoint, recurrence rates fell to a mere 3–5%.1 The definition of CTI block as the ablation endpoint allowed performing ablation during sinus rhythm, improving catheter stability in some cases. Further progress was made by designing special catheter curves or using guiding sheaths to improve stability of the ablation electrode on the CTI, but the main breakthrough was the use of larger electrodes (8–10 mm in length) allowing the … *Corresponding author. Tel: +34 91 683 0781; fax: +34 91 624 7313, Email: fgarciacosio.hugf{at}salud.madrid.org