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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.

Atrial fibrillation, a commonly encountered arrhythmia, has in recent years, been the subject of increased interest and intensive clinical research. There is also increasing awareness that atrial fibrillation is a major cause of embolic events which in 75% of cases are complicated by cerebrovascular accidents[1,2]. Atrial fibrillation is often associated with heart disease but a significant proportion of patients (about 30%) have no detectable heart disease[3]. Symptoms, occasionally disabling, haemo-dynamic impairment and a decrease in life expectancy are among the untoward effects of atrial fibrillation, resulting in an important morbidity, mortality and an increased cost for the health care provider[4]. The Working Group of Arrhythmias of the European Society of Cardiology created a Study Group on Atrial Fibrillation in order to establish recommen-dations for the better management of this arrhythmia and to promote multicentre studies. The purpose of this paper is to briefly outline the state of our knowledge on the clinical presentation, the causes, the mechanisms and therapeutic approaches currently available and to propose recommendations for management. Although atrial flutter can coexist with atrial fibrillation, it is considered a different arrhythmia and will not be covered in the present paper.

Nothing in arrhythmia management should be taken for granted. Errors and mistakes over the last 30 years must now force reappraisal of the arrhythmia risks and the risk-benefits of their treatment. Supraventricular tachycardias have attracted great interest from electrophysiologists and the fundamental mechanisms of many are now well established. Surprisingly, however, very little is known of the long-term implications of supraventricular tachycardias in terms of quality and quantity of life. Not even for asymptomatic WPW syndrome is there consensus in this regard. The extent of our deficiencies in knowledge need to be appreciated and more must be done to understand the natural history of these events.

The aim of this study was to quantify electrocardiographic changes during the onset and early stages of ventricular fibrillation. Thirty recordings of ventricular fibrillation (mean duration 57 s, range 24–160 s) were obtained from 23. Coronary Care Unit patients. Each recording was investigated using frequency analysis on 1 s epochs of data. A significant rise in the mean dominant frequency of ventricular fibrillation from 3·9 Hz (SD 0·8 Hz) to 5·9 Hz (SD 1·0 Hz) was observed between 1 s and 30 s ( P

Dilated cardiomyopathy is a global myocardial abnormality in which it is likely that there are relatively homogeneous electrical conditions. The pattern of arrhythmic complications, especially atrial ectopic beats, ventricular ectopic beats and the brief salvoes of polymorphic ventricular tachycardia which are characteristic of the condition, suggest that triggered automaticity is a more likely arrhythmia mechanism than reentry. Although treatment with 'conventional' antiarrhythmic agents has an important place, drugs which alter myocardial loading conditions (and thus, thereby, a possible mechanism of triggered automaticity) may be effective. Therapeutic strategies directed against the basic disease processes are in an early stage of clinical development but they hold great promise for the future.

Fascicular tachycardia in young patients without overt heart disease constitutes a rare but electrophysiologically distinct arrhythmia entity. Microreentry within the left posterior fascicle has been proposed as its mechanism, but evidence for this is inconclusive. This report details a patient with incessant fascicular tachycardia. The electrophysiological features, in particular the pattern of resetting response, provided strong evidence for reentry as the tachycardia mechanism. Satisfactory long-term arrhythmia control was achieved with flecainide.

Diuretics and angiotensin-converting enzyme inhibitors currently are the mainstay of both acute and chronic heart failure management. They have earned their place by bringing measurable and reliable clinical benefit to patients with all grades and types of heart failure. Other treatments--digoxin, vasodilators and inotropes--offer less secure efficacy and their clinical role is at times controversial. The need for new remedies is inescapable. Despite current therapy, heart failure causes a distressing reduction in both quality and quantity of life. As knowledge of the pathophysiology of heart failure is gained, more selective treatment options may become available offering hitherto unknown specificity but demanding remarkable levels of diagnostic accuracy.

Low plasma potassium and magnesium concentrations have been advanced as risk factors for ventricular fibrillation (VF). For potassium, this assertion is based almost exclusively on retrospective data; for magnesium the evidence shows an association with ventricular arrhythmias but no direct association with VF. We studied the relationship between these electrolytes and VF prospectively. Plasma potassium and serum magnesium concentrations were measured on admission to our coronary care unit. Drug therapy, time from onset of symptoms, ECG, enzyme changes and clinical status were all recorded. VF was confirmed by analysis of 24 h monitoring tapes. Mean plasma potassium in the 21 patients with VF who had measurements prior to their arrhythmia was 3.49 +/- 0.54 mmol/l, lower than that of the 1165 patients without VF (mean K 3.88 +/- 0.57 mmol/l, p < 0.05). Plasma potassium concentrations in the 17 patients with myocardial infarction and VF were lower (mean 3.58 +/- 0.41 mmol/l) than in those without VF (n = 417, mean 3.89 +/- 0.61 mmol/l) (p < 0.05). Mean serum magnesium in the 12 patients with VF, measured prior to their arrhythmia (all with myocardial infarction) was 0.80 +/- 0.07 mmol/l, which was not different from the mean for patients without VF (n = 781, 0.82 +/- 0.09 mmol/l) or from the mean of 0.81 +/- 0.08 mmol/l for those with infarction but not VF (n = 331). Low plasma potassium concentrations are associated with increased risk of ventricular fibrillation, but low serum magnesium concentrations are not.

Ventricular ectopic complex ( VEC ) activity is seen frequently, both in patients with cardiovascular disease and in normal subjects. It has been claimed to be predictive of cardiovascular disease but in the asymptomatic individual it may be benign. Unifocal ventricular ectopic complexes with activity greater than 2 per 100 on the resting electrocardiogram of an applicant for a flying licence should be assessed. Further investigation including exercise electrocardiography and tape monitoring may be indicated. Even following investigation, empirically high counts may be acceptable only for multi-crew operation. Complex ventricular ectopic activity including multiformity, pairs, ventricular tachycardia, R-on-T ectopic beats, bigeminy and trigeminy, and parasystole, are incompatible with unrestricted certification and most are incompatible with any form of certification as individual risk-stratification is not yet possible. Of these, bigeminal arrhythmias are, however, likely to be the most benign, while R-on-T ectopic complexes and ventricular tachycardia are the most malignant.

Signal averaging to detect abnormalities in the terminal phase of ventricular depolarization has been performed in several groups of patients with various manifestations of ischaemic heart disease. Late potentials were common in patients with VT and in a group of patients having cardiac surgery. Findings in the surgical group highlighted the close correlation of late potentials with delayed, fragmented epicardial activation supporting the hypothesis that late potentials reflect a myocardial substrate which would support re-entrant VT. The findings in the surgical group allowed a definition of late potentials which could be applied to other patients in the study, and also demonstrated a spectrum of late depolarization abnormalities. Signal averaging is technically feasible in the noisy CCU environment but late potentials were detected in few patients early in AMI. Late potentials were also rarely seen in patients with VF and therefore cannot be construed as a predictive index of this arrhythmia.

A simple method was developed for recording epicardial monophasic action potentials intraoperatively in man. Potentials were recorded rapidly and reliably from multiple epicardial sites using a hand-held probe. The feasibility of repolarization mapping was assessed in 30 patients. It was possible to record technically adequate signals from most left ventricular and posterior right ventricular sites (success rates 72% and 61%, respectively), but it was more difficult to achieve satisfactory recordings over the free wall of the right ventricle (success rate 36%). The onset of cardiopulmonary bypass resulted in a transient rise in action potential duration of approximately 30-40 ms in the first minutes of bypass. An approximate steady state was achieved thereafter. Reproducibility of the method was assessed by mapping a small number of sites repeatedly. The 95% confidence limits for an estimate of repolarization time, based on a single potential, were +/- 21 ms. With 4 probe applications at each site, the confidence limits of the estimated site mean were reduced to +/- 8 ms. Based on this approach, statistically significant differences between sites were demonstrated in 9 of 10 patients, confirming that the method is sensitive enough to provide information on regional differences in repolarization. Intraoperative epicardial repolarization mapping has been shown to be a practical possibility. The technique holds promise as a means of assessing the role of dispersion of repolarization in arrhythmogenesis in man.