Natural history of sinus node disease treated with atrial pacing in 213 patients: implications for selection of stimulation mode.

OBJECTIVES. This study was designed to analyze the incidence and determinants of complications and long-term survival in sinus node disease treated with atrial pacing. BACKGROUND. Knowledge of the natural history of sinus node disease treated with different pacing modes is imperfect, and controversy exists regarding the optimal pacemaker therapy. METHODS. A consecutive series of 213 patients with sinus node disease initially treated with atrial pacing was studied for a median follow-up period of 60 months. The end points studied were permanent atrial fibrillation, high grade atrioventricular (AV) block, P wave undersensing, pacing mode change, reoperation and death. Several prognostic factors were evaluated statistically and the survival rate was compared with that of a matched general population. RESULTS. The incidence rate of permanent atrial fibrillation during follow-up was 7% (1.4%/year). The risk of this arrhythmia increased substantially with age greater than or equal to 70 years at pacemaker implantation. Only 2 of the 15 patients who developed permanent atrial fibrillation required ventricular pacing. High grade AV block occurred in 8.5% (1.8%/year) and its incidence was much greater in patients with complete bundle branch block or bifascicular block (35%) than in patients without such conduction disturbances (6%). A change to ventricular or dual-chamber stimulation was necessary in 14% of all patients, primarily because of early lead dislodgment or high grade AV block. Surgical intervention with maintenance of atrial pacing was required in 7% of patients. The survival rates of 97% at 1 year, 89% at 5 years and 72% at 10 years did not differ significantly from those of a matched general population. CONCLUSIONS. In sinus node disease, atrial pacing can be successfully applied during long-term follow-up. Patients with complete bundle branch or bifascicular block in addition to sinus node disease should initially receive a dual-chamber pacemaker, but routine application of dual-chamber stimulation does not appear to be warranted.     

Incidence of arrhythmias after atrial or dual-chamber pacemaker implantation

The incidence of sustained atrial, pacemaker-mediated and ventricularrhythm disturbances was studied retrospectively in a consecutiveseries of112 patients without a history of preexisting atrialtachy arrhythmias, receiving an atrial or dual-chamber pacemaker. Early atrial fibrillation (during the first week) was recordedtwice. Late atrial fibrillation was seen in seven patients,flutter in one, yielding a total incidence of 8.9% for 22 months.There were no significant differences with respect to age, aetiology,electrocardiographic diagnosis, pacing history, or the measuredintracardiac P wave between the group with and the group withoutatrial fibrillation. Treatment with digoxin reverted three patientsto sinus rhythm, association of digoxin and amiodarone, sixpatients. One patient with congestive heart failure remainedin atrial fibrillation. Pacemaker-mediated tachycardia was not a major problem. Onepatient of a subgroup with known ventricular arrhythmia hada non-sustained ventricular tachycardia during programming atfollow-up; sustained ventricular tachycardia was not recorded.Reprogramming to VDD, DVI or VVI was done in 6/100patients. The incidence of atrial fibrillation or flutter in highly selectedpatients with dual-chamber or atrial pacing is moderately low.It is not possible to identify patients with a high risk fordevelopment of atrial fibrillation; when it occurs, it is easilycontrolled with drugs. DDD pacing seems to be safe in patients with a history of seriousventricular arrhythmias, treated with appropriate drugs.     

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.     

Multiple syncope mechanisms coexisting in a Brugada syndrome patient requiring a single therapeutic approach

We report the case of a Brugada syndrome patient with a history of syncopal and presyncopal episodes and evidence of sinus node and atrioventricular (AV) conduction abnormalities. The patient developed sinus bradycardia, sinoatrial conduction abnormalities, prolonged HV interval, early appearance of AV block, AV nodal reentrant tachycardia and polymorphic ventricular tachycardia in the electrophysiological study. He was treated with a dual-chamber pacemaker defibrillator. At the 9-year follow-up, the patient remained asymptomatic with several episodes of 1:1 AV-relationship tachycardia, interrupted with antitachycardia pacing, while the predominant pacing states of the device were AP-VS and AS-VP for most of the time.     

Schrittmachertherapie bei Patienten mit Vorhofflimmern

Pacemaker therapy in patients with atrial fibrillation means the best current pacemaker therapy for patients with bradycardias with the aim to avoid the onset of atrial fibrillation and to establish DDD pacing despite of a history of atrial tachyarrhythmias. The newer application of pacing is the suppression of atrial arrhythmias in patients with medical refractory atrial tachyarrhythmias. Patients with slow ventricular rates and permanent atrial fibrillation should receive a VVI-pacemaker, if the bradycardias causes syncope, dizziness or a decrease of their exercise tolerance. In case of chronotropic incompetence the pacemaker should provide rate responsive pacing. Patients with sick sinus syndrome should receive an atrial (AAI) or dual-chamber (DDD) pacemaker, because patients with these in contrast to VVI-pacemakers develop less often atrial fibrillation and subsequent complications such as atrial thromboembolism. A dual-chamber or VDD-pacemaker—the latter connected to a VDD-single-lead—is indicated in patients with advanced AV-block. Atrial fibrillation occurs in 3 to 6% of the patients with no history of arrythmia and is, if pacemakers have no automatic mode switch, an often reason to program the devices to the VVI-pacing mode. Nowadays, most DDD(R)-pacemakers provide an automatic mode switch: During an atrial tachycardia the pacemaker switches to a VVI/VVIR mode and restores the initial DDD(R)-pacing mode with termination of the arrhythmia. In respect to the newer applications, one approach to prevent atrial tachyarrhythmias is permanent atrial pacing. As lower pacing rates of 80 to 90 ppm are usually needed and many patients hardly tolerate these pacing rates, new algorithms are under clinical investigation. Another approach is the simultaneous depolarization of the right and left atrium. Biatrial pacing is performed with one lead in the high right atrium and another lead in the coronary sinus. Another solution is bifocal atrial pacing with leads placed in the high right atrium and in the coronary sinus ostium. One effect of the new pacing techniques is to shorten interatrial conduction times. Therefore, biatrial pacing has become a therapy to prevent atrial arrhythmias deriving from delayed interatrial conduction times. As atrial reentry circuits seem to be important in atrial fibrillation, multisite atrial pacing is also performed in patients with medical refractory paroxysmal atrial fibrillation. Preliminary results suggest a more effective prevention of atrial fibrillation; nevertheless, these techniques should be still restricted to patients enrolled in clinical studies.     

Pacemaker hemodynamics: Clinical implications

Our review of the current literature and experience in caring for pacemaker patients suggests that a consideration of hemodynamics is a logical way to approach pacemaker selection and programming. Multiple clinical factors enter into the selection of a pacemaker or pacemaker programming settings in each case. It appears that in patients with sinus node disease, atrial-inhibited or dual-chamber pacing provides the best chance for preventing the development of chronic atrial fibrillation with its attendant risks of embolism and stroke. It is clear that AV synchrony has beneficial hemodynamic effects at rest in most patients. The results of Labovitz would suggest that in patients with marked left atrial enlargement, this may be less so. The results of Stewart et al would further suggest that in patients with retrograde VA conduction, dual-chamber pacing is preferable. Retrograde VA conduction can be intermittent and this makes it difficult to use its absence on a single test to decide on the type of pacemaker to use. It appears that baseline left ventricular function does not determine the relative improvement in cardiac output observed with AV synchrony or rate-adaptive pacing. However, in patients with severe congestive heart failure even a small improvement in cardiac output may result in significant clinical improvement. Studies have shown that in any given patient, there may be an optimal AV interval at rest. In general, this ranges from 100 to 150 milliseconds. In normal individuals the optimal AV interval shortens with increased heart rate during exercise in a predictable and linear fashion. The hemodynamic benefits of a shortened AV interval with faster heart rates in pacemaker patients have not yet been shown. Intuitively, however, this would appear to be a desirable approach and will probably be added to the design of future generations of dual-chamber pacemakers. Studies of the effect of different pacing modes on secretion of atrial natriuretic factor are intriguing and may contribute more to our understanding of pacing hemodynamics in the future. During exercise, heart rate increase is more important than AV synchrony and this has been shown by several studies. Thus, in active patients with chronotropic incompetence due to sick sinus syndrome, the addition of rate-adaptive pacing is important. Because single-chamber rate-adaptive atrial pacing leaves the patient exposed to the risk of future development of AV block and DDD pacing does not provide chronotropic support, it is likely that the new rate-adaptive dual-chamber (DDDR) devices will be used in a significant number of these patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

Late ventricular arrhythmia and sudden death following direct-current catheter ablation of the atrioventricular junction.

Early reports of direct-current catheter ablation (DCCA) of the atrioventricular (AV) junction for resistant AV tachycardias documented efficacy of DCCA with little morbidity. Nine patients underwent DCCA at our institution 4 to 9 years ago: 3 patients had DCCA in the coronary sinus for permanent junctional reciprocating tachycardia, 2 patients had His ablation, 2 had coronary sinus and His ablation for permanent junctional reciprocating tachycardia, and 2 had DCCA for congenital tachycardia, and 2 had DCCA for congenital junctional ectopic tachycardia. Shocks (total 1 to 5) ranged from 12.5 to 400 J. Five patients had pacemaker implant at the time of DCCA. During follow-up, 3 patients developed clinical ventricular tachycardia: all 3 had DCCA of the His bundle. One asymptomatic patient with ventricular tachycardia, who had DCCA of the bundle of His, died suddenly 6 years later with ventricular fibrillation. Autopsy revealed 2 ventricular scars: 1 extending from the AV junction and 1 in the outflow tract. No patient with DCCA limited to the coronary sinus developed ventricular tachycardia. DCCA of the His bundle can result in late ventricular arrhythmias, possibly a result of extension of the DCCA lesion into the ventricle. These late findings should be considered in evaluating the safety and efficacy and follow-up for patients undergoing radiofrequency ablation.     

Electrophysiologic manifestations of ventricular tachyarrhythmias provoking appropriate defibrillator interventions in high-risk patients with hypertrophic cardiomyopathy

Introduction: Our objective was to determine features of ventricular tachyarrhythmias triggering appropriate implantable cardioverter-defibrillator (ICD) interventions in hypertrophic cardiomyopathy (HCM).
Methods and Results: The study cohort was 68 high-risk HCM patients who received ICDs for primary sudden cardiac death prevention from 1995 to 2003. All episodes of sustained ventricular tachyarrhythmias identified by stored intracardiac electrograms were analyzed. Nine patients had 51 episodes of sustained ventricular tachyarrhythmic events that required device therapy (mean follow-up, 3.4 ± 2.2 years; cumulative event rate, 3.2% per year): five had 47 episodes of monomorphic ventricular tachycardia (VT); four each had one episode of ventricular fibrillation (VF). Sinus tachycardia or atrial fibrillation was the initiating rhythm in five of nine patients and in 43 of 51 episodes of events. Of the 17 episodes of monomorphic VT detected in the VT zone, 16 (94%) were terminated by antitachycardia pacing. Thirty episodes of monomorphic VT were detected in the VF zone and were terminated by defibrillation.
Conclusion: Sustained monomorphic VT is common in a high-risk cohort with HCM. Sinus tachycardia is often the initiating rhythm, suggesting that high sympathetic drive may be proarrhythmic when a susceptible substrate is present. Antitachycardia pacing is highly effective in terminating VT in this patient population.     

Transvenous catheter ablation of the His bundle in ventricular tachycardia

The usefulness of transvenous catheter ablation of the His bundle in three patients with recurrent ventricular tachycardia (VT), in which the initiating mechanism was recognized during a rapid atrial rhythm, is reported. Tachycardia was refractory to conventional treatment and required transthoracic direct-current shocks in all patients. In patient No. 1 double tachycardia (atrial flutter and VT) was documented and VT was easily induced by rapid atrial pacing. In patients Nos. 2 and 3 initiation of VT during junctional reciprocating and atrial tachycardia, respectively, was observed. Interruption of the His bundle was performed by means of fulguration. Stable atrioventricular (AV) block was observed in patient No. 1 after the ablative procedure; patient No. 2 showed anterograde conduction over a posterior septal accessory pathway with no evidence of conduction over the normal conduction system in both the anterograde and retrograde directions. In patient No. 3, transient AV block was observed; AV conduction resumed 2 days later and the cardiac rhythm showed persistent ectopic atrial tachycardia with second-degree AV block. Patients Nos. 1 and 2 underwent pacemaker implantation, but patient No. 2 was not pacemaker dependent. After the procedure, VT no longer occurred in any of the patients (follow-up: 2 years, 5 months, and 6 months).     

Indications for dual-chamber cardioverter defibrillators at implant and at 1 year follow-up: a retrospective analysis in the single-chamber defibrillator era.

AIM: This retrospective four-centre study assessed the current indications for dual-chamber implantable cardioverter defibrillators (ICDs) at implant and during a medium-term follow-up period in a group of patients treated by single-chamber ICD in the pre dual-chamber ICD era. METHODS AND RESULTS: The study population consisted of 153 consecutive patients (127 males, mean age 58 +/- 6 years) treated by single-chamber ICD for ventricular tachycardia and/or ventricular fibrillation. Definite indications for having a dual-chamber ICD included the presence of sinus node dysfunction and of second- or third-degree atrioventricular (AV) block, while possible indications were represented by paroxysmal atrial fibrillation or flutter and first-degree AV block. At implant, dual-chamber ICD would appear definitely indicated in 10.5% of cases, and possibly indicated in an additional 17.5% of cases. During 12 +/- 10 months follow-up, such percentages remained stable (11 and 19.5%, respectively). Inappropriate ICD intervention was documented in five of 13 patients (38%), with episodes of paroxysmal atrial fibrillation or flutter. CONCLUSION: In this non-selected study population, a dual-chamber ICD would have potentially benefited approximately 30% of the patients. During medium-term follow-up, there was no progression towards increasing dual-chamber ICD indications. The 15% cumulative incidence of paroxysmal atrial tachyarrhythmias justifies the activation of dedicated detection algorithms.     

The Response of Paroxysmal Supraventricular Tachycardia to Overdrive Atrial and Ventricular Pacing:

Pacing During Supraventricular Tachycardia. Introduction: Standard electrophysiologic techniques generally allow discrimination among mechanisms of paroxysmal Supraventricular tachycardia. The purpose of this study was to determine whether the response of paroxysmal Supraventricular tachycardia to atrial and ventricular overdrive pacing can help determine the tachycardia mechanism. Methods and Results: Fifty-three patients with paroxysmal Supraventricular tachycardia were studied. Twenty-two patients had the typical form of atrioventricular (AV) junctional (nodal) reentry, 18 patients had orthodromic AV reentrant tachycardia, 10 patients had atrial tachycardia, and 3 patients had the atypical form of AV nodal reentrant tachycardia. After paroxysmal Supraventricular tachycardia was induced, 15-beat trains were introduced in the high right atrium and right ventricular apex sequentially with cycle lengths beginning 10 msec shorter than the spontaneous tachycardia cycle length. The pacing cycle length was shortened in successive trains until a cycle of 200 msec was reached or until tachycardia was terminated. Several responses of paroxysmal Supraventricular tachycardia to overdrive pacing were useful in distinguishing atrial tachycardia from other mechanisms of paroxysmal Supraventricular tachycardia. During decremental atrial overdrive pacing, the curve relating the pacing cycle length to the VA interval on the first beat following the cessation of atrial pacing was flat or upsloping in patients with AV junctional reentry or AV reentrant tachycardia, but variable in patients with atrial tachycardia. AV reentry and AV junctional reentry could always be terminated by overdrive ventricular pacing whereas atrial tachycardia was terminated in only one of ten patients (P < 0.001). The curve relting the ventricular pacing cycle length to the VA interval on the first postpacing beat was flat or upsloping in patients with AV junctional reentry and AV reentry, but variable in patients with atrial tachycardia. The typical form of AV junctional reentry could occasionally be distinguished from other forms of paroxysmal Supraventricular tachycardia by the shortening of the AH interval following tachycardia termination during constant rate atrial pacing. Conclusions: Atrial and ventricular overdrive pacing can rapidly and reliably distinguish atrial tachycardia from other mechanisms of paroxysmal Supraventricular tachycardia and occasionally assist in the diagnosis of other tachycardia mechanisms. In particular, the ability to exclude atrial tachycardia as a potential mechanism for paroxysmal Supraventricular tachycardia has important implications for the use of catheter ablation techniques to cure paroxysmal Supraventricular tachycardia.     

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 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.     

Conventional and biventricular pacing in patients with first-degree atrioventricular block

Recent reports suggest that first-degree atrioventricular block is not benign. However, there is no evidence that shortening of the PR interval can improve outcome except for symptomatic patients with a very long PR interval ≥0.3 s. Because these patients require continual forced pacing, biventricular pacing should be used according to accepted guidelines for third-degree AV block. Functional atrial undersensing may occur in patients with conventional dual-chamber pacing and first-degree AV block because the sinus P-wave tends to be displaced into the post-ventricular atrial refractory period (PVARP) an arrangement that may cause a pacemaker syndrome. Prevention requires programming a shorter AV and PVARP that is feasible because retrograde conduction is rare in first-degree AV block patients. A relatively new pacing mode to minimize right ventricular stimulation has been designed by eliminating the traditional AV interval but with dual-chamber backup. This pacing mode permits the establishment of very long AV intervals that may cause pacemaker syndrome. About 50% of patients undergoing cardiac resynchronization therapy (CRT) have a PR interval ≥200 ms. The CRT patients with first-degree AV block are prone to develop electrical desynchronization more easily than those with a normal PR interval. The duration of desynchronization after exceeding the upper rate on exercise is also more pronounced. AV junctional ablation is rarely necessary in patients with first-degree AV block but should be considered for symptomatic functional atrial undersensing or when the disturbances caused by first-degree AV block during CRT cannot be managed by programming.     

Pseudo failure of sensing in patients with universal pacemakers and junctional rhythms

Ventricular fibrillation has been only rarely observed as a complication of cardiac pacing after the advent of demand pacemakers. Automatic AV sequential pacing (DDD) may provide the setting for ventricular fibrillation in patients with junctional rhythms. In this report we present two patients with implanted DDD pacemakers in whom ventricular pacemaker spikes were seen occurring on top of the T wave during episodes of junctional rhythm. This apparent lack of sensing of QRS complexes does not represent pacemaker malfunction, but rather, is the result of physiologic lack of sensing (blanking) which occurs 56 to 100 msec. following the output of the atrial and ventricular channels. During junctional rhythm when the atrial spike occurs at the beginning of a QRS complex the ventricular channel is blanked and does not sense the intrinsic ventricular activity and thus, ventricular output occurs during repolarization. Increasing the maximum pacemaker rate and decreasing the AV delay will reduce the chance occurrence of this phenomenon.     

The role of pacing mode in the development of atrial fibrillation.

Asynchronous ventricular pacing has been shown to increase the risk of development of atrial fibrillation (AF) because of various mechanisms: retrograde atrioventricular (AV) conduction with increase in atrial pressure causing acute atrial stretch and reverse flow in the pulmonary veins, mitral regurgitation, reduced coronary blood flow, adverse neuroendocrine reactions, etc. Dual-chamber pacing preserves atrioventricular synchrony. However, in randomized multicentre trials comparing VVI(R) with DDD(R) pacing, AF is only slightly less frequent in the dual-chamber mode. This is most likely due to unnecessary ventricular pacing, which is frequent in dual-chamber pacing. At nominal values, dual-chamber devices usually do not permit intrinsic AV conduction but promote delivery of the ventricular stimulus at an inappropriate time in an inappropriate place. Programming of long AV delays facilitates spontaneous AV conduction but usually cannot completely avoid unnecessary ventricular pacing and causes other problems in the dual-chamber mode. Atrial septal lead placement can improve left-sided AV synchrony and promote spontaneous AV conduction. Programming of the AAI(R) mode is superior to the dual-chamber mode but cannot be used if AV conduction is impaired intermittently or permanently. Therefore, dedicated algorithms enhancing spontaneous AV conduction in the dual-chamber mode are desirable for a large proportion of pacemaker patients.     

Worldwide clinical experience with a new dual-chamber implantable cardioverter defibrillator system

INTRODUCTION: Management of atrial tachyarrhythmias represents a significant challenge in patients with implantable cardioverter defibrillators (ICDs). Drug therapy of these arrhythmias is limited by moderate efficacy, ventricular proarrhythmia, and drug-device interactions. This study tested the safety and efficacy of a new dual-chamber ICD to detect and treat atrial as well as ventricular tachyarrhythmias. METHODS AND RESULTS: A dual-chamber ICD (Medtronic 7250 Jewel AF) was implanted in 293 of 303 patients at 49 centers in Europe, Canada, and North America. Specific data were collected at implant and during a mean follow-up period of 7.9+/-4.7 months. There were no clinically evident failures to detect and treat ventricular arrhythmias. In patients with at least one of the dual-chamber detection criteria activated, 1,056 of 1,192 episodes of ventricular tachycardia or fibrillation detected were judged to be appropriate (89% positive predictive accuracy). Therapy efficacy was 100% in the ventricular fibrillation zone and 98% in the ventricular tachycardia zone. Positive predictive accuracy for detection of atrial episodes was 95% (1,052/1,107). For episodes classified as atrial tachycardia by the device, the efficacy of atrial antitachycardia pacing and high-frequency (50-Hz) burst pacing was 55% and 17%, respectively. High-frequency burst pacing terminated 16.8% of episodes classified as atrial fibrillation, and atrial defibrillation had an estimated efficacy of 76%. The actuarial estimates of 6-month complication-free survival and total survival were 88% and 94%, respectively. CONCLUSION: This novel dual-chamber ICD is capable of safely and effectively discriminating atrial from ventricular tachyarrhythmias and of treating atrial tachyarrhythmias without compromising detection and treatment of ventricular tachyarrhythmias.     

Use of intravenous adenosine in sinus rhythm as a diagnostic test for latent preexcitation

In a proportion of patients with left free wall accessory connections, preexcitation is apparent only during atrial arrhythmias or atrial pacing (latent preexcitation). These patients may be at risk of a rapid ventricular response to atrial fibrillation despite the absence of preexcitation in sinus rhythm. The ability of intravenous adenosine to unmask latent preexcitation was evaluated in 22 patients with a history of documented supraventricular tachycardia and a normal electrocardiogram during sinus rhythm. Preexcitation was unmasked in response to adenosine in 4 patients: all 4 were shown to have latent preexcitation at electrophysiologic study. In 12 patients atrioventricular (AV) nodal conduction delay or block was induced without preexcitation after adenosine (first-degree AV block in 8, second-degree block in 4): at subsequent electrophysiologic study none of these patients was found to have latent preexcitation. Five patients had little or no PR prolongation in response to adenosine: of these, 2 were shown to have latent preexcitation at electrophysiologic study. Atrial fibrillation was induced in 1 patient and a narrow complex regular tachycardia in another after intravenous adenosine. Intravenous adenosine during sinus rhythm is capable of producing AV nodal conduction delay or block in 73% of patients with a history of supraventricular tachycardia: in these patients adenosine provides a diagnostic test that is both 100% sensitive and 100% specific for latent preexcitation. In those patients in whom adenosine does not produce AV conduction delay or block, further investigation is required to establish or refute the diagnosis of latent preexcitation.     

Prävention von Vorhofflimmern durch Schrittmacherstimulation

Several prospective randomized clinical trials have reported that atrial-based "physiological" pacing is associated with a lower incidence of paroxysmal and permanent atrial fibrillation than single-chamber ventricular pacing in patients with conventional pacemaker indication. Whether atrial pacing itself is antiarrhythmic remains still uncertain. By contrast, right ventricular pacing is considered to beget atrial fibrillation, even in preserved AV synchrony during dual-chamber pacing. A number of clinical trials investigated the impact of sitespecific atrial pacing and advanced atrial pacing algorithms on the secondary prevention of atrial fibrillation. Multisite pacing (dual-site right atrial or biatrial pacing) was demonstrated to add only minimal benefit for the prevention of atrial fibrillation. By contrast, in some studies septal pacing and specific atrial pacing algorithms were reported to reduce the recurrence of atrial fibrillation in selected patients. At present, however, it remains unclear how to identify these patients. In clinical practice, the effectiveness of specific atrial pacing algorithms and/or septal pacing has to be tested out in the individual case. These therapeutic options should be considered in patients with a conventional indication for antibradycardia pacing and, additionally, symptomatic atrial fibrillation.     

Pacing therapy for atrial tachyarrhythmias

The use of pacing techniques for the treatment of atrial tachyarrhythmias has been advocated for more than 30 years. Although it has played a beneficial role in the management of paroxysmal supraventricular tachycardia (PSVT) in drug-refractory patients, tachycardia acceleration and development of atrial fibrillation has been the major drawback. With the availability of radiofrequency catheter ablation therapy, the use of implantable antitachycardia devices for PSVT is currently negligible. From retrospective and small control studies it has been shown that atrial or dual-chamber pacing in patients with sick sinus syndrome has been associated with a lower incidence of paroxysmal atrial flutter or fibrillation than in those who received a ventricular pacemaker. Furthermore, recent studies have reported the potential benefit of reducing frequency of paroxysmal atrial flutter and fibrillation with multisite atrial pacing. As a result, there is a resurgence of research interest in antitachycardia pacing for prevention of atrial tachyarrhythmias. This paper briefly describes the basic aspects of antitachycardia pacing, reviews the data on the use of implantable antitachycardia devices for PSVT and the selection of patients, and assesses the current status of research on atrial pacing for prevention of paroxysmal atrial flutter and fibrillation.