A case of appropriate inappropriate device therapy: hyperkalemia-induced ventricular oversensing

The present case describes a patient who received inappropriate, but potentially life-saving, therapy from her implantable cardioverter defibrillator (ICD) in the setting of acute hyperkalemia (plasma potassium concentration = 8 mM). Hyperkalemia was associated with the development of a slow sinusoidal ventricular tachycardia, at a rate of 100 beats/min to 125 beats/min (610 ms to 480 ms) in a patient who is pacemaker-dependent. There was associated fractionation of the ICD electrogram and T wave oversensing, leading to ventricular oversensing with resultant detection in the ventricular fibrillation rate zone. This was followed by shock therapy, even though the ventricular tachycardia rate was below the programmed detection rate of the ICD. The subsequent emergency treatment of the hyperkalemia normalized the electrogram, corrected the ventricular oversensing and arrhythmia, and restored rate-adaptive single-chamber ventricular pacing.     

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.     

Clinical use of transoesophageal atrial stimulation in terminating ventricular tachycardia

This study was performed to evaluate whether transoesophageal atrial pacing could also stop ventricular tachycardias with low rates and no haemodynamic impairment. Prior to resorting to ventricular endocardial pacing, seven male patients, aged between 15 and 73 years, were treated by transoesophageal atrial pacing for 10 spontaneous episodes of sustained ventricular tachycardia at rates between 105 and 160 beats per minute, without haemodynamic impairment. When atrial pacing did not allow ventricular capture, atropine sulphate was administered. Transoesophageal atrial pacing led to ventricular capture in seven episodes, which made overdriving possible, and blocked six episodes of ventricular tachycardia. In no case did transoesophageal atrial pacing lead to an acceleration of ventricular tachycardia or to degeneration into ventricular fibrillation. Transoesophageal atrial pacing can block low-rate sustained ventricular tachycardias (less than or equal to 150 beats per minute). For low-rate sustained ventricular tachycardias without haemodynamic impairment, transoesophageal atrial pacing can thus be used as the method of choice thanks to its good ratio of risk to efficiency.     

Termination of ventricular tachycardia with bursts of rapid ventricular pacing

Bursts of rapid ventricular pacing used during 573 episodes of ventricular tachycardia in 23 patients terminated 5 12 episodes (89 percent), with burst rates averaging 56 beats/min above the ventricular tachycardia rate, for 5 to 10 captures. Tachycardia was accelerated by pacing bursts to rates below 300 beats/min in 16 episodes (3 percent); 10 of these terminated spontaneously or responded to further bursts. Acceleration of heart rate to more than 300 beats/min or ventricular fibrillation occurred six times (1 percent), each episode requiring direct current cardioversion. Pacing bursts had no effect in 38 instances (7 percent), mostly in patients with terminal cardiogenic shock. Implantable pacemakers delivering bursts of rapid ventricular pacing were placed in two patients who have used these units at home. No deaths were associated with bursts of rapid ventricular pacing, which is an effective, rapid, pleasant alternative to repeated direct current cardioversion and a useful tool during electrophysiologic testing in patients with recurrent tachycardia.     

Effect of atrial fibrillation on atrial blood flow in conscious dogs

This study was undertaken to examine the independent effects of atrial tachycardia, ventricular tachycardia, and atrial fibrillation (AF) on atrial and ventricular blood flow in conscious, heart-blocked dogs using radioactive microspheres. Atrial blood flow averaged 0.54 ± 0.08 ml/min/g during the control period at an atrial rate of 124 beats/min and a ventricular rate of 90 beats/min. Atrial flow increased to 0.72 ± 0.12 ml/min/g during atrial pacing at 236 beats/min, but was not significantly altered by ventricular pacing at 200 beats/min. AF at a ventricular rate of 90 beats/min resulted in atrial flow values of 0.91 ± 0.08 ml/min/g. The ratio of atrial flow to left ventricular flow during AF averaged 1.18 ± 0.08. Administration of a maximal vasodilating dose of adenosine during AF further increased atrial flow to 2.18 ± 0.16 ml/min/g. Atrial tachycardia or AF did not significantly affect ventricular blood flow. These data indicate (1) that atrial blood flow increases significantly during AF, reaching flow values per gram of tissue comparable to those of the left ventricle, and (2) that this flow is regulated by the metabolic needs of the atrial tissue and does not represent maximal vasodilation.     

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.     

Supraventricular tachycardia-ventricular tachycardia discrimination algorithms in implantable cardioverter defibrillators: state-of-the-art review

To reduce inappropriate therapy of supraventricular tachycardia (SVT), implantable cardioverter defibrillators (ICDs) include algorithms to discriminate ventricular tachycardia (VT) from SVT. Dual-chamber algorithms analyze atrial and ventricular rates or AV relationship. They provide advantages over single-chamber algorithms, but introduce new ways to detect SVT as VT inappropriately and to underdetect VT. Unlike pacemakers, dual-chamber ICDs require accurate atrial sensing during high ventricular rates. A postventricular atrial blanking period prevents oversensing of far-field R waves as atrial electrograms, but causes underdetection of atrial fibrillation during high ventricular rates. Tachycardias with 1:1 AV relationship and VT during atrial tachyarrhythmias present specific SVT-VT discrimination problems. The first dual-chamber algorithms performed comparably to single-chamber algorithms. Present dual-chamber algorithms correct some limitations of earlier versions.     

Initial clinical experience with the pacemaker-cardioverter-defibrillator

The implantation of a new multiprogrammable pacemaker-cardioverter-defibrillator is reported in four patients suffering from drug-refractory ventricular tachycardia or fibrillation. The generator (PCD 7215; Medtronic Inc) was interfaced to the epicardium by three countershock patch electrodes and one ventricular myocardial screw-in lead for sensing/pacing. The device employs separate rate detection criteria for ventricular tachycardia and ventricular fibrillation with automatic delivery of up to four therapies per episode. Therapeutic options include: antitachycardia burst or autodecremental pacing, synchronized cardioversion, defibrillation and ventricular demand pacing at 30 to 90 beats/min. Four men and one woman (ages 29 to 75 years) underwent intraoperative implant evaluation, and the device was implanted in the four men. Over a follow-up of 1.5 to 23 months, 161 spontaneous episodes of ventricular tachycardia and nine episodes meeting ventricular fibrillation criteria (cycle length less than 280 to 290 ms) were detected and treated by the device. Ramp pacing was initially employed to terminate 140 ventricular tachycardia episodes and was successful 88.5% of the time while 10 (7.2%) required low energy epicardial cardioversion (4 to 10 J). Six (4.3%) episodes terminated spontaneously prior to therapy delivery. All nine spontaneous episodes of ventricular fibrillation were defibrillated using 10 to 15 J. Two patients continue to do well with the device functioning reliably. The device was removed at the time of heart transplant in one patient, while another patient died suddenly from drug overdose. No other complications, device malfunctions or inappropriate therapy delivery have been observed. These early results demonstrate the potential usefulness of a programmable device which provides graded therapy for ventricular tachycardia with added defibrillation and bradycardia pacing capability.     

Ein neuartiges Zwei-Kammer-Defibrillationssystem: Dauer, Frequenz und zirkadiane Variation supraventrikulärer Tachyarrhythmierezidive

BACKGROUND: The treatment of concomitant atrial tachyarrhythmias in patients with malignant ventricular tachyarrhythmias is a major challenge for new defibrillator devices. Atrial fibrillation is not only responsible for inappropriate ventricular therapies, but also reduced left ventricular performance, especially in patients with heart failure and severely depressed left ventricular function. Furthermore, it is a strong risk factor for the development of thromboembolism. NEW SYSTEM: A new dual-chamber implantable defibrillator is capable of tiered atrial therapies for both regular and irregular atrial tachyarrhythmias. In first investigations a high sensitivity and specificity could be shown as well as a promising therapy efficacy of atrial antitachycardia ramp and burst pacing for the treatment of atrial tachycardias. Atrial ramp pacing has shown to be successful for regular atrial tachyarrhythmias in up to 60 to 70% of all episodes. The results have supported a programming of a high first shock energy for treatment of atrial fibrillation. The incidence of atrial fibrillation in patients with a history of atrial fibrillation or without is much higher in the present investigated patient populations than expected. CONCLUSION: The more complicated and subtle new dual-chamber detection algorithm has proven to be safe and effective both for the detection of ventricular tachycardia but also in terms of an increase of specificity and a reduction of inappropriate ventricular therapies for atrial tachyarrhythmias.     

Characterization of sustained atrial tachycardia in dogs with rapid ventricular pacing-induced heart failure

INTRODUCTION: Atrial arrhythmias often complicate congestive heart failure (CHF). We characterized inducible atrial tachyarrhythmias and electrophysiologic alterations in dogs with CHF and atrial enlargement produced by rapid ventricular pacing. METHODS AND RESULTS: Endocardial pacing leads were implanted in the right ventricle, right atrium, and coronary sinus in 18 dogs. The right ventricular lead was connected to an implanted pacemaker capable of rapid ventricular pacing. The atrial leads were used to perform electrophysiologic studies in conscious animals at baseline in all dogs, during CHF induced by rapid ventricular pacing at 235 beats/min in 15 dogs, and during recovery from CHF in 6 dogs. After 20 +/- 7 days of rapid ventricular pacing, inducibility of sustained atrial tachycardia (cycle length 120 +/- 12 msec) was enhanced in dogs with CHF. Atrial tachycardia required a critical decrease in atrial burst pacing cycle length (< or = 130 msec) for induction and often could be terminated by overdrive pacing. Calcium antagonists (verapamil, flunarizine, ryanodine) terminated atrial tachycardia and suppressed inducibility. Effective refractory periods at 400- and 300-msec cycle lengths in the right atrium and coronary sinus were prolonged in dogs with CHF. Atrial cells from dogs with CHF had prolonged action potential durations and reduced resting potentials and delayed afterdepolarizations (DADs). Mitochondria from atrial tissue from dogs with CHF were enlarged and had internal cristae disorganization. CONCLUSIONS: CHF promotes inducibility of sustained atrial tachycardia. Based on the mode of tachycardia induction, responses to pacing and calcium antagonists, and presence of DADs, atrial tachycardia in this CHF model has a mechanism most consistent with DAD-induced triggered activity resulting from intracellular calcium overload.     

Successful treatment by overdrive pacing of recurrent quinidine syncope due to ventricular tachycardia

A 54 year old patient who experienced recurrent ventricular tachycardia subsequent to quinidine administration for conversion of atrial fibrillation is described. Over a 10 hour period, 25 sustained episodes of ventricular tachycardia occurred for which electrical cardioversion was required in addition to numerous self-terminating paroxysms. Medical therapy with lidocaine, procainamide and propranolol was unsuccessful in controlling the arrhythmia. However, placement of a transvenous right ventricular pacemaker with overdrive pacing at a rate of 110 beats/min abrupty terminated all further ventricular ectopic activity during the period of quinidine elimination. Temporary overdrive pacing may be the treatment of choice for refractory, recurrent, ventricular tachycardia associated with quinidine therapy.     

Optimal programming of ICDs for prevention of appropriate and inappropriate shocks

Expansion of indications for implantable cardioverter-defibrillators (ICDs) has led to a significant increase in the number of patients receiving ICDs and the number of lives saved because of ICD therapy. However, appropriate or inappropriate shocks are frequent and may result in a significant decrease in quality of life in patients with ICDs. Atrial fibrillation with rapid ventricular response, sinus tachycardia, atrial tachycardia or atrial flutter with rapid conduction, and other supraventricular tachycardias are the most common arrhythmias causing inappropriate therapy. Other causes include oversensing of diaphragmatic potentials or myopotentials, T-wave oversensing, double or triple counting of intracardiac signals, lead fractures or header connection problems, lead chatter or noise, and electromagnetic interference. Strategies to reduce inappropriate therapy using device programming rely on the ability to distinguish supraventricular and atrial arrhythmias from ventricular tachycardia. Avoiding therapy for nonsustained ventricular arrhythmias and increasing the role of antitachycardia pacing to terminate ventricular tachycardia are key approaches to reducing shocks for ventricular arrhythmias. Optimal programming holds great promise for decreasing the overall incidence of shock therapy and increasing ICD acceptance.     

Predictors of inducible sustained ventricular tachyarrhythmias in patients with coronary artery disease

To determine predictors of inducible sustained ventricular tachycardia or fibrillation by programmed electrical stimulation in patients with coronary artery disease and ventricular tachyarrhythmias, 14 clinical and angiographic variables were analyzed in 60 consecutive patients. All patients had angiographically documented coronary artery disease and symptomatic ventricular arrhythmias (sustained ventricular tachycardia in 21, ventricular fibrillation in 21 and nonsustained ventricular tachycardia in 18). Baseline programmed electrical stimulation while the patient was not taking antiarrhythmic drugs was performed with use of single, double and triple extrastimuli and burst pacing from two right ventricular sites. The variables analyzed were presenting arrhythmia; presence, frequency and complexity of ventricular ectopic activity on baseline 24 h electrocardiographic (Holter) monitoring; greater than or equal to 70% narrowing in either the left anterior descending, proximal left anterior descending, right coronary or circumflex coronary artery (independently assessed); single, double or triple vessel coronary disease; anterior, apical or inferior wall motion abnormalities; segmental dyskinesia and ejection fraction. Thirty-seven patients (62%) had inducible sustained ventricular tachycardia (rate greater than 100 beats/min, duration greater than 30 s or requiring cardioversion) and two patients (3%) had ventricular fibrillation induced. Eleven patients (18%) had nonsustained ventricular tachycardia (duration greater than or equal to 3 beats, less than 30 s) induced and 10 patients (17%) had no inducible arrhythmia (duration less than 3 beats). Multivariate stepwise logistic regression analysis identified three independent variables predictive of inducible sustained ventricular arrhythmias: sustained ventricular tachycardia as the presenting arrhythmia (p = 0.004), proximal left anterior descending artery lesion (p = 0.002) and anterior wall motion abnormality (p = 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

The Duration of Induced Ventricular Tachycardia as Related to Clinically Sustained Ventricular Tachycardia

Programmed electrical stimulation has been extremely useful in the management of patients with sustained ventricular tachycardia or cardiac arrest. However, the definition of sustained ventricular tachycardia is controversial, and the relationship between the duration of induced ventricular tachycardia and the risk for spontaneous ventricular tachycardia has not been adequately defined. Thus, we examined the records of 64 patients with at least three beats of induced ventricular tachycardia during EP studies using single and double premature stimuli in sinus rhythm and during ventricular paced rhythm (two sites, up to three drive cycle lengths) and using ventricular burst pacing to correlate maximum length of induced ventricular tachycardia with the nature of their spontaneous arrhythmias. Forty-nine patients (77%) had ventricular tachycardia requiring intervention to terminate it, which we called sustained. Nine patients (14%) had ten or fewer beats of ventricular tachycardia; four patients (6%) had 11 to 20 beats of ventricular tachycardia; and two patients (3%) had more than 20 beats of ventricular tachycardia which did not require intervention for termination. Inducible sustained ventricular tachycardia had a sensitivity of 88% and a specificity of 92% for identifying patients with clinical sustained ventricular tachycardia or fibrillation. More than 20 beats of inducible ventricular tachycardia had a sensitivity of 92% and a specificity of 92%. More than 10 beats of inducible ventricular tachycardia achieved a sensitivity of 98% and a specificity of 91% for identifying patients with sustained ventricular tachycardia or fibrillation. The criteria used for the duration of inducible ventricular tachycardia are arbitrary and the interpretation of inducible nonsustained ventricular tachycardia must depend on the purpose of the test and the prior probability of each result.     

Diagnosis and therapy of atrial tachyarrhythmias in the dual chamber implantable cardioverter defibrillator

INTRODUCTION: Devices capable of monitoring and treating atrial tachyarrhythmias provide information about the natural history of the arrhythmias and potentially can influence their natural course by electrical therapy early after onset. METHODS AND RESULTS: Types of atrial arrhythmias and efficacy of device therapies were evaluated in 30 patients implanted with the Medtronic model 7250 Jewel AF implantable cardioverter defibrillator (ICD). All patients had structural heart disease and documented sustained ventricular and atrial arrhythmias (27 with atrial fibrillation [AF]) before implant. Twenty patients were taking amiodarone, and three were taking sotalol. During 20+/-10 months of follow-up, 600 atrial arrhythmia recurrences were documented in 50% of patients. AF was diagnosed in 19%, fast polymorphic atrial tachycardia (AT) in 20%, fast monomorphic AT in 57%, and slow AT in 4% of episodes. The two adaptive pacing therapies, burst and ramp, together with the 50-Hz burst, were successful in 57% of detected atrial arrhythmias. Burst and ramp were responsible for 49% and 50-Hz burst for 51% of successfully treated arrhythmias; 33% of the episodes terminated spontaneously. No ventricular proarrhythmia was observed due to atrial pacing therapies. In 30% of episodes, dual chamber pacing was required due to post termination bradycardia. Atrial arrhythmia recurrences in patients with dilated cardiomyopathy were not amenable to pacing therapies. Several aspects of atrial arrhythmia diagnosis, therapy, and documentation that are specific for functioning of the Jewel AF are discussed. CONCLUSION: Atrial arrhythmias in ICD patients with diseased hearts who are taking Class III antiarrhythmics frequently had longer cycle lengths than AF. Half of these arrhythmias could be terminated with pacing therapies; one third terminated spontaneously.     

Ventricular fibrillation during programmed ventricular stimulation: Incidence and clinical implications

Ventricular fibrillation occurred in 10 (3.3 percent) of 300 patients consecutively studied with programmed ventricular stimulation. One hundred twenty-five of these patients were studied with double ventricular extrastimuli including 68 patients with and 57 patients without documented or suspected ventricular tachycardia or fibrillation, or both. Ventricular fibrillation did not develop in response to a single ventricular extrastimulus delivered during sinus rhythm, ventricular pacing or ventricular tachycardia or in response to ventricular pacing at cycle lengths of 300 msec or greater and occurred only in response to double ventricular extrastimuli. All 10 patients who manifested ventricular fibrillation during programmed stimulation were in the group of patients with suspected or documented ventricular tachycardia or fibrillation. Ventricular fibrillation was initiated in seven patients with double ventricular extrastimuli delivered during sinus rhythm or ventricular pacing and in three patients with double ventricular extrastimuli delivered during ventricular tachycardia. Four patients had spontaneous conversion to sinus rhythm and the remainder underwent defibrillation without sequelae. Recurrent ventricular fibrillation occurred clinically in 7 of the 10 patients. This study suggests that ventricular fibrillation occurs uncommonly during programmed ventricular stimulation and only in response to double ventricular extrastimuli in patients in whom spontaneous episodes are likely to occur.     

Termination of pacemaker-mediated tachycardia by adenosine

A 30-year-old woman was referred for follow-up right- and left-heart catheterization 4 years after cardiac transplantation. She had an implanted epicardial pacemaker for bradycardia; this was programmed to the DDD mode. At the time of her catheterization, as a pigtail catheter was pulled back across the aortic valve, runs of premature ventricular complexes occurred and tachycardia with ventricular pacing spikes and ventricular capture was initiated at a rate of 126 beats/min. Adenosine 6 mg was given intravenously through a femoral venous sheath and within 20 s the tachycardia broke. The tachycardia was consistent with pacemaker-mediated tachycardia (PMT), a circus movement tachycardia occurring when ventricular pacing causes retrograde atrial depolarization followed by triggering of ventricular pacing. With reprogramming of the pacemaker to an AV delay of 160 ms and a postventricular atrial refractory period of 300 ms, no further episodes of PMT have occurred. This case illustrates that intravenous adenosine can effectively terminate PMT by causing ventriculoatrial block, thus interrupting the reentrant circuit by eliminating retrograde atrial activation.     

体外无创性起搏终止快速心律失常的临床观察

为评价体外无创性程控起搏终止快速心律失常的疗效、安全性和患者的耐受性，对３１例房室折返性心动过速（ＡＶＲＴ）、１６例房室结折返性心动过速（ＡＶＮＲＴ）、１例房性心动过速、３例心房扑动和２例室性心动过速患者进行体外程控起搏终止心动过速的治疗。４７例ＡＶＲＴ和ＡＶＮＲＴ患者的６７次发作中６１次（９１．０％）被成功终止，其中ＡＶＲＴ的有效率（９３．５％）高于ＡＶＮＲＴ（８５．７％），Ｐ＜０．０５。１例室性心动过速被终止。所有房性心律失常都未被终止。同一输出电流强度下，递减刺激法终止ＡＶＲＴ和ＡＶＮＲＴ的总成功率（８６．４％）高于期前刺激法（４１．０％）和短阵超速抑制法（５５．０％），Ｐ均＜０．０５。部分患者有胸部皮肤疼痛感，但大多数患者能够耐受，且无心肌损伤。因此，体外无创性程控起搏可作为一种终止ＡＶＲＴ和ＡＶＮＲＴ的紧急治疗手段运用于临床     

Questionable dysfunction of a dual-Chamber pacemaker in a 17-year-old female: differential diagnoses of missing ventricular beats

The case of a 17-year-old female who had been implanted a dual-chamber DDD pacemaker because of third-degree atrioventricular block is reported. There is a history of continued dizziness and even occasional syncopes. At heart rates of 111/min to 124/min, 24-h Holter electrocardiography revealed isolated missing ventricular beats in an otherwise continuous atrially sensed and triggered, ventricularly paced rhythm. Differential diagnoses of a putative pacemaker dysfunction are presented, comprising 2:1-block at maximum programmed heart rate, intermittent lead fracture, anti-pacemaker-mediated tachycardia algorithm, ventricular oversensing, P wave signal undersensing, and atrial oversensing.