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PubMed1996

[Complications of radiofrequency ablation: A French experience. Le Groupe de Rythmologie de la Société Francaise de Cardiologie].

The multiplication of the indication of radiofrequency for curative or palliative treatment of cardiac arrhythmias motivated the Rhythmology Working Group to set up a register of the complications related to this technique. Five thousand six hundred and eighty nine cases from 19 French centres were recensed up to March 1996. There were 2765 ablations of a Bundle of Kent, 1579 ablations of slow pathways, 621 ablations of atrial flutter, 25 ablations of atrial tachycardia, 200 ablations of ventricular tachycardia and 499 ablations of the Bundle of His. Eighty five complications (1.5%), two of which were lethal (0.04%), were reported. The complications of catheterization (27% of all complications) were pneumothorax (n = 6), arterial thrombosis (n = 3), venous thrombosis with and without pulmonary embolism (n = 8), haematoma (n = 2), femoral pseudoaneurysm (n = 1), arteriovenous fistula (n = 1), infection (n = 2), valvular disease with mitral or aortic regurgitation (n = 3). Other complications were specific to the ablation itself:skin burns at the site of the patch (n = 2), ventricular fibrillation (n = 3), coronary events (n = 2), vascular events (n = 2), tamponade (n = 12), one of which was lethal, and transient or permanent complete atrioventricular block (n = 32) complicating ablation of antero and posteroseptal accessory pathways, atrial flutter and slow intranodal reentry pathways (n = 25). One lethal cerebral haemorrhage occurred the day after an ablation procedure. It was not possible to identify a predictive factor in these complications apart from the operator's experience. There were 1.4% of complications in Kent bundle ablations, 1.9% in ablation of slow pathway, 0.6% in atrial flutter and tachycardia, 1.5% for ventricular tachycardia and 1.9% for Bundle of His. The authors concluded that the prevalence of complications, though small with minimal risk of mortality (0.04%), should incite physicians to reserve this technique for symptomatic patients or those with potentially lethal arrhythmias.

Arrhythmias, Cardiac↗
PubMed1978

[2 or 3 level blocks in the Tawara node during atrial tachycardia].

In atrial flutter (or paroxysmal atrial tachycardia), the ventricular response is dependant on the passage through 3 superposed zones of conduction in the Tawara node, the zone of decremential conduction being the central zone N. When the ventricular response is between half and a quarter of the atrial rate there are two possible explanations: type B alternate Wenckebach period (mobitz I block in the central zone N, 2/1 block at the nodo-ventricular junction) or type A alternate Wenckebach period (Mobitz I block in the central zone N and 2/1 block at the atrio-nodal junction). These two responses may alternate in the same patient depending on the drug therapy or vagal activity due to a phenomenon similar to the "GAP" phenomenon. Inexactitudes in the working out of the arithmetic formulae may easily be explained by a certain degree of concealed conduction of blocked activation in one zone or more rarely by hisian extrasystoles. Type A alternate Wenckebach periods are always easier to construct than type B. Perfect 3/1 atrial flutter can only be explained by a type B alternate Wenckebach period with a 3/2 period with a 3/2 period in the N zone and a 2/1 block in the NH zone. When the ventricular rhythm is permanently very slow or when the RR intervals are greater than four times the atrial cycle, 3 zones of block are usually at issue (the third being located in the inferior part of the node or superior part of the bundle of His). Examples of 5/1, 6/1 flutter are thereby analysed. Rapid atrial pacing after termination of the atrial arrhythmia allows a better analysis of its mechanism and the successive reproduction of conduction defects in each zone of block.

Atrioventricular Node↗
PubMed2000

Electroanatomic mapping to identify breakthrough sites in recurrent typical human flutter.

The accuracy of conventional techniques in localizing previous radiofrequency (RF) ablation sites and thus breakthrough sites of recurrent atrial flutter is somewhat limited. We investigated the role of electroanatomic mapping for identifying breakthrough sites or "gaps" at the tricuspid annulus and inferior vena cava (IVC)/eustachian ridge isthmus to help RF ablation in patients with recurrent typical flutter. Twelve patients (8 men, 4 women, age 63 +/- 10 years) with recurrent typical atrial flutter were included in the study. An electroanatomic mapping system (CARTO) was used to create a voltage map and activation and propagation patterns in the right atrium. Detailed voltage, activation, and propagation mapping of the tricuspid annulus and IVC/eustachian ridge isthmus allowed precise identification of gaps in all 12 patients at the tricuspid annulus (eight sites), IVC ridges (two sites), mid-isthmus region (one site), and tricuspid annulus and IVC ridges (one site). Radiofrequency energy directed at these sites eliminated atrial flutter in all 12 patients, confirmed by noninducibility of atrial flutter and demonstration of conduction block during atrial pacing on either side of the lesion lines. During a mean follow-up of 14.8 +/- 3.5 months (range 8-19 months), paroxysmal atrial flutter recurred in only one patient and was subsequently treated with amiodarone, although this had been ineffective prior to ablation. Electroanatomic mapping can precisely identify gaps in the lesion line responsible for breakthrough of recurrent typical atrial flutter at the tricuspid annulus and at the IVC/eustachian ridge isthmus. These sites can be targeted with RF ablation with a high degree of success.

Atrial Flutter↗
PubMed2003

Arrhythmias in the intensive care patient.

PURPOSE OF REVIEW: Atrial fibrillation, atrial flutter, AV-nodal reentry tachycardia with rapid ventricular response, atrial ectopic tachycardia, and preexcitation syndromes combined with atrial fibrillation or ventricular tachyarrhythmias are typical arrhythmias in intensive care patients. Most frequently, the diagnosis of the underlying arrhythmia is possible from the physical examination, the response to maneuvers or drugs, and the 12-lead surface electrocardiogram. In all patients with unstable hemodynamics, immediate DC-cardioversion is indicated. Conversion of atrial fibrillation to sinus rhythm is possible using antiarrhythmic drugs. Amiodarone has a conversion rate in atrial fibrillation of up to 80%. However, caution in the use of short-term administration of intravenous amiodarone in critically ill patients with recent-onset atrial fibrillation is absolutely necessary, and the duration of therapy should not exceed 24 to 48 hours. Ibutilide represents a relatively new class III antiarrhythmic agent that has been reported to have conversion rates of 50% to 70%; it seems that ibutilide is even successful when intravenous amiodarone failed to convert atrial fibrillation. RECENT FINDINGS: Newer studies compared the outcome of patients with atrial fibrillation and rhythm- or rate-control. Data from these studies (AFFIRM, RACE) clearly showed that rhythm control is not superior to rate control for the prevention of death and morbidity from cardiovascular causes. Therefore, rate-control may be an appropriate therapy in patients with recurrent atrial fibrillation after DC-cardioversion. Acute therapy of atrial flutter in intensive care patients depends on the clinical presentation. Atrial flutter can most often be successfully cardioverted to sinus rhythm with energies less than 50 joules. Ibutilide trials showed efficacy rates of 38-76% for conversion of atrial flutter to sinus rhythm compared with conversion rates of 5-13% when intravenous flecainide, propafenone, or verapamil was administered. In addition, a high dose (2 mg) of ibutilide was more effective than sotalol (1.5 mg/kg) in conversion of atrial flutter to sinus rhythm (70% versus 19%). SUMMARY: There is general agreement that bystander first aid, defibrillation, and advanced life support is essential for neurologic outcome in patients after cardiac arrest due to ventricular tachyarrhythmias. The best survival rate from cardiac arrest can be achieved only when (1) recognition of early warning signs, (2) activation of the emergency medical services system, (3) basic cardiopulmonary resuscitation, (4) defibrillation, (5) management of the airway and ventilation, and (6) intravenous administration of medications occurs as rapidly as possible. Public access defibrillation, which places automatic external defibrillators in the hands of trained laypersons, seems to be an ideal approach in the treatment of ventricular fibrillation. The use of automatic external defibrillators by basic life support ambulance providers or first responder in early defibrillation programs has been associated with a significant increase in survival rates. Drugs such as lidocaine, procainamide, sotalol, amiodarone, or magnesium were recommended for treatment of ventricular tachyarrhythmias in intensive care patients. Amiodarone is a highly efficacious antiarrhythmic agent for many cardiac arrhythmias, ranging from atrial fibrillation to malignant ventricular tachyarrhythmias, and seems to be superior to other antiarrhythmic agents.

Aged↗
PubMed1979

Metoprolol in the treatment of supraventricular tachyarrhythmias.

Twenty one patients with either paroxysmal supraventricular tachycardia (group A), atrial flutter (group B), or atrial fibrillation (group C) were treated with intravenous metoprolol in the dose range 2--20 mg. Sinus rhythm was restored in 3 out of 6 patients in group A, 3 out of 7 patients in group B and one out of 8 patients in group C. In patients who did not convert to sinus rhythm a remarkable decrease in ventricular rate occurred in 3 patients with atrial flutter and 4 patients with atrial fibrillation. In patients with systolic blood pressure greater than 100 mm Hg but without an acute myocardial infarction the risk of hypotension necessitating treatment was small. Metoprolol appears to be an effective and safe drug in the treatment of supraventricular tachycardia.

Adult↗
PubMed2003

Occurrence of atrial fibrillation after flutter ablation: the significance of intra-atrial conduction and atrial vulnerability.

Atrial vulnerability and intra-atrial conduction delay are important substrates for paroxysmal atrial fibrillation (AFib); however, their significance is unknown in patients undergoing atrial flutter ablation. Antegrade (high right atrium to coronary sinus: HRA-CS) and retrograde (CS-HRA) intra-atrial conduction times and AFib inducibility were assessed in 61 patients undergoing ablation for type I atrial flutter. Twenty-three patients had structural heart disease and 18 AFib before the procedure. After 16 +/- 12 months of follow-up 17 patients experienced AFib, 5 of which progressed into chronic AFib. During the study, AFib was easily inducible in 14 patients, 7 of which developed AFib (P =.03). Patients with post- ablation AFib were older (59 +/- 11 vs. 44 +/- 15 years, P =.001), had longer intra-atrial conduction times before (98 +/- 17 ms vs. 68 +/- 20 ms, P <.001) and after ablation (91 +/- 19 ms vs. 73 +/- 21 ms, P =.01) than those without AFib. Discriminant analysis revealed that only age, previous AFib and inta-atrial conduction delay (>90 ms) were independent predictors of postablation AFib. Patients without a history of AFib and with normal intra-atrial conduction had a 3% risk of AFib, while patients with both factors had a 90% risk of AFib after ablation. Intra-atrial conduction delay is an important electrophysiological factor predicting atrial fibrillation after successful flutter ablation.

Age Factors↗
PubMed1997

Arrhythmia and mortality after the Mustard procedure: a 30-year single-center experience.

OBJECTIVES: Our purpose was to assess the risk factors for late mortality, loss of sinus rhythm and atrial flutter after the Mustard operation. BACKGROUND: The Mustard operation provides correction of cyanosis with low surgical risk in transposition of the great vessels. However, right ventricular failure, loss of sinus rhythm, atrial flutter and death are frequent long-term complications. METHODS: Records of 534 children who underwent the Mustard operation at a single center since 1962 were reviewed for demographic, anatomic, electrocardiographic and physiologic predictors and outcomes. RESULTS: There were 52 early deaths (9.7%). Survival analysis was undertaken for 478 early survivors with a mean follow-up interval of 11.6 +/- 7.2 years. There were 77 late deaths (16.1%), with sudden death (n = 31) the most frequent cause. Survival estimates were 89% at 5 years and 76% at 20 years of age. Risk factors were an earlier date of operation, operative period arrhythmia and an associated ventricular septal defect. Risk (hazard) of late death declined in the first decade, with further peaks in the second decade. Sinus rhythm was present in 77% at 5 years and 40% at 20 years. Loss of sinus rhythm was associated with previous septectomy, postoperative bradycardia and late atrial flutter. Freedom from atrial flutter was 92% at 5 years and 73% at 20 years of age. Risk factors for atrial flutter were the occurrence of perioperative bradyarrhythmia, reoperation and loss of sinus rhythm during follow-up. Risk of atrial flutter demonstrates a late increase. CONCLUSIONS: Ongoing loss of sinus rhythm and late peaks in the risk of atrial flutter and death necessitate continued follow-up.

Arrhythmias, Cardiac↗
PubMed1990

Clinical evaluation in therapy of patients with atrial fibrillation or flutter.

The weight of evidence clearly indicates that both atrial fibrillation and atrial flutter are due to a reentrant mechanism. Atrial fibrillation seems almost certainly due to multiple circulating reentrant wavelets of the leading circle type, whereas atrial flutter appears to be caused by single reentrant circuit located in the right atrium. The diagnosis of both atrial fibrillation and atrial flutter should always be possible using either old or new techniques. The interruption of atrial flutter should be possible using pacing or direct current cardioversion techniques, and the conversion of atrial fibrillation to sinus rhythm also is most often possible by direct current cardioversion or antiarrhythmic drug therapy. Long-term antiarrhythmic drug therapy to suppress recurrent atrial fibrillation and atrial flutter may be a problem, but availability of newer antiarrhythmic agents holds promise for finding an effective regimen. Catheter ablation techniques may be used to cause complete heart block in the treatment of either atrial fibrillation or atrial flutter when these rhythms cannot be satisfactorily suppressed and are associated with unacceptably rapid ventricular response rates. Finally, recent data suggest that atrial flutter may be successfully treated on a chronic basis with an antitachycardia pacing device, may be cured with catheter ablation techniques applied to a critical portion of the atrial flutter reentry circuit, and may be treated successfully with innovative surgical techniques. The latter is also true for atrial fibrillation.

Anti-Arrhythmia Agents↗
PubMed1995

Prevention of embolic events after cardioversion of atrial fibrillation. Current and evolving strategies.

We review the incidence of embolic events following cardioversion of atrial fibrillation, as well as the literature that forms the basis for the current strategy of anticoagulation before, and following, cardioversion to reduce the risk of post-cardioversion embolism. We evaluate a new strategy that uses transesophageal echocardiography to identify patients in atrial fibrillation without atrial thrombi who may be safely cardioverted without preceding anticoagulation and we also address the embolic event and anticoagulation issues in patients with atrial flutter. Cardioversion of atrial fibrillation to sinus rhythm is associated with a small but significant risk of thromboembolic events (average incidence, 1.5%; range, 0% to 7%). Anticoagulating these patients before cardioversion appears to significantly reduce this risk, and because of the delay in return of atrial contraction, anticoagulation should be continued for several weeks following cardioversion. The current guidelines for anticoagulating patients in atrial fibrillation who are to be cardioverted is based primarily on clinical observations, numerous uncontrolled case series, two retrospective trials, and one prospective nonrandomized controlled trial. Anticoagulation for 3 weeks before cardioversion followed by 4 weeks of anticoagulation after cardioversion is a theoretically sound and effective approach to reduce the risk of thromboembolic events. The use of transesophageal echocardiography to rule out thrombus and thus identify low-risk patients who may undergo cardioversion without preceding anticoagulation has been supported by several small studies that successfully used this strategy. However, the demonstration of a postcardioversion atrial and atrial appendage "stunning" suggests that anticoagulation needs to be given at the time of, and following, cardioversion. While promising, this transesophageal echocardiography--guided strategy for cardioversion of patients in atrial fibrillation requires more rigorous study before its routine use can be recommended. The current management of pure atrial flutter requires no anticoagulation before cardioversion; however, several clinical observation suggest theoretical risks for embolic events in these patients, thus further investigation of this strategy may be warranted.

Anticoagulants↗
PubMed2001

Radiofrequency ablation in pediatric and adult patients: comparative results.

BACKGROUND: Radiofrequency (RF) catheter ablation has been widely and successfully employed to cure adult and pediatric patients of a variety of arrhythmias. Only limited data exist which compare the results in these two groups. The aim of this study was to compare the efficacy and safety of RF catheter ablation in pediatric versus adult patients performed by an adult electrophysiology (EP) team. METHODS: The study group included 327 consecutive pediatric (n=47) and adult (n=280) patients, aged 7-82 years (mean 40+/-19), with symptomatic tachyarrhythmias, who underwent RF ablation during the last 6 years. All but ten patients underwent a full EP study during the same session. Procedures were performed in all but five patients with use of local anesthesia and deep or light sedation. The left heart was approached with use of transaortic (n=36) or transseptal (n=55) or both (n=6) techniques. RF ablation was performed for manifest or concealed accessory pathways in 132 patients, AV nodal slow pathway in 119, atrial tachycardia in 24, atrial flutter in 15, atrial fibrillation in one, ventricular tachycardia in 29, and AV node/His bundle in 7 patients. RESULTS: RF ablation was successful in 271 (96.8%) patients in the adult group and in all patients (100%) in the pediatric group, with a mean of 15+/-18 (median: 8) vs 12+/-10 (median: 8) RF applications respectively (P=NS). Complications occurred in four patients (1.4%) in the adult group and in one patient (2.1%) in the pediatric group (P=NS). Fluoroscopy time averaged 43+/-40 min vs 39+/-27 min and procedures lasted for 3.0+/-1.9 hours vs 2.8+/-1.4 hours respectively (P=NS). During long-term follow-up of 25+/-19 months, there were 12 (4.4%) recurrences among the adult patients, and three (6.4%) recurrences in children, with nine of them successfully treated with repeat RF ablation. Procedural variables were dependent on the type of arrhythmia ablated, rather than on patient's age. Patients with multiple accessory pathways or atrial flutter required the greatest number of RF applications and the longest fluoroscopy exposure and duration of the procedure; the lowest values of these variables concerned ablation of the slow AV nodal pathway or the AV node/His bundle. CONCLUSION: RF ablation in adult and pediatric patients performed by an adult EP team is equally efficacious and safe offering cure of symptomatic cardiac tachyarrhythmias in both patient populations.

Adolescent↗
PubMedDate not supplied

Incessant atrial tachycardias in a dog with tricuspid dysplasia. Clinical management and electrophysiology.

In a dog, tricuspid regurgitation due to congenital tricuspid dysplasia resulted in extreme right heart enlargement and right heart failure. Incessant supraventricular tachycardias were present, requiring the intravenous administration of verapamil to reduce the ventricular rate. Oral therapy using a combination of verapamil and quinidine was partially effective in controlling the ventricular rate during the following week. At that time, electrophysiologic studies were performed. They revealed that a succession of several atrial tachycardias with different cycle lengths, including one episode of atrial flutter, was present. Atrial activity was spanning the majority of the cycle length in all these arrhythmias. Epicardial mapping was performed during the atrial flutter. This enabled the detection of a depolarization wave-front traveling counterclockwise from the dorsolateral right atrium toward the right appendage, following the tricuspid valve annulus. No areas of abnormal conduction were detected. Because programmed electric stimulation maneuvers could not be performed, definitive conclusions about the mechanism of the arrhythmia could not be drawn. The two most likely possibilities were circus movement using part of the dilated tricuspid valve annulus as an anatomic barrier or a leading circle type of re-entry.

Animals↗
PubMed2001

Dofetilide: a new class III antiarrhythmic agent.

Dofetilide is a new, pure class III antiarrhythmic agent that prolongs the refractory period and action potential duration without having beta-blocking or calcium channel-blocking properties, making it unique among established class III agents. Dofetilide is effective in converting atrial and ventricular arrhythmias, and in maintaining sinus rhythm after cardioversion. Interestingly, it is more effective in converting atrial flutter than atrial fibrillation. It appears to be safe in patients with left ventricular dysfunction and postmyocardial infarction. In small studies, intravenous dofetilide was superior to flecainide, procainamide and amiodarone in converting atrial fibrillation and flutter. Dofetilide can be administered orally or intravenously with no significant effect on heart rate or blood pressure, but it can prolong QT interval and cause torsade de pointes in 3% to 4% of patients receiving it intravenously and in 0.8% to 1.5% of patients receiving it orally. So far, it is recommended that therapy be initiated in hospital under electrocardiogram monitoring for at least two days, with particular care to avoid torsade de pointes in high risk patients such as women, and those with bradycardia, hypokalemia, hypomagnesia and renal dysfunction. Studies have failed to show any extracardiac side effects.

Anti-Arrhythmia Agents↗
PubMedDate not supplied

[Heart rhythm disorders of supraventricular origin in children].

An analysis and updating is made, of the main supraventricular heart rhythm disturbances encountered in children, excepting paroxysmal supraventricular tachycardia, which remains the major clinical entity in this field, but was presented by the same authors in a previous issue of this journal. A review is made of vasovagal syncope, of sinusal tachy- and bradycardia, of atrial extrasystolic arrhythmia, of the sinus node disease, of atrial flutter, and of atrial fibrillation. On the basis of modern studies in the field of electrophysiology, including endocavitary electrophysiology, the major mechanisms are presented, involved in triggering all types of heart tachyarrhythmias, namely: abnormal automatism (automatic ectopic focuses), the "re-entry mechanism" and the "triggered dysrhythmia". Particular attention is given to extrasystolic arrhythmias of atrial origin, and to the sinus node disease, of which the first is important because of its frequency while the second one is remarkable because of the considerable mass of new data that have been published in the literature. A review is made of etiologic aspects, as well as clinical, electrocardiographic, and therapeutical data related to heart rhythm disturbances of supraventricular origin, as well as a series of considerations in relation to evolution and prognosis. The authors stress certain difficulties of diagnosis, especially with electrocardiograms, as is the case, for instance, with blocked bigeminal atrial extrasystoles, with the sinus node disease, etc. In the final part of the paper two more rarely encountered disturbances are presented; atrial fibrillation and atrial flutter. These two entities are also defined on the basis of clinical and electrocardiographic data, and their analysis is also made from the viewpoint of their etiology. A discussion is made concerning the therapeutic aspects, and their evolution and prognosis.

Arrhythmias, Cardiac↗
PubMed1991

Effects of procainamide on refractoriness, conduction, and excitable gap in canine atrial reentrant tachycardia.

The effects of procainamide were studied in a model of atrial flutter around the tricuspid valve in seven open chest, chloralose-anesthetized dogs (31 +/- 3 kg). A Y-shaped incision in the intercaval area extending to the right atrial appendage was made and five bipolar electrodes were sutured on the atrial epicardium around the tricuspid valve. Reentry tachycardia was induced in the absence and presence of drug by burst pacing. Procainamide (15 mg/kg bolus followed by 0.075 mg/kg/min infusion) produced stable plasma levels (38 +/- 9 microM) during the study. At a pacing cycle length of 200 msec, mean (+/- SD) diastolic threshold at the five sites increased from 1.6 +/- 1.5 to 2.0 +/- 1.7 mA and mean atrial effective refractory period from 125 +/- 9 to 140 +/- 16 msec on drug (P less than 0.05). Procainamide prolonged the cycle length of atrial flutter from 144 +/- 10 to 160 +/- 13 msec and slowed conduction velocity during atrial flutter around the tricuspid valve from 73 +/- 6 to 66 +/- 6 cm/sec (P less than 0.05). A reset response curve was determined by introducing premature stimuli during atrial flutter. Procainamide prolonged effective refractory period during atrial flutter from 101 +/- 13 to 116 +/- 17 msec but did not change the duration of the excitable gap (38 +/- 9 vs 40 +/- 18 msec). Although the reset response curve was predominantly increasing, in six of seven experiments there was present a flat portion at long coupling intervals approaching the atrial flutter cycle length that comprised 23% +/- 10% of the excitable gap.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Slow abnormal conduction in the low right atrium: its anatomic basis and relevance to atrial reentry.

To characterize slow abnormal conduction in the low right atrium, which is known to be responsible for atrial flutter, electrophysiologic findings were correlated with anatomic features in a canine model of atrial flutter with ligation of the crista terminalis in the midright atrium. Activation in the low right atrium was mapped with a patch electrode containing 52 bipolar electrodes and a multiplexing system. A particular region in the low right atrium showed atrioventricular node-like electrophysiologic properties, a rate-dependent conduction delay, and Wenckebach periodicity. This area coincided with an area responsible for slow conduction during atrial flutter and unidirectional block at its initiation. Both pilsicainide and E-4031 preferentially blocked conduction in the specific area, leading to the termination of atrial flutter. Although refractoriness could not explain the abnormal conduction, anatomic studies consistently found the specific region to be in or around a thick muscle bundle, that is, the crista terminalis, or a thick pectinate muscle branching from the crista, located perpendicular to the wavefront of the pacing impulse and atrial flutter. These electrophysiologic and anatomic findings suggest that slow abnormal and atrioventricular node-like conduction over a thick muscle bundle, which is a normal anatomic feature of the low right atrium, plays a role in the initiation, maintenance, and termination of atrial reentry.

Animals↗
PubMed2004

Stable secondary arrhythmias late after intraoperative radiofrequency ablation of atrial fibrillation: incidence, mechanism, and treatment.

INTRODUCTION: Intraoperative radiofrequency (RF) ablation is an effective treatment of atrial fibrillation (AF). However, secondary arrhythmias late after ablation may complicate the patient's course. We report on the incidence, mechanisms, and treatment of gap-related atrial flutter and other secondary arrhythmias during long-term follow-up. METHODS AND RESULTS: In 129 patients who underwent intraoperative RF ablation with placement of left atrial linear lesions using minimally invasive surgical techniques, secondary arrhythmias were analyzed during long-term follow-up (20 +/- 6 months). Transient atrial arrhythmias during the first 3 postoperative months were excluded. In 8 (6.2%) of 129 patients, sustained stable secondary arrhythmias were documented. Left atrial, gap-related atrial flutter was observed in 4 patients (3.1%). The flutter was treated by percutaneous RF ablation in 3 patients (2.3%) and with drugs in 1 patient (0.8%). In 2 patients (1.6%), right atrial isthmus-dependent atrial flutter occurred and was treated successfully by percutaneous RF ablation. In 2 patients (1.6%), ectopic right atrial tachycardias occurred and were treated with percutaneous RF ablation. CONCLUSION: Late after intraoperative RF ablation of atrial fibrillation, three types of stable secondary arrhythmias were observed in 6% of patients: left atrial gap-related atrial flutter, right atrial isthmus-dependent atrial flutter, and ectopic atrial tachycardia. Gaps after intraoperative RF ablation due to noncontinuous or nontransmural linear lesions may lead to stable left atrial macroreentrant tachycardias, requiring new interventional therapy.

Atrial Fibrillation↗
PubMed1999

Prospective clinical evaluation of a programmed atrial stimulation protocol for induction of sustained atrial fibrillation and flutter.

UNLABELLED: We sought to define a minimum standardized protocol for induction of atrial fibrillation [AF] and/or atrial flutter. In contrast to ventricular stimulation protocols, a stimulation protocol for induction of AF or atrial flutter has not been critically evaluated. Since suppression of inducible AF or atrial flutter is used as one of the endpoints of success of pharmacologic and ablation therapies, there is an obvious need to define a minimally appropriate electrical stimulation protocol for induction of AF or atrial flutter. We prospectively evaluated 70 patients, 44 with spontaneous atrial flutter or AF and 26 controls without documented atrial arrhythmias. A standardized programmed stimulation protocol, which employed up to three atrial extrastimuli delivered at two atrial sites at two atrial drive pacing lengths, was used in attempt to reproduce sustained AF and atrial flutter. The study endpoint was induction of sustained (> 30 s) AF or atrial flutter. Sustained AF or atrial flutter was induced in 39/44 (89%) patients and 2/26 (7%) of controls (p < 0.01). The arrhythmia induced was atrial flutter in 19/21 (91%) of atrial flutter patients, AF in 17/18 (94%) AF patients, both atrial flutter and AF in 5 AF/atrial flutter patients (100%). Two patients with atrial flutter had both AF/atrial flutter and 1 patient with AF had atrial flutter induced. The arrhythmia was induced from first stimulation site in 37 patients (85%) using a single extrastimuli in 9 (20%) patients, double extrastimuli 18 (41%) patients and triple extrastimuli in 10 (23%) patients. Two patients (5%) required stimulation from second site with two and three extrastimuli, respectively. The overall sensitivity and specificity of this stimulation protocol were 89% and 92%, respectively with a positive predictive accuracy of 95%. CONCLUSIONS: 1. Up to three atrial extrastimuli and two atrial sites are needed to increase yield of AF/atrial flutter induction at electrophysiologic study. 2. Induction of either AF or atrial flutter correlates well with the presence of a similar spontaneous arrhythmia. 3. A baseline determination of the induction mode may be desirable prior to evaluation of interventions directed at AF or atrial flutter.

Aged↗
PubMed1976

Atrial tachyarrhythmias in acute myocardial infarction.

Causative factors, clinical consequences and treatment of atrial tachyarrhythmias were reviewed in 917 monitored patients with definite acute myocardial infarction. Significant atrial tachyarrhythmias were found in 104 (11 per cent) of them and included atrial fibrillation in 67, atrial flutter in 29 and paroxysmal atrial tachycardia in 33. These episodes were single in 79 patients and multiple in 25, and began within the first four days of acute myocardial infarction in 90 per cent of the patients. Fifty per cent of these atrial tachyarrhythmias were heralded by premature atrial contractions. The incidence of atrial tachyarrhythmia was not related to the location of the acute myocardial infarction or to the presence or degree of power failure; however, atrial tachyarrhythmias were significantly more frequent in patients with pericarditis. Atrial tachyarrhythmias were well tolerated in almost one fifth of the patients, caused marginal compromise in almost two thirds and led to severe clinical deterioration in one fifth. Paroxysmal atrial tachycardia rarely required specific treatment, atrial fibrillation was best managed with intravenous administration of digoxin except when associated with severe clinical compromise, and atrial flutter generally required cardioversion or rapid intravenous therapy and usually caused severe clinical deterioration. Over-all, atrial tachyarrhythmia was not associated with a significantly increased mortality, and in those who died, death was not related specifically to the atrial tachyarrhythmia but rather to the severity of the underlying acute myocardial infarction. However, persisting atrial tachyarrhythmias, particularly atrial flutter which tends to be refractory to both heart rate control and cardioversion, may contribute indirectly to morbidity and mortality.

Adult↗