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This report presents the outcome of a cohort of 94 patients with atrial fibrillation from the Canadian Registry of Atrial Fibrillation, in which we paid particular attention to the probability of stroke and death. We also evaluated warfarin use over time and compared left atrial dimensions in patients with atrial flutter with those with atrial fibrillation.
The association of different types of tachycardia in a given patient is a well-known phenomenon and the development of ablative methods rises hopes that treatment of one of them may suppress the others. The aim of this study was to determine the significance of induction of atrial flutter or fibrillation (AF) during electrophysiological investigation of patients investigated for paroxysmal junctional tachycardia. The initial population of 500 patients was limited to 485 patients, aged 12 to 86, with a normal intercritical ECG and without a Wolff-Parkinson-White syndrome, who underwent electrophysiological investigation for junctional tachycardias since 1978 and in whom the tachycardia could be reproduced. The study was performed by the endocavitary approach in 262 cases and by the transoesophageal approach in 213 cases with a similar protocol, programmed atrial stimulation with 1 and 2 extrastimuli under basal conditions, eventually completed by the repetition of the protocol with low doses of isoproterenol. The electrophysiological study showed that the tachycardia involved a latent bundle of Kent in 103 cases, a double nodal pathway in 343 cases or another circuit in 39 cases. During this study, sustained AF was induced in 66 cases (13.5%) with a similar incidence in Kent bundles (14.5%), intranodal reentry (11%) and other forms of reentry (11%). During follow-up, ranging from 6 months to 10 years, 7 patients with induced AF and 9 without inducible tachycardia, developed permanent AF. The occurrence of the arrhythmia was significantly correlated with the mechanism of reentry (latent Kent 8/103 cases, intranodal reentry 8/343 cases, p < 0.05), and with the induction of the same arrhythmia by oesophageal investigation alone (p < 0.001). The initiation of the arrhythmia by endocavitary stimulation did not seem to have any positive predictive value. In conclusion, the induction of atrial flutter or fibrillation during investigation of a subject with paroxysmal junctional tachycardia without a patent Wolff-Parkinson-White syndrome, does not seem to be predictive of future development of atrial flutter or fibrillation, unless the investigation was undertaken by the oesophageal approach.
INTRODUCTION: The "flutter isthmus," the part of the lower right atrium between the eustachian valve and the tricuspid annulus inferior to the coronary sinus os, is considered the crucial zone for conduction delay necessary for the genesis of atrial flutter. However, the underlying mechanism remains unclear. METHODS AND RESULTS: We studied the "flutter isthmus" in 50 hearts obtained at autopsy from patients without atrial tachyarrhythmias. The muscular trabecular arrangement was dissected carefully by peeling off the endocardium. Documentation of the trabecular arrangement focused, in particular, on the question of whether there was a uniform pattern of well-aligned muscle trabeculae or a nonuniform architecture. It appeared that a nonuniform trabecular pattern prevailed (37/50 [74%]). In these hearts, the muscular arrangement showed abundant cross-overs and interlacing trabeculae, particularly in the zone immediately inferior to the coronary sinus os. Connections also occurred along the inferior rim of the os. CONCLUSION: The normal anatomy of the lower right atrium favors nonuniform muscular trabeculation, with interlacing bundles and a multitude of cross-overs. The potential for conduction delay is present in the vast majority of normal hearts. This raises the question as to what has changed in the hearts of patients with atrial flutter such that the potential for conduction delay and reentry has become effective.
AIMS: Trials of rate control vs. rhythm control for atrial fibrillation or flutter included few patients with new-onset arrhythmia. Our objective was to assess the relapse rate and the effect of the relapse of new-onset atrial arrhythmias on mortality after direct-current cardioversion (DCCV). METHODS AND RESULTS: A cohort of 351 patients with atrial fibrillation (new onset in 179) and 126 patients with atrial flutter (new onset in 78) was followed-up after DCCV. Cox proportional hazard models were used. Median age was 74.6 years. Mean follow-up for relapse was 7.7 months; for death, 29.4 months. Patients with new-onset atrial flutter [adjusted hazard ratio (HR) = 1] were more likely to maintain sinus rhythm than the patients with recurrent atrial flutter (adjusted HR = 2.5, P < 0.01), new-onset atrial fibrillation (adjusted HR = 2.4, P < 0.01), or recurrent atrial fibrillation (adjusted HR = 2.7, P < 0.01). Patients with new-onset atrial fibrillation were as likely to have relapses as patients with recurrent atrial fibrillation or flutter. Relapse of atrial arrhythmia after DCCV was associated with increased mortality (adjusted HR= 3.1, P < 0.01). CONCLUSION: DCCV is more successful in maintaining sinus rhythm in patients with new-onset atrial flutter than in patients with new-onset atrial fibrillation. Relapse of atrial arrhythmia after cardioversion is associated with increased mortality.
AIMS: To evaluate the clinical and electrophysiological features of atypical atrial flutter (AAF) and its response to radiofrequency catheter ablation. METHODS AND RESULTS: In 90 consecutive patients referred for sustained atrial flutter, bipolar recordings were obtained from the tricuspid annulus, coronary sinus, interatrial septum and left atrium. AAF was defined by the absence of concealed entrainment from the inferior vena cava--tricuspid annulus isthmus. Target sites were identified by early, fragmented or double potentials and by concealed entrainment. Linear lesions were created between target sites and nearby anatomical barriers in a temperature-controlled mode: 20 episodes of AAFs were documented in 19/90 (21%) patients. Mitral valve disease and surgery were significantly more frequent in patients with AAF. Target sites were identified in the right atrial free wall (n=8), interatrial septum (n=6), left atrium (n=4) and coronary sinus (n=2). Effective ablation was obtained in 15/19 patients (79%). After a 15.7 +/- 10.7 month follow-up, AAF recurred in 0/15 patients with a successful and 3/4 (75%) with a failed procedure (P<0.05). CONCLUSIONS: Conventional mapping techniques enable identification of critical sites of AAF and allow successful ablation in the majority of cases.
A rare case of clinical cardiac arrest after acute DC cardioversion is presented. The patient was a 64-year-old man with acute haemodynamically unstable atrial flutter. He was known to have had episodes of atrial flutter requiring DC cardioversion, and he was treated with propafenone (300 mg twice daily). Synchronised DC cardioversion resulted in cardiac arrest. Resuscitation was initiated and after 2-3 minutes the patient regained sinus rhythm and pulse. There were no sequelae. We conclude that cardiac arrest is a rare complication to DC cardioversion.
An 87-year-old man was referred to our institution to undergo radiofrequency catheter ablation for typical atrial flutter. A decapolar electrode catheter with an interelectrode spacing of 1mm positioned at the cavotricuspid isthmus (CTI) exhibited 2 discrete potentials. The first electrogram was recorded at a site close to the tricuspid annulus and the second at a site close to the inferior vena cava at the CTI. Entrainment study showed that the first component was crucial to maintain the artrial flutten; however, the second one was found to function as a bystander portion of the reentrant circuit. Radiofrequency energy application at the site where the first potential was inscribed could terminate the atrial flutter creating a complete bidirectional conduction block at the CTI.
Much of our understanding of the mechanisms of macro re-entrant atrial tachycardia comes from study of cavotricuspid isthmus (CTI) dependent atrial flutter. In the majority of cases, the diagnosis can be made from simple analysis of the surface ECG. Endocardial mapping during tachycardia allows confirmation of the macro re-entrant circuit within the right atrium while, at the same time, permitting curative catheter ablation targeting the critical isthmus of tissue located between the tricuspid annulus and the inferior vena cava. The procedure is short, safe and by demonstration of an electrophysiological endpoint - bidirectional conduction block across the CTI - is associated with an excellent outcome following ablation. It is now fair to say that catheter ablation should be considered as a first line therapy for patients with documented CTI-dependent atrial flutter.
A patient with sick sinus syndrome (SSS) presented with episodic lightheadedness and weakness. The electrocardiographic features were marked supraventricular bradyarrhythmias and paroxysmal atrial flutter. The symptoms lasted for four years and disappeared with the onset of stable atrial flutter which has persisted for the past seven years. Over the 11-year period of observation, there has been progressive involvement of the His-Purkinje system manifested by the development of left anterior fascicular block, right bundle-branch block, and prolongation of the HV conduction time. The patient has refused pacemaker implantation. In the absence of angina and in the presence of a normal heart size, the etiology of his SSS is postulated to be idiopathic fibrosis of his conduction system.
An 8 1/2-year-old child without heart disease developed nonsustained atrial flutter by programmed atrial stimulation. Atrial re-entry was the underlying mechanism.
We describe a case of isthmus-dependant atrial flutter ablation with a superior approach due to an anomalous inferior vena cava (IVC), azygos, and emiazygos continuation. A 56-year-old man was referred to our institution for the treatment of a common atrial flutter. Two years prior, the patient had an attempted electrophysiological study not performed due to the inability to advance the guidewire through IVC. A computed tomography of the abdominal venous system revealed the absence of the subrenal IVC, azygos, and emiazygos continuation. Following double puncture of the left subclavian vein, two catheters were inserted into the coronary sinus and into the right atrium. Programmed atrial stimulation was performed and a sustained isthmus-dependant right atrial tachycardia was obtained. After 11 applications of radiofrequency energy with an inversion technique, sinus rhythm was restored and a repeat atrial programmed stimulation failed to induce any arrhythmia.
Little information is available about rate dependent changes in electrical activity of human myocardial cells. We therefore studied, in vitro, the electrical activity of adult human atrial fibres driven at frequencies near that of atrial flutter by means of the standard microelectrode technique. Thirty two atrial samples exhibiting "normal" responses with fast upstroke were selected. At very high frequencies, the action potential (AP) upstroke arose from the repolarisation phase of the preceding AP in spite of marked frequency induced shortening of the plateau. As the stimulation rate was progressively increased, the take off potential (TOP) was less and less negative and the maximal rate of depolarisation (Vmax) decreased. Moreover, in most preparations, a clear alternation between two types of action potentials occurred. Calcium channel inhibitors cobalt (5 mM) or diltiazem (5 x 10(-6) M) shortened AP duration, increased Vmax and markedly reduced alternation. Sodium channel inhibitors, tetrodotoxin (7.5 10(-6) M) or lignocaine (10(-5) M) shortened AP duration and induced a transient increase in Vmax. Ouabain (10(-6) M) prolonged AP duration, decreased Vmax, enhanced alternation and finally suppressed the 1:1 capture of the atrial tissue. Our results show that, at high driving rates corresponding to the frequencies of atrial flutter, slight variations in action potential duration induced by drugs are associated with marked concomitant variations in Vmax and probably with consequent modifications of the conduction velocity.
OBJECTIVE: To determine how well dofetilide and Betapace AF (sotalol, approved solely for atrial fibrillation and atrial flutter), with their detailed dosing and monitoring guidelines for safety, were accepted into clinical practice during the 2 calendar years after their introduction. METHODS AND RESULTS: We reviewed the number of new, refill, and total prescriptions of all antiarrhythmic agents in the United States from April 2000-December 2001 to assess use of dofetilide and Betapace AF in the drug market. Both were prescribed very infrequently throughout the study period. In addition, the infrequent reported use of these drugs for patients with atrial fibrillation and flutter indicated poor acceptance of these agents by prescribing physicians. We speculated that the restricted distribution and required educational program for dofetilide, as well as the availability of generic sotalol products, may have discouraged physicians from prescribing both dofetilide and Betapace AE CONCLUSION: A common goal for both the dofetilide risk-management program and the creation of a sotalol product indicated solely for atrial fibrillation and atrial flutter was to provide safer treatment for patients with these arrhythmias. Unfortunately, limited penetration of dofetilide and Betapace AF into the U.S. market suggests that drugs without a risk-management program or detailed dosing guidelines were more likely than dofetilide or Betapace AF to be selected for treatment of atrial fibrillation and atrial flutter.
BACKGROUND: Radiofrequency energy has demonstrated its efficacy in catheter ablation of atrial flutter (AFl). However, long-term recurrences of AFl have been reported frequently after initial, apparently successful ablation. To date, criteria for prediction of late recurrences are lacking. METHODS AND RESULTS: Twelve patients (10 men; mean age, 53.6 years; range, 26 to 69 years) were referred for AFl ablation. Duodecapolar and decapolar catheters were used for detailed mapping of the tricuspid ring, the inferior vena cavatricuspid annulus (IVC-TA) isthmus, and the coronary sinus ostium (CSOs) area. Additional multipolar catheters were used for recording activation of the coronary sinus and the CSOs-TA isthmus. AFl was present at baseline in 9 patients and was induced by proximal coronary sinus (PCS) pacing in 3. Counterclockwise right atrial activation was recorded in all patients. Primary success of ablation was defined as when AFl was no longer inducible even during isoproterenol infusion. AFl was successfully ablated in all 12 patients, with a median of 4 pulses delivered at the IVC-TA isthmus. In the 3 patients in whom AFl was induced, during PCS pacing in sinus rhythm before ablation, a collision of descending and ascending wave fronts was observed at the middle lateral right atrium (LRA). This activation pattern of the LRA also was noted after unsuccessful radiofrequency applications. Noninducibility of AFl after radiofrequency applications was associated with a change of activation pattern at the LRA and with an inversion of the activation sequence of the IVC-TA isthmus (from clockwise to counterclockwise) in 9 patients when pacing from the PCS. In 2 of 3 patients, despite noninducibility of atrial flutter, ablation was pursued to obtain evidence of permanent block of conduction at the IVC-TA isthmus. Finally, a completely descending LRA wave front was observed when pacing from the PCS in all patients except one. Low LRA pacing was also performed in 4 patients and showed evidence for block in the counterclockwise direction at the isthmus. During a follow-up of 9 +/- 3 months, AFl recurred in 1 patient; this was the only patient who showed no conduction block at the isthmus after the procedure. CONCLUSIONS: Direction of impulse propagation at LRA and block of propagation at the IVC-TA isthmus during PCS and low LRA pacing appear to be of interest in predicting long-term success of AFl ablation.
OBJECTIVE: The purpose of this study is to determine the reliability of activation sequence mapping in assessing the presence of bidirectional conduction block (BCB) in typical atrial flutter (AFL) ablation. INTRODUCTION: Radiofrequency ablation (RFA) can cure typical AFL by creating BCB across the right atrial isthmus. Effective conduction block across this region can prevent AFL recurrence, but accurate assessment of isthmus conduction may be flawed. METHODS: BCB was measured before and after RFA by pacing at multiple rates on both sides of the isthmus during sinus rhythm. Pacing was performed from a low lateral tricuspid annulus site (proximal to the isthmus) and a coronary sinus Os site (distal to the isthmus), while recording simultaneously from 8-10 right atrial sites bordering the isthmus (4-5 free wall sites; 4-5 septal sites) as well as from an isthmus site. After ablation reinduction of atrial flutter was attempted from both sides of the block with rapid atrial pacing after BCB was established in all patients. In some patients lines of conduction block were evident at the isthmus (using the ablation catheter to map). RESULTS: Of 65 patients undergoing RFA of AFL, 59 had typical AFL. In all 59 patients, BCB was demonstrated at all pacing cycle lengths 30 min after RFA applications. In 6 of these 59, AFL was inducible with atrial pacing despite apparent BCB. Further RFA resulted in non inducibility in all 6 patients. In the remaining 53/59 patients, BCB was associated with noninducibility at 30 min. A total of 8 recurrences were seen during a mean 19.3 +/- 8.3 (SD) month follow-up. CONCLUSION: Apparent BCB as determined by activation sequence mapping outside of the isthmus is an excellent marker, but, as measured, may be a misleading method of assessing the presence or absence of conduction through the isthmus. It is necessary to attempt reinduction of AFL after apparent success. Elimination of typical AFL does not preclude other AFLs.
This report describes a patient with the pulmonary edema after cardioversion for paroxysmal atrial flutter without organic heart disease. A 68-year-old man was admitted to hospital for paroxysmal atrial flutter. Antiarrhythmic agents were not effective, and direct current cardioversion was performed on the 4th hospital day. Three hours after cardioversion, the patient complained of dyspnea, and a chest X-ray showed pulmonary edema. He responded to oxygen, intravenous furosemide and drip infusion of nitroglycerine. During tapering of the medication, his condition remained stable. The patient was discharged on the 7th day after admission. Echocardiographic findings indicated that transient left ventricular diastolic dysfunction due to direct current shock was the most likely cause of the lung edema.
OBJECTIVES: To assess the effect of atrial flutter (AFL) on exercise tolerance in patients with grown-up congenital heart (GUCH), exercise tests with modified Bruce protocol were performed in 20 patients aged 21 to 62 years with GUCH (11 females, 9 males) during symptomatic AFL and again 24 to 48 hours after DC conversion to sinus rhythm (SR). At the same time, cardiac function was assessed by means of transthoracic Doppler echocardiography. RESULTS: Mean exercise duration was significantly less during AFL (6.4 +/- 4.1 min) versus SR (10.9 +/- 3.7 min) (P <.001). Heart rate was faster at rest and peak exercise while in AFL (106 +/- 21 beats/min vs 77 +/- 14 beats/min, P <.001, and 157 +/- 31 beats/min vs 129 +/- 24 beats/min, P <.01, respectively). Systolic blood pressure was lower at peak exercise with AFL (112 +/- 25 mm Hg vs 137 +/- 24 mm Hg, P <.001), as was mean blood pressure increase (5.3 +/- 24.3 mm Hg vs 22.6 +/- 15.8 mm Hg) compared with SR (P <.01). Four of the 6 patients after Fontan surgery had a decrease of 16 mm Hg in systolic blood pressure at peak exercise when in AFL. The reasons for exercise termination during AFL were mainly breathlessness, chest pain, or presyncope, whereas in SR it was caused by fatigue. Echocardiography during AFL showed shorter isovolumic relaxation time (40 +/- 20 ms) compared with SR (50 +/- 20 ms) (P <.05). Ventricular long-axis excursion was reduced (left 1.0 +/- 0.3 cm vs 1.2 +/- 0.4 cm, septal 0.5 +/- 0.2 cm vs 0.7 +/- 0.3 cm, and right 0.7 +/- 0.2 cm vs 0.9 +/- 0.4 cm respectively, P <.001 for all), as were peak pulmonary and aortic flow velocities (85 +/- 30 cm/s vs 105 +/- 50 cm/s, P <.001, and 137 +/- 118 cm/s vs 143 +/- 114 cm/s, P <.02) compared with sinus rhythm. There was a close correlation between exercise duration and blood pressure increase (r = 0.6), left-sided long-axis excursion and blood pressure increase (r = 0.57), and between aortic flow velocity and right-sided long-axis excursion (r = 0.71). CONCLUSIONS: Atrial flutter causes dramatic reduction in exercise tolerance in patients with GUCH, and the combination of fast heart rate and hypotension may contribute to the development of presyncope, particularly in those with Fontan surgery. Marked improvement in effort tolerance and cardiac dynamics occurs after regaining SR. Thus, improving the quality of life in patients with GUCH requires maintaining SR.
The mechanisms of action of antiarrhythmic drugs at atrial level are multiple. Antiarrhythmics may act at three levels in the prevention of paroxysmal atrial fibrillation: on the arrhythmogenic atrial substrate, the initiating extrasystoles including those of the pulmonary veins, and in the modulation of the autonomic nervous system. However, there are many modes of initiation which are not well understood so that the preventive role of the antiarrhythmic drugs remains imprecise. Cardioversion of persistent atrial fibrillation has been better analysed in healthy hearts: Class I antiarrhythmics in particular, despite their depressive effects on the conduction which are potentially arrhythmogenic, are beneficial by decreasing the number of reentry circuits, prolonging the atrial refractory period on short cycles and, paradoxically, by increasing the period of excitability in AF. All have a preferential action on anisotropic conduction, especially at the pivotal point of reentry. On the other hand, their role in electrophysiological remodelling in the prevention of immediate recurrences and in pathological atria, remains poorly understood. As for atrial flutter, despite many clinical and experimental studies with antiarrhythmics, the current predominant role of radiofrequency ablation greatly limits the value of these pharmacological studies.