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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.

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

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.

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.

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 …

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.

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.

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

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

Abstract —Current nomenclature for the atrioventricular (AV) 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, although the mouth of the coronary sinus is shown as being posterior. Although this nomenclature has served its purpose for the description and treatment of arrhythmias dependent on accessory pathways and atrioventricular nodal reentry, 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 for description of the AV junctions, establishing the principles of this new nomenclature.

BACKGROUND The mechanisms of common atrial flutter entrainment have not been directly studied in humans. METHODS AND RESULTS Endocardial mapping in six cases of common flutter showed large right atrial (RA) reentry circuits. Activation was craniocaudal in the anterolateral right atrium and caudocranial in the septum. The inferior vena cava-tricuspid isthmus (IVC-TV) closed the circuit. The high right atrium was paced at progressively shorter cycle lengths (CLs) in all, and the IVC-TV was paced in three cases. We recorded six to eight simultaneous RA electrograms from septum and anterior wall. Transient entrainment was recognized from all sites by capture of all electrograms at two or more paced CLs, with total or partial preservation of baseline flutter sequence and return to baseline after pacing. Antidromic circuit penetration was documented in five cases during high RA pacing and in one with IVC-TV pacing. Short CLs induced orthodromic conduction delays that resulted in a postpacing pause longer than basal flutter CL. ECG fusion with high RA pacing correlated poorly with antidromic septal penetration. This was related to overlap of orthodromic septal activation with anterior wall activation of the following cycle. Pacing disorganized flutter into a brief irregular rapid rhythm in two cases and atrial fibrillation in one case. In two cases, complete antidromic septal penetration led to sudden flutter interruption, and in another case it led to circuit inversion. CONCLUSIONS Direct recordings confirm orthodromic and antidromic penetration of flutter circuits by high and low RA pacing. Short CLs modify the circuit. Disorganization is the most common mode of flutter interruption.

The electrophysiologic substrates of atrial flutter and fibrillation (AFF) have been studied in patients with paroxysmal arrhythmias. Atrial repetitive responses to extrastimuli are a nonspecific response, even though they can precipitate AFF. AFF inducibility is rather sensitive, but not very specific, in separating patients from controls. There is no established protocol to explore vulnerability in this fashion. Atrial refractoriness is abnormal in some patients. Some authors have found a tendency toward short effective refractory periods (AERP) and others have found a poor adaptation of AERP to decreases in cycle length. Unfortunately, these abnormalities are neither sensitive nor specific enough. Atrial conduction may be abnormal basally, but subtler abnormalities are shown by premature stimulation. Early extrastimuli are conducted with increased conduction delays in patients with paroxysmal AFF in relation to controls. Again, there is not enough sensitivity and specificity in the findings to make them of diagnostic value. Electrophysiologic abnormalities are detectable in patients with AFF, but larger studies, including reproducibility and the effect of drugs on the abnormal parameters, will be necessary to develop clinical applications.