Mode-Switch-Algorithmen: Programmierbarkeit und Nutzen

BACKGROUND: Automatic mode switching is defined as the ability of a pacemaker to reprogram itself from tracking to non-tracking mode in response to atrial tachyarrhythmias, and to regain tracking mode as soon as the tachyarrhythmia terminates. In contrast to upper rate behavior, mode switching does not only limit atrial tracking at a certain rate but actively drives the ventricular pacing rate back to lower rate or sensor rate as long as the atrial tachyarrhythmia persists. In contrast to DDD with mode switch, AV synchrony may be lost in DDIR mode if the sinus rate exceeds the sensor rate. DDD pacing with mode switching represents a valuable option in patients with AV block and paroxysmal atrial tachyarrhythmias. It may prevent the transition from paroxysmal to permanent atrial fibrillation after AV node ablation to a higher extent than VVI(R) pacing. On the other hand, patients with sinus node disease and normal AV conduction may benefit from DDIR mode with long AV interval. Mode switching should provide a rapid, sensitive and specific detection of atrial tachyarrhythmias, fast switch to non-tracking mode without ventricular pacing at the upper rate limit, adequate ventricular rate during the atrial tachyarrhythmia, rapid, sensitive and specific detection of conversion to sinus rhythm and fast switch back to tracking mode. In addition, oscillations between DDD and DDI mode with sudden ventricular rate changes should be avoided. MODE-SWITCHING ALGORITHMS: To achieve these aims, different mode-switching algorithms have been developed which all show specific disadvantages: reliable but slow response to atrial tachyarrhythmias, fast but unspecific switch to non-tracking mode, mode oscillations, inclination to inadequate mode-switching due to ventricular far-field sensing, failure to perform modeswitching during atrial flutter or intermittent atrial undersensing. Some of these problems can be avoided by careful atrial lead implantation providing atrial signals above 2 mV and avoiding ventricular far-field signals. Programming of mode-switching related parameters (e.g. atrial rate and number of fast beats required for mode switch), atrial blanking times, and atrial sensitivity can solve some of the problems with mode switching. Clinical results show a strong influence of device programming and atrial undersensing on mode-switching performance. Some data suggest a superiority of fast mode-switching algorithms with regard to clinical symptoms. However, loss of AV synchrony during sinus rhythm due to premature or inadequate mode switching may limit the benefit of fast mode switching. FURTHER DEVELOPMENTS: Improved performance may be achieved by a combination of different mode-switching algorithms (e.g. one algorithm for detection of atrial fibrillation, another one for detection of atrial flutter). In addition, programmability of several algorithms (e.g. mean atrial rate, beat-to-beat, x out of y) within the same device and atrial cycle-dependent sensitivity adjustment similar to automatic gain control in implantable defibrillators may further increase the clinical use of automatic mode switching.     

Mode-Switch-Algorithmen: Programmierbarkeit und Nutzen

Hintergrund: Die Funktion des automatischen Mode-Switch bezeichnet die Fähigkeit eines Schrittmachers, atriale Tachykardien zu erkennen und selbständig aus dem triggernden Betrieb (DDR[R], VDD[R]) in den nicht triggernden (DDI[R], VDI[R]) zu wechseln, solange die Tachyarrhythmie anhält, sowie zurück in den triggernden Betrieb, sobald die Tachyarrhythmie terminiert. Patienten mit AV-Block und paroxysmalen Vorhoftachyarrhythien (einschließlich Patienten nach AV-Knoten-Ablation wegen medikamentös therapierefraktärem paroxysmalen Vorhofflimmern) benötigen eine derartige Funktion für eine AV-synchrone Stimulation während Sinusrhythmus einerseits und zur Vermeidung einer schnellen Überleitung von Vorhoftachyarrhythmien andererseits. Mode-Switch-Systeme: Im Folgenden wird erläutert, wie verschiedene Systeme einen automatischen Mode-Switch durchführen und welche spezifischen Probleme sich dabei ergeben. Es werden Hinweise zur Optimierung der Programmierung gegeben, da sowohl inadäquater als auch ausbleibender Mode-Switch nicht selten sind. Klinische Ergebnisse weisen auf ein verbessertes subjektives Befinden unter schnellen Mode-Switch-Algorithmen hin. Neue atriale Sensing-Algorithmen: Eine weitere Verbesserung der Erkennung atrialer Tachyarrhythmien und Abgrenzung vor allem gegenüber ventrikulären Fernfeldsignalen ist von neuen atrialen Sensing-Algorithmen zu erwarten, die analog zu Detektionsalgorithmen in implantierbaren Kardioverter/Defibrillator-Systemen arbeiten. Background: Automatic mode switching is defined as the ability of a pacemaker to reprogram itself from tracking to non-tracking mode in response to atrial tachyarrhythmias, and to regain tracking mode as soon as the tachyarrhythmia terminates. In contrast to upper rate behavior, mode switching does not only limit atrial tracking at a certain rate but actively drives the ventricular pacing rate back to lower rate or sensor rate as long as the atrial tachyarrhythmia persists. In contrast to DDD with mode switch, AV synchrony may be lost in DDIR mode if the sinus rate exceeds the sensor rate. DDD pacing with mode switching represents a valuable option in patients with AV block an paroxysmal atrial tachyarrhythmias. It may prevent the transition from paroxysmal to permanent atrial fibrillation after AV node ablation to a higher extent than VVI(R) pacing. On the other hand, patients with sinus node disease and normal AV conduction may benefit from DDIR mode with long AV interval. Mode switching should provide a rapid, sensitive and specific detection of atrial-tachyarrhythmias, fast switch to non-tracking mode without ventricular pacing at the upper rate limit, adequate ventricular rate during the atrial tachyarrhythmia, rapid, sensitive and specific detection of conversion to sinus rhythm and fast switch back to tracking mode. In addition, oscillations between DDD and DDI mode with sudden ventricular rate changes should be avoided. Mode-Switching Algorithms: To achieve these aims, different mode-switching algorithms have been developed which all show specific disadvantages: reliable but slow response to atrial tachyarrhythmias, fast but unspecific switch to non-tracking mode, mode oscillations, inclination to inadequate mode-switching due to ventricular far-field sensing, failure to perform modeswitching during atrial flutter or intermittent atrial undersensing. Some of these problems can be avoided by careful atrial lead implantation providing atrial signals above 2 mV and avoiding ventricular far-field signals. Programming of mode-switchig related parameters (e. g. atrial rate and number of fast beats required for mode switch), atrial blanking times, and atrial sensitivity can solve some of the problems with mode switching. Clinical results show a strong influence of device programming and atrial undersensing on mode-switching performance. Some data suggest a superiority of fast mode-switching algorithms with regard to clinical symptoms. However, loss of AV synchrony during sinus rhythm due to premature or inadequate mode switching may limit the benefit of fast mode switching. Further Developments: Improved performance may be achieved by a combination of different mode-switching algorithms (e. g. one algorithm for detection of atrial fibrillation, another one for detection of atrial flutter). In addition, programmability of several algorithms (e. g. mean atrial rate, beat-to-beat x out of y) within the same device and atrial cycle-dependent sensitivity adjustment similar to automatic gain control in implantable defibrillators may further increase the clinical use of automatic mode switching.     

Electrocardiographic and Electrophysiologic Characterization of Atypical Atrial Flutter in Man:

Atypical Atrial Flutter. Introduction : Although the circuit in typical counterclockwise atrial flutter has been clearly delineated, the mechanisms of "atypical atrial flutters" have been less well characterized. The purpose of this study was to investigate the ECG and electrophysiologic (EP) characteristics of atypical atrial flutter.
Methods and Results : Thirty-three patients with at least one form of atypical atrial flutter underwent EP evaluation with multipolar atrial activation and entrainment mapping. Nineteen patients with clockwise flutter had: (1) stereotypic ECG morphology; (2) same cycle length as counterclockwise flutter; (3) clockwise activation around the tricuspid annulus; (4) recording of discrete split potentials along the length of the crista terminalis, suggesting the presence of conduction block; (5) concealed entrainment from the low right atrial isthmus; (6) successful ablation in this isthmus. Twenty patients with atypical flutter not consistent with a clockwise mechanism ("true atypical flutter") showed: (1) heterogeneous ECG morphology; (2) cycle length shorter than that of clockwise flutter; (3) frequent transitions from and to atrial fibrillation; (4) could be entrained in only six patients and, when accomplished, demonstrated surface fusion when entraining from the low right atrial isthmus.
Conclusions : Atypical flutter falls into two broad categories. Clockwise flutter uses the same circuit with the same endocardial barriers as its counterclockwise counterpart and is best con sidered a form of typical flutter. True atypical flutter induced in the EP laboratory is a hetero geneous group of arrhythmias that are transitional to atrial fibrillation. Although it may superficially resemble clockwise or counterclockwise flutter based on the 12-lead ECG alone, the distinction can be readily made from a combined evaluation including activation and entrainment mapping.     

Intravenous cibenzoline in the management of acute supraventricular tachyarrhythmias

Summary Intravenous cibenzoline was evaluated in 37 patients with acute supraventricular tachyarrhytymias and a ventricular rate >120 beats/min. The presenting arrhythmia was atrial fibrillation in 15 patients, atrial flutter in 5, ectopic atrial tachycardia in 11, and paroxysmal atrioventricular (AV) junctional reentrant tachycardia in 6 patients. Intravenous cibenzoline was administered as a bolus given over 2 minutes, at a dose of 1 mg/kg in the first 26 patients and 1.2 mg/kg in the subsequent 11 patients, 15 minutes following failure of placebo (isotonic glucose). The results were evaluated 15 minutes after the intravenous injection. Restoration of sinus rhythm was obtained in 3 out of 6 patients with paroxysmal AV junctional tachycardia (50%) and in 7 out of 31 patients (23%) with atrial tachyarrhythmias (5 out of 15 patients with atrial fibrillation and 2 out of 16 patients with ectopic atrial tachycardia or atrial flutter). Five additional patients with atrial tachyarrhythmias had slowing of ventricular rate below 100 beats/min. Therefore, a satisfactory result, that is, restoration of sinus rhythm or slowing of ventricular rate, occurred in 15 patients (40.5%). Side effects were transient, including visual disturbance (one patient), asymptomatic widening of QRS complex (three patients), incessant reciprocating tachycardia (one patient), and acceleration of ventricular rate (eight patients), resulting in 1:1 flutter, with poor tolerance in two patients. In conclusion, intravenous cibenzoline may be useful in selected patients with supraventricular tachyarrhythmias. Careful monitoring is recommended during therapy in view of the possible occurrence of 1:1 atrial flutter.     

Atrial fibrillation is common after ablation of isolated atrial flutter during long-term follow-up

BACKGROUND: Previous studies have shown that the incidence of atrial fibrillation after atrial flutter ablation is approximately 20% among patients presenting with typical atrial flutter and no history of fibrillation. However, studies involving this population have been small, with follow-up typically less than 2 years. OBJECTIVE: The purpose of this study was to provide a more accurate perspective on the long-term risk of atrial fibrillation in patients presenting with isolated typical flutter. METHODS: Clinical records of consecutive patients who had flutter ablations at Presbyterian Medical Center between 1999 and 2004 were assessed (n = 254). Patients with no apparent history of atrial fibrillation before their flutter ablation were identified. Retrospective follow-up data on these patients were obtained by review of medical records from our institution, from patients' cardiologists and primary care physicians, and by direct patient questionnaires. Postablation atrial fibrillation and other arrhythmias were identified by electrocardiography, Holter monitoring, and subsequent clinical records. RESULTS: Postablation atrial fibrillation was identified in 40 (50%) of 80 patients, and an additional three patients presented with atypical atrial flutter, after a mean follow-up of 29.6 +/- 21.7 months. The incidence of atrial fibrillation was progressive, with 49% occurring after 2 years. There was no difference in age, left atrial size, hypertension, structural heart disease, or left ventricular dysfunction in patients who developed atrial fibrillation compared with those who did not. CONCLUSION: Atrial fibrillation occurs in over half of patients who present with isolated typical flutter after cavotricuspid isthmus ablation. Asymptomatic patients should be screened for recurrent arrhythmias indefinitely after ablation. In certain patients, atrial fibrillation and flutter may be different expressions of the same electrical disease, and eradication of the flutter circuit will not prevent the eventual manifestation of atrial fibrillation.     

Atypical Atrioventricular Nodal Reentry Tachycardia with Atrioventricular Block Mimicking Atrial Tachycardia:

AVNRT Mimicking Atrial Tachycardia, Introduction : Fast-intermediate form AV nodal reentry tachycardia (AVNRT) sometimes may mimic atrial tachycardia or atrial flutter and render the diagnosis difficult when the tachycardia rate is fast and AV block occurs during tachycardia.
Methods and Results : A 45-year-old woman with paroxysmal supraventricular tachycardia was referred to this institution. Initially, the tachycardia was thought to be an atrial tachycardia because of: (1) a short cycle length of the tachycardia with 2:1 and Wenckebach AV block; (2) a difference in the atrial activation sequence during tachycardia and during ventricular pacing; and (3) failure of burst ventricular pacing to affect the atrial rate and the atrial activation sequence during tachycardia. An accurate diagnosis of fast-intermediate form AVNRT was subsequently made based on the finding that the tachycardia was induced following delivery of a third ventricular extrastimulus, which showed a sequence of V-A-H and a change on atrial activation sequence of the induced beat. Successful radiofrequency ablation was achieved only after accurate diagnosis of the tachycardia was made.
Conclusion : Fast-intermediate form AVNRT sometimes may masquerade as atrial tachycardia. Accurate diagnosis is mandatory for successful ablation therapy.     

Variations in Human Atrial Flutter Cycle Length Induced by Ventricular Beats: Evidence of a Reentrant Circuit with a Partially Excitable Gap

Variations in Atrial Flutter Cycle Length. Introduction : The purpose of this investigation was to study the mechanisms responsible for small variations in atrial flutter cycle lengths. Methods and Results : In a study group of 11 patients with common atrial flutter, atrial electrograms were recorded from an intraesophageal lead together with a surface lead (V₁). Upon the onset of the QRS complex, atrial flutter intervals consistently increased by an average of 1.8% (SD± 0.9; P <0.01) and subsequently decreased by 2.1% (SD ± 0.8; P <0.01) before returning to the average flutter rate. Carotid sinus massage, which temporally prevented ventricular activation, markedly reduced the variations in atrial flutter intervals. Ventricular pacing at different rates clearly demonstrated that the pattern in atrial flutter intervals was coupled to the moment of ventricular contraction. The hypothesis was formulated that these periodic variations in atrial flutter intervals following a ventricular contraction were caused by the influence of stretch of the atrial myocardium on the conduction properties of a circulating impulse in the atrium. The secondary decrease in flutter rate could be explained if a partial excitable gap is assumed between head and tail of the circus movement. This hypothesis was tested in a simulation study, which revealed that the alternation in intervals as found in patients could only be reproduced if the excitable gap in the circus movement was partially excitable. Conclusion : In conclusion, the analysis of variations in atrial flutter cycle lengths points to a mechanism of circus movement with a partially excitable gap in common atrial flutter.     

Autodecremental pacing for the interruption of ventricular tachycardia and atrial flutter

The efficacy and safety of autodecremental pacing (ADP) to interrupt ventricular tachycardia (VT) and atrial flutter was examined. Once tachycardia was recognized, ADP was initiated using a short train of stimuli with gradual shortening (3%) of the interstimulus interval. ADP was applied to 13 consecutive patients during 75 episodes of VT (mostly following induction by ventricular stimulation). Successful interruption of VT occurred in 88% of the episodes. In 6 episodes (8%), ADP resulted in ventricular fibrillation and in 3 episodes VT was unaffected by ADP. The only significant discriminator between the failure or success of ADP was the rate of VT. ADP was also applied to 17 consecutive patients with an atrial flutter that was resistant to conventional antiarrhythmic agents. Successful conversion of atrial flutter to sinus was seen in only 8 patients (47%). A temporary acceleration to atrial fibrillation appeared in 3 patients (18%), and in 6 patients atrial flutter was unaffected by ADP. ADP was successful in 70% (7/10) of patients with type 1 (< 300 beats/min) atrial flutter. The authors conclude that ADP is beneficial in the interruption of VT and atrial flutter in a selected group of patients, especially with a slower rate of tachyarrhythmia (atrial rate during atrial flutter < 300 beats/min and ventricular tachycardia < 180 beats/min).     

Incidence and clinical significance of transformation of atrial fibrillation to atrial flutter in patients undergoing long-term antiarrhythmic drug treatment.

AIMS: To investigate the rate of transformation of atrial fibrillation to atrial flutter in patients taking antiarrhythmic drugs for the prophylaxis of atrial fibrillation, we retrospectively analysed data from 305 consecutive patients with paroxysmal atrial fibrillation (155 male; mean age 63 +/- 11 years) treated with ventricular rate controlling drugs, antiarrhythmic drugs, or without drugs. METHODS AND RESULTS: At a mean follow-up of 9 months (range 1-24) all patients experienced recurrence of arrhythmia: 48 (14.6%, Group A) suffered Type 1 atrial flutter, and 257 (85.4%, Group B) atrial fibrillation. The relative rate of recurrence of atrial flutter vs atrial fibrillation was similar in patients without treatment or with ventricular rate controlling drugs (from 6.8% to 14.6%, P=ns). However, recurrence was higher (25%) in patients administered antiarrhythmic drug therapy. The relative risk in these patients was 3.02 times greater, compared with patients without treatment, or treated with rate controlling drugs (P<0.001). There were no differences between groups concerning the baseline clinical characteristics and the clinical consequences of the recurrence; patients with atrial flutter had a lower rate of conversion to sinus rhythm (42% vs 64%) and a higher rate of hospital admission (69% vs 36%) compared with those with atrial fibrillation. Six patients (8.5%) experienced 1:1 atrioventricular conduction during atrial flutter with a ventricular rate of 240-280 beats x min(-1). CONCLUSION: Our data suggest that the use of antiarrhythmic drugs for the prophylaxis of atrial fibrillation is associated with a threefold increase in the probability of Type 1 atrial flutter recurrence, as opposed to atrial fibrillation, which may have important clinical consequences, but which did not in our study.     

Impact of congestive heart failure and left ventricular systolic function on the prognostic significance of atrial fibrillation and atrial flutter following acute myocardial infarction

BACKGROUND: Reports on the prognostic importance of atrial fibrillation following myocardial infarction have provided considerable variation in results. Thus, this study examined the impact of left ventricular systolic function and congestive heart failure on the prognostic importance of atrial fibrillation in acute myocardial infarction patients that might explain previous discrepancies. METHODS: The study population was 6676 patients consecutively admitted to hospital with acute myocardial infarction. Information on the presence of atrial fibrillation/flutter, left ventricular systolic function and congestive heart failure were prospectively collected. Mortality was followed for 5 years. RESULTS: In patients with left ventricular ejection fraction<0.25, atrial fibrillation/atrial flutter was associated with an increased in-hospital mortality (OR=1.8 (1.1-3.2); p<0.05) but not an increased 30-day mortality. In patients with 0.250.35. In patients with congestive heart failure, atrial fibrillation/atrial flutter was associated with an increased in-hospital mortality (OR=1.5 (1.2-1.9); p<0.001) and increased 30-day mortality (OR=1.4 (1.1-1.7); p<0.001) but not in patients without congestive heart failure. In hospital survivors, atrial fibrillation/atrial flutter was associated with an increased long-term mortality in all subgroups except those with left ventricular ejection fraction<0.25. CONCLUSIONS: Atrial fibrillation/atrial flutter is primarily associated with increased in-hospital mortality in heart failure patients. Long-term mortality is increased in all subgroups except those with left ventricular ejection fraction<25%.     

Dual chamber arrhythmia detection in the implantable cardioverter defibrillator

INTRODUCTION: Dual chamber implantable cardioverter defibrillator (ICD) technology extended ICD therapy to more than termination of hemodynamically unstable ventricular tachyarrhythmias. It created the basis for dual chamber arrhythmia management in which dependable detection is important for treatment and prevention of both ventricular and atrial arrhythmias. METHODS AND RESULTS: Dual chamber detection algorithms were investigated in two Medtronic dual chamber ICDs: the 7250 Jewel AF (33 patients) and the 7271 Gem DR (31 patients). Both ICDs use the same PR Logic algorithm to interpret tachycardia as ventricular tachycardia (VT), supraventricular tachycardia (SVT), or dual (VT+ SVT). The accuracy of dual chamber detection was studied in 310 of 1,367 spontaneously occurring tachycardias in which rate criterion only was not sufficient for arrhythmia diagnosis. In 78 episodes there was a double tachycardia, in 223 episodes SVT was detected in the VT or ventricular fibrillation zone, and in 9 episodes arrhythmia was detected outside the boundaries of the PR Logic functioning. In 100% of double tachycardias the VT was correctly diagnosed and received priority treatment. SVT was seen in 59 (19%) episodes diagnosed as VT. The causes of inappropriate detection were (1) algorithm failure (inability to fulfill the PR相似文献   

Contemporary catheter ablation of arrhythmias in geriatric patients: patient characteristics, distribution of arrhythmias, and outcome.

AIMS: Catheter ablation is a treatment of first choice for many arrhythmias. Data in geriatric patients are still limited, mostly focusing on single arrhythmia types. The aim of the study was to investigate characteristics of contemporary ablation therapy in the very elderly, focusing on patient characteristics, arrhythmia spectrum, and outcome in a large cohort. METHODS AND RESULTS: We studied 131 consecutive patients aged 80 and older (mean age 83 +/- 3) undergoing ablation for any indication from 1998 until 2004. Sixty-eight patients (52%) had structural heart disease. Most common indications were typical atrial flutter (54%), atrioventricular nodal re-entrant tachycardia (AVNRT) (22%), and atrial fibrillation (AF) (18%). Patients with structural heart disease had more often atrial flutter (72 vs. 35%, P < 0.001) and less AVNRT (7 vs. 38%, P < 0.001) than those without structural heart disease. In almost all patients with AF, ventricular rate control was achieved by elimination of atrioventricular conduction and pacemaker implantation. Success rate exceeded 97% for all ablation types. There was one major complication (0.8%), a stroke after isthmus ablation. CONCLUSION: Almost half of the very elderly patients undergoing ablation have structural heart disease. Indications have changed significantly in recent years, typical atrial flutter is nowadays the predominant indication. The arrhythmia spectrum differs significantly between patients with and without structural heart disease. Regardless of the presence or absence of structural heart disease, success is excellent. Catheter ablation is an excellent therapy option for geriatric patients with arrhythmias.     

The effectiveness and safety of d,l-sotalol in the ambulatory treatment of atrial fibrillation and flutter]

Data on short and long term efficacy and safety of d,l sotalol in patients with atrial fibrillation or atrial flutter is limited. The aims of this study were to (1) assess the antiarrhythmic efficacy of d,l sotalol maintaining normal sinus rhythm in patients with refractory atrial fibrillation or flutter, (2) evaluate the efficacy of d,l sotalol in preventing recurrences of paroxysmal atrial fibrillation or flutter, (3) evaluate the control of ventricular rate in patients with paroxysmal or refractory atrial fibrillation or flutter unsuccessfully treated with other antiarrhythmic agents, (4) determine predictors of efficacy (5) assess the safety of d,l sotalol in this setting. Two hundred patients with chronic or paroxysmal atrial fibrillation or atrial flutter or both, who had failed one to six previous antiarrhythmic drug trials were treated with d,l sotalol 80 to 440 mg/day orally. Fifty four percent was female, age 47 +/- 16 years (range 7-79), follow up period 7 +/- 7 months (range 1 to 14 months), 79% of patients had the arrhythmia for more than one year. The atrial fibrillation in 37.5% of patients was chronic and paroxysmal in 23.5. The atrial flutter was chronic in 31% of patients and paroxysmal in 8%. Eighty two percent of patients was in functional class I (NYHA) and 82% had cardiac heart disease: left atrial (LA) size 44 +/- 10 mm, right atrial (RA) size 37 +/- 7 mm and left ventricular ejection fraction (LVEF) 58 +/- 8%. Total success was achieved in 58% of patients (atrial fibrillation 40% and 18% in atrial flutter), partial success in 38% (atrial fibrillation in 18% and 20% in atrial flutter) and 4% of patients failure. It was p < 0.07 when compared total success vs partial success among atrial fibrillation and atrial flutter groups. Patients with cardiac heart disease responded worst (p = 0.10) to the drug than those without it, specially if the heart was dilated. We concluded that d,l sotalol has moderate efficacy to convert and maintain normal sinus rhythm, as well as it acts controlling paroxysmal relapses and ventricular heart rate.     

Atrial tracking (synchronous) pacing in a pediatric and young adult population

One hundred pediatric and young adult patients underwent implantation of an atrial tracking pacemaker. Seventy-four pacemakers paced in an atrioventricular (AV) sequential mode at the lower rate limit (DDD) while 26 paced in a ventricular demand mode at the lower rate limit (VDD). Five patients required reoperation during follow-up of 1 month to 2.5 years (mean 1.5 years). Six additional patients required programming to ventricular demand (3) or AV sequential (3) pacing, because of development of sinus bradycardia (2), atrial sensing problems (1) or pacemaker-mediated tachycardia (3). Pulse generators that could sense atrial signals less than 1.0 mV and had a programmable atrial refractory period did not require reprogramming out of the atrial tracking mode. No patient developed atrial flutter or fibrillation. Sensing problems during exercise occurred in 37% of the first 60 pacemakers but in none of the last 40, which had improved electronic components. Atrial tracking pacing is feasible in pediatric and young adult patients.     

Apical hypertrophic cardiomyopathy associated with life-threatening paroxysmal atrial flutter with a slow ventricular response: a case report

A 58-year-old male patient had apical hypertrophic cardiomyopathy (HCM) associated with a life-threatening tachycardia due to atrial flutter. Following palpitation and dyspnea for 2-3 h, he became unconscious because of circulatory catastrophe, but was fully resuscitated. An electrocardiogram recorded just before the loss of consciousness revealed atrial flutter at a rate of 260 beats/min with a 2:1 ventricular response. He was diagnosed as having apical HCM based on the echocardiographic and left ventriculographic findings. Atrial stimulation at a rate of 150 pacings/min for 1 min caused a marked drop in systemic systolic blood pressure from 170 to 120 mmHg. The patient was treated with 150 mg of cibenzoline per day to prevent supraventricular tachyarrhythmias and to improve left ventricular diastolic function. At the time of the recent follow-up at 2 and a half years, he felt quite well.     

Long-Term Outcome of Radiofrequency Catheter Ablation for Topical Atrial Flutter: Risk Prediction of Recurrent Arrhythmias

RF Catheter Ablation for Atrial Flutter. Introduction: Little is known about the predictors of recurrent atrial flutter or fibrillation after successful radiofrequency ablation of typical atrial flutter. In addition, there is only limited evidence suggesting that elimination of atrial flutter would modify the natural history of atrial fibrillation in patients who experienced both of these arrhythmias. The aims of the present study were to investigate the long-term results of radiofrequency catheter ablation and to examine the predictors for late occurrence of atrial fibrillation in a large population with typical atrial flutter. Methods and Results: The study population consisted of 144 patients (mean age 56 ± 18 years) with successful ablation of clinically documented typical atrial flutter. In the first 50 patients, successful ablation was defined as termination and noninducibility of atrial flutter; for the subsequent 94 patients, successful ablation was defined as achievement of bidirectional isthmus conduction block and no induction of atrial flutter. The clinical and echocardiographic variables were analyzed in relation to the late occurrence of atrial flutter or fibrillation. Over the follow-up period of 17 ± 13 months, 14 (9.7%) patients had recurrence of typical atrial flutter. In the first 50 patients, 8 (16%) had recurrence of atrial flutter, compared with only 6 (6%) of the following 94 patients. Patients with incomplete isthmus block had a significantly higher incidence of recurrent atrial flutter than those with complete isthmus block (6/16 vs 0/78, P < 0.0001) in the following 94 patients. There was no predictor for recurrence of atrial flutter after successful ablation as determined by univariate and multivariate analysis. Although successful ablation of atrial flutter eliminated atrial fibrillation in 45% of patients with a prior history of atrial fibrillation, 31 (21.5%) of 144 patients undergoing this procedure developed atrial fibrillation during the follow-up period. Univariate analysis revealed that three clinical variables were related to the occurrence of atrial fibrillation: (1) the presence of structural heart disease; (2) a history of atrial fibrillation before ablation; and (3) inducible sustained atrial fibrillation after ablation. By multivariate analysis, only a history of atrial fibrillation and inducible sustained atrial fibrillation could predict the late development of atrial fibrillation after atrial flutter ablation. Conclusion: Radiofrequency catheter ablation of typical atrial flutter is highly effective and associated with a low recurrence rate of atrial flutter, but atrial fibrillation continues to be a long-term risk for patients undergoing this procedure. The presence of structural heart disease and prior spontaneous or inducible sustained atrial fibrillation increases the risk of developing atrial fibrillation.     

Flecainide acetate for conversion of acute supraventricular tachycardia to sinus rhythm

The efficacy of intravenous flecainide acetate (maximum 2 mg/kg or 150 mg given at a rate of 15 mg/min) was assessed in patients with acute supraventricular tachycardia (SVT) (within 24 hours). Fifty patients were studied, 46 with spontaneous SVT and 4 with induced SVT at electrophysiologic assessment. Conversion to sinus rhythm was achieved within 45 minutes in 76%: in 25 patients with atrial fibrillation (76% conversion), 15 with atrioventricular (AV) nodal or AV reentrant tachycardia (100% conversion) and 10 with atrial flutter or atrial reentrant tachycardia (40% conversion). Adverse effects were noted in 21 patients (42%): paresthesia in 9, drowsiness in 8, nausea in 2, accelerated ventricular rate in 5, ventricular tachycardia in 1, sinus bradycardia in 1 and hypotension in 5. Adverse effects were associated with larger dosage and atrial flutter or atrial reentrant tachycardia. Thus, flecainide acetate is effective in converting to sinus rhythm acute atrial fibrillation and AV nodal and AV reentrant tachycardias, but not atrial flutter or atrial reentrant tachycardia.     

Electrophysiological studies in four patients with atrial flutter with 1:1 atrioventricular conduction

Electrophysiological studies of atrioventricular conduction during rapid atrial overdrive pacing and during programmed premature atrial stimulation are reported in four patients with an unusually rapid 1:1 ventricular response to atrial flutter (ventricular rates 240 to 310 per minute). Second-degree AV block developed during atrial overdrive pacing at rates well below those during which 1:1 AV conduction was sustained during spontaneous atrial flutter. Although none of the four patients showed evidence of pre-excitation on the standard 12-lead electrocardiogram, evidence suggesting a partial AV nodal bypass was demonstrated at electrophysiological study in one case. It is postulated that the profile of the atrial wavefront presented to the normal AV node by atrial flutter differs from that during high right atrial pacing and may account for the lower ventricular rates achieved during high right atrial overdrive pacing than during spontaneous atrial flutter in the remaining three cases.     

The contribution of artificial pacemaking to understanding the pathogenesis of arrhythmias

Right atrial or ventricular pacing was performed on 36 occasions in 26 patients in an attempt to terminate a variety of tachyarrhythmias. Of 16 episodes of atrial flutter, 13 were terminated successfully; in 9 of the 13, sinus rhythm or the patient's pre-flutter rhythm was restored immediately, whereas in 4 patients, intervening atrial fibrillation or unstable atrial flutter occurred. Pacing terminated paroxysmal atrioventricular junctional or paroxysmal atrial tachycardia on 3 occasions; in a fourth patient, this tachyarrhythmia terminated during catheter manipulation. Six episodes of pacemaker-induced ventricular tachycardia were abolished by ventricular pacing. In 2 patients, atrial tachycardia was only transiently suppressed, and in 1 of these patients, d-c cardioversion produced a similar effect. Atrial fibrillation, spontaneously converting to atrial flutter, resulted during pacing for atrial tachycardia with block; the latter arrhythmia returned when the atrial flutter was terminated. Atrial fibrillation in 7 patients remained unaffected by atrial pacing. Based on the different electrophysiologic mechanisms responsible for reentrant excitation and automatic pacemaker discharge, an attempt has been made to determine the pathogenesis of the tachyarrhythmia by its response to pacing.     

Continuous rapid atrial pacing to control recurrent or sustained supraventricular tachycardias following open heart surgery.

A technique is described to control recurrent or sustained supraventricular tachycardia associated with rapid ventricular rates following open heart surgery. The technique utilizes a pair of temporarily implanted atrial epicardial wire electrodes to pace the heart. In one group of patients with recurrent atrial flutter and 2:1 A-V conduction, continuous rapid atrial pacing at 450 beats/min produced and sustained atrial fibrillation. The ventricular response rate immediately slowed when compared to that during atrial flutter, and if further slowing was required, it was easily accomplished by the administration of digitalis. Another group of patients with different arrhythmias (recurrent paroxysmal atrial tachycardia, sustained ectopic atrial tachycardia, or sinus rhythm with premature atrial beats which precipitated runs of atrial fibrillation) was treated with continuous rapid atrial pacing to produce 2:1 A-V block. In all instances, the continuous rapid atrial pacing suppressed the supraventricular tachycardia and maintained the ventricular response rate in a therapeutically desirable range. It was demonstrated that the technique is safe, effective, and reliable.