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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.

We read with interest the 2012 focused update of the ESC Guidelines for the management of atrial fibrillation (AF), and more specifically the recommendations formulated for catheter ablation (CA).1 A class I-level of evidence (LoE) A recommendation is attributed to CA for paroxysmal AF in symptomatic drug-refractory patients. In randomized controlled trials (RCTs), AF recurs off-antiarrhythmic drug (AAD) in one-third of patients, 1 year after a single CA.2,3 We have documented that AF recurs in up to 50% after 2 years, which is in line with other observational studies.4,5 The procedure has a …

The objective of the European Myocardial Infarct Amiodarone Trial (EMIAT) is to assess the efficacy of amiodarone on mortality of patients with depressed left ventricular (LV) function following myocardial infarction (Ml). The rationale for the trial is as follows: patients with poor LV function after acute Ml have a high sudden cardiac death (SCD) mortality; amiodarone is a successful prophylactic therapy against SCD in patients with ventricular arrhythmias; a number of small studies (Canadian Amiodarone Myocardial Infarction Arrhythmia Trial [CAMIAT] pilot study, Basel Antiarrhythmic Study & Infarct Survival [BASIS], and the Polish Amiodarone Trial [PAT]) of prophylactic amiodarone post AMI have shown a beneficial response attributable to amiodarone. Patients are enrolled between 5 and 21 days after acute MI if LV ejection fraction (assessed by multiplegated image acquisition nuclear angiography) is ≤40%. The study group is stratified according to ejection fraction (stratum 1,31–40%; stratum 2, 700 patients are enrolled from >60 centers (13 countries). The total study mortality (10% at 500 days) and the differential mortality of both strata are as anticipated. Side effects have been infrequent and very few patients have been withdrawn from the study. Trial conclusion is forecast for October 1995.

Visible T wave changes of the 1st sinus beat following a ventricular premature beat (VPB) are sometimes observed in the electrocardiograms (ECG) of both healthy subjects and cardiac patients. We hypothesized that ventricular repolarization of the post-VPB beat can be modulated even without visible T wave changes. We analyzed 12-lead ECGs acquired in 7 healthy subjects, with at least 1 VPB/ECG with no visible changes of the 1st post-VPB beat. The spatial T loop of each sinus beat was reconstructed in derived XYZ leads and was characterized by 5 parameters. The 1st post-VPB beat was compared with the 2nd and 3rd pre-VPB beats. In 6 subjects, 1 to 3 T-loop parameters were significantly modified with an average change from -18.9% to 30.1% signifying increased repolarization heterogeneity. In conclusion, heterogeneity of the post-VPB sinus beat can be increased in the absence of visible T wave changes.

A computer model reproduced atrio-ventricular (AV) reentrant tachycardia and its termination by overdrive on-circuit pacing. The model simulated activation waves radiating along a one-dimensional circular pathway, the portions of which represent the atrial, AV nodal, His-Purkinje, ventricular, and bypass parts of the tachycardia circuit. The modeled pathway was composed of 289 elements, and the model distinguished only the depolarized and resting states of constituent elements and introduced differential refractoriness and conduction velocity for each element. Cycle length dependence of AV nodal decremental conduction is also introduced. The experiments with the model examined the capability of overdrive on-circuit pacing to terminate the tachycardia. The results of the study suggest that the usual impression of a regular recovery wave and of a regular excitable window moving uniformly along the macro-reentrant circuit is incorrect. >

A computer model is used to reproduce atrioventricular (AV) reentrant tachycardia in order evaluate the possibility of its termination by overdrive 'on-circuit' pacing. The model simulates activation waves radiating along a one-dimensional circular pathway composed of 289 elements. Experiments examined the capability of overdrive on-circuit pacing to terminate the tachycardia and its dependence on various factors. The results suggest the following: (A) the general impression of a regular recovery wave and of a regular excitable window moving uniformly along the macroreentrant circular path is incorrect; (B) the use of overdrive bursts of several stimuli with a short coupling interval has unpredictable effects; and (C) the use of bursts with coupling interval only slightly shorter than the tachycardia cycle length is more safe (with respect to tachycardia reinitiation) and for certain combinations of the coupling interval and cycle length, prolonged bursts do not reinitiate the tachycardia. >

Objective: Atrial fibrillation (AF) is the most common arrhythmia and it is associated with a five-fold risk of stroke. Atrial fibrillation associated ischaemic strokes and embolisms are more disabling and fatal. We aimed to investigate the time to ischemic stroke/embolism after the diagnosis of AF in patients who never used warfarin. Methods: We analyzed the records of 402674 patients over the age 18 who had the diagnosis of non-valvular atrial fibrillation (AF) according to ICD-10 code I48 from a nation-wide claims and utilization management system which processes claims for all health insurance funds in Turkey since 2007. In this study we have used completely anonymized data. Time-to-event analysis were used to measure the time to ischemic stroke/embolism after being diagnosed with AF. Results: A total of 28187 AF patients (7 %) had ischemic stroke or emboli. Time to ischemic stroke and emboli was 61,25 0,05 months from the first diagnosis of AF. Stroke/emboli was observed earlier in the patients with CHA2DS2-VASc score >1⁄4 2; mean 60,72 0,06 months. Stroke/emboli was observed in patients with CHA2DS2-VASc score 0 and 1 in mean 65,39 0,11 months and mean 65,02 0,09 months respectively. Conclusions: Stroke/emboli was observed in a significant portion of AF patients in 5 years, and increased risk score decreased time to ischemic/embolic event. Stroke/emboli is one of the most important adverse events in AF patients and contributes to mortality and observed earlier in patients with higher risk scores. Therefore anticoagulation and strict control is needed. Figure 1. Warfarin Use according to CHA2DS2-VASc Score -OP-243 Results of Anticoagulation in Patients with CHADS2 Score of 0 and CHA2DS2VASC Score of 1; An Investigation Using the National Turkish Atrial Fibriallation (TRAF) Registry. B. Yavuz, N. Ata, E. Oto, K. Aytemir, S. Okutucu, B. Evranos, D.K. Ozturk, R. Koselerli, E. Ertugay, Y.G. Ilhan, A.J. Camm, A. Oto. Kecioren Teaching and Research Hospital; Social Security Institution; Hacettepe University Faculty of Medicine; MITS; St George’s Medical School, London. The American Journal of Cardiology MARCH 13e16, 2014 10 IN AND C Objective: Atrial fibrillation is associated with ischaemic strokes. Stroke risk is not homogenous and is identified by risk stratification schemes created by adding the risk factors.A new risk score, CHA2DS2VASC risk scheme was developed to decrease the intermediate risk group of CHADS2 risk scheme and to decrease the confusion about anticoagulation. But it has also created a new confusion on anticoagulation of very low risk group of patients. Therefore to detect the effect of anticoagulation in CHADS2 score of 0 and CHA2DS2VASC score of 1 patients we compared offwarfarin and onwarfarin patientswhoseCHADS2 score was 0 and CHA2DS2VASC score was 1. Methods: We analyzed the records of 402674 patients over the age 18 who had the diagnosis of non-valvular atrial fibrillation (AF) according to ICD-10 code I48 from a nation-wide claims and utilization management system which processes claims for all health insurance funds in Turkey since 2007. In this study we have used completely anonymized data. Results: Twenty one percent of on warfarin group and 16% of off warfarin group was hospitalized over 5 years follow up. Major hemorrhage was more frequently encountered in on warfarin group than off warfarin group (2,7% and 1,3 respectively). Stroke/TIA/Systemic Embolism/Death composite endpoint was higher in on warfarin group than off warfarin group, (7,8% and 4,6% respectively). Conclusions: This analysis showed that both hospitalization and major hemorrhages were higher in on warfarin group and warfarin did not decrease the joint endpoint of thromboembolism and death in this low risk group. Therefore this result directs us to question the intermediate risk categorization of CHA2DS2VADSc risk scheme.

Two patients with dystrophia myotonica showed high-grade atrio-ventricular block. Both underwent electrophysiological studies which revealed sinus and A-V nodal disease with normal intraventricular conduction in 1 case and His-Purkinje conduction disease in the other. Dystrophia myotonica may, therfore, involve all parts of the cardiac conduction system and may affect the generation of cardiac impulses. Pacemaker implantation may be necessary especially if drugs such as procainamide, which in addition to controlling myotonic symptoms may aggravate conduction disorders, are to be used.

Summary A 25 year old man had experienced virtually incessant ventricular tachycardia since the age of 16 years, and complained of increasing lethargy and shortness of breath over the past 5 years. Despite medical therapy with numerous conventional antiarrhythmic agents, no single drug or combination of drugs had successfully controlled the tachycardia. Isotope and contrast angiography revealed an enlarged left ventricle with poor function. Electrophysiological studies demonstrated earliest endocardial activation at the left ventricular apex. No electrical procedure terminated tachycardia. Following institution of amiodarone, continuous ECG monitoring revealed periods of sinus rhythm alternating with periods of ventricular bigeminy. Repeat isotope angiography indicated a considerable improvement in L.V. function. There was a corresponding reduction in heart size on the chest radiograph. Clinical improvement was evidenced by disappearance of lethargy and shortness of breath. This report demonstrates that amiodarone, a new antiarrhythmic agent, may suppress long standing incessant ventricular tachycardia resistant to other antiarrhythmic agents. The marked reduction in heart size on amiodarone may suggest that the associated cardiomegaly is secondary to tachycardia.

A computer simulation model of cardiac rhythm disturbances and of the heart/pacemaker interaction has been created and implemented on a NORD-100 minicomputer. The model incorporates important properties including cycle length dependence of the refractory periods of different parts of the heart and of the atrioventricular nodal conduction speed. Computational experiments produce an explicit timetable of polarisation changes, a simulated one-channel electrocardiographic record and a pacemaker marker channel. The simulation program is written infortran and uses discrete event simulation techniques. The heart is modelled using instances of nine simulation process prototypes. The paper presents and discusses several examples in the form of simulated electrocardiographic records and the results show that the model is clinically relevant. Included in the examples are the modelling of rhythm disturbances, pacemaker actions, pacing for tachycardia prophylaxis and atrioventricular nodal conduction disorders.

A computer simulation model of cardiac rhythm and heart-pacemaker interactions has been used to examine the possibility of short atrial-ventricular (AV) delay DDD pacing to prevent junctional reentry tachycardia. The experiments compared the actions of two pacemaker models: a clinically realistic DDD mode operating with quasi-Wenckebach prolongation of the AV delay, and a modification of the DDD mode which is programmed according to atrial and ventricular refractoriness of the heart and the conduction delays of pathological bypass tracts. The pathological phenomena modeled in the experiments simulate different possibilities of tachycardia initiation. The computational results prove that many possible mechanisms of initiation of junctional reentry tachycardia are beyond the prophylactic capabilities of current sophisticated DDD pacemakers. The results also show that the suggested pacing mode improves antitachycardia prophylaxis even when responding to complex pathological episodes of natural cardiac activity. >

Symptomatic myopotential interference was observed in a patient with a respiratory-dependent rate modulated pacemaker (RDP3). During treadmill exercise, prolonged interference suspended the rate responsive function and resulted in reversion to the interference mode with the pacing rate falling back to the basic frequency during the interference. This loss of rate response resulted in severe impairment of exercise tolerance and reduction in cardiac output during exercise. The unit was replaced with a bipolar activity sensing rate modulated pacemaker.

Modern haemodynamic techniques have allowed a greater degree of understanding of the effects of cardiac arrhythmias. The haemodynamic consequences relate to a number of factors which include: the ventricular rate and the regularity of the rhythm, the presence or absence of cardiac disease, the relationship between atrial and ventricular systole, the synchronicity of ventricular contraction, the preservation and level of autonomic tone and disease in other organs1,2.