The Use and Interaction of Permanent Pacemakers and the Automatic Implantable Cardioverter Defibrillator

The adverse interactions of permanent pacemakers and automatic implantable cardioverter defibrillators (AICD) were studied in nine patients in whom both devices were implanted. Both unipolar and bipolar pacemakers were evaluated. The permanent pacemakers were also used to do noninvasive electrophysiological studies and to induce ventricular fibrillation. Undersensing of ventricular fibrillation by the permanent pacemakers caused inappropriate pacemaker stimuli, which caused undersensing of ventricular fibrillation by the AICD in three of four patients with unipolar pacemakers. After an AICD discharge, pacemaker noncapture was seen in eight of 22 episodes for an average 4.9 seconds and inability to sense was seen in 11 of 20 episodes for an average 9.0 seconds. Counting of pacemaker stimuli and QRS by the AICD caused inappropriate discharges. Noninvasive electrophysiological testing by the pacemakers correlated with invasive testing. Furthermore, induction of ventricular fibrillation was successful in four of five patients attempted, though requiring long bursts at high outputs at the shortest cycle lengths obtainable by these pacemakers. Operation of the AICD and permanent pacemakers must be clearly understood to avoid adverse interactions of these devices.     

Electrosurgery-induced ventricular fibrillation during pacemaker replacement — a unique mechanism

Arrhythmias and pacemaker malfunction are known to occur from the use of an electrosurgical device. The present case report describes a patient with sick sinus syndrome who experienced ventricular fibrillation while undergoing surgery. During replacement of his non-functioning cardiac pacemaker under general anesthesia, electrosurgery was used to ensure hemostasis. Electric current may have stimulated myocardial leads present in the surrounding tissue, leading to ventricular fibrillation. The patient was resuscitated from the episode without any residual sequelae. Microshock and possible mechanisms that can lead to ventricular arrhythmias in patients with pacemakers during electrosurgery are discussed.     

Electrosurgery-induced ventricular fibrillation during pacemaker replacement — a unique mechanism

Arrhythmias and pacemaker malfunction are known to occur from the use of an electrosurgical device. The present case report describes a patient with sick sinus syndrome who experienced ventricular fibrillation while undergoing surgery. During replacement of his non-functioning cardiac pacemaker under general anesthesia, electrosurgery was used to ensure hemostasis. Electric current may have stimulated myocardial leads present in the surrounding tissue, leading to ventricular fibrillation. The patient was resuscitated from the episode without any residual sequelae. Microshock and possible mechanisms that can lead to ventricular arrhythmias in patients with pacemakers during electrosurgery are discussed.     

Importance of Pacemaker Noise Reversion as a Potential Mechanism of Pacemaker-ICD Interactions

Numerous types of interactions between pacemakers and implantable cardioverter defibrillators (ICDs) have been described. Pacemaker outputs preventing appropriate detection of ventricular tachycardia or ventricular fibrillation by the ICD is one of the more serious. Asynchronous pacemaker activity during ventricular arrhythmias maybe caused by either nonsensing of the arrhythmia or by noise reversion, which is an algorithm that causes the pacemaker to switch to asynchronous pacing when repetitive sensing at a high rate occurs. We analyzed the mechanisms underlying asynchronous pacemaker activity in ventricular arrhythmias using pacemaker telemetry during the arrhythmia. Thirty-nine induced arrhythmias from 26 different procedures in 19 patients with both pacemakers and ICDs were analyzed. Of the 39 arrhythmias, asynchronous pacemaker activity occurred in 16. The underlying mechanism was nonsensing in 4 episodes and noise reversion in 12 episodes. Clinically significant interference with detection arose on three occasions. Conditions favoring the occurrence of noise reversion include specific pacemaker models, arrhythmia cycle lengths in the range causing noise reversion of the individual pacemaker model, long noise sampling periods, and VVI pacing mode. Noise reversion can be diagnosed by telemetering the pacemaker marker channel during ventricular arrhvthmias as a part of routine pacemaker-ICD interaction evaluation. It can be prevented or minimized by programming short ventricular refractory periods or using pacemakers with shoii retriggerable refractory periods.     

Prognostic implications of arrhythmias during primary percutaneous coronary interventions for ST-elevation myocardial infraction

The authors reviewed current knowledge on occurrence, clinical and prognostic significance, and management of sustained ventricular arrhythmias, atrial fibrillation and bradyarrhythmias in patients with ST-elevation myocardial infarction undergoing primary percutaneous coronary interventions (PCI). Cardiac arrhythmias worsen clinical course and prognosis in patients with ST-elevation myocardial infarction undergoing primary PCI. Sustained ventricular arrhythmias developing during or early after PCI and associated with mechanical restoration of coronary flow and reperfusion do not affect mortality, whereas those related to incomplete revascularization and ongoing ischemia are associated with poor prognosis. New-onset atrial fibrillation increases mortality and stroke rates in patients undergoing primary PCI. Among bradyarrhythmias, high-degree atrioventricular block is associated with short- and long-term mortality. Prompt and complete revascularization is the cornerstone of arrhythmia management. Arrhythmias related to reperfusion do not usually require specific treatment, whereas those because of ongoing ischemia, incomplete revascularization and presence of substrate require adequate management including nonpharmacological and pharmacological therapies.     

Automatic scanning extrastimulus pacemaker to treat ventricular tachycardia

Many investigators have reported the use of various permanent pacemaking modes in the long-term management of patients with recurrent ventricular tachycardia. The three general types of antitachycardic pacemakers are: (1) underdrive; (2) burst; and (3) scanning pacemakers. Such devices have been activated externally or have had automatic activation. Each antitachycardic pacemaking modality has known technical and physiologic limitations. A serious limitation of dual-demand underdrive pacemakers is that they are usually successful only for tachycardias with a rate below 160 bpm because a random stimulus is needed for conversion. Therefore, this modality is seldom useful in patients with symptomatic sustained ventricular tachycardia in which rates are generally greater than 160 bpm and/or hemodynamic compromise occurs rapidly. Although others have reported the successful use of burst pacemakers in the control of ventricular tachycardia, this technique may cause acceleration of ventricular tachycardia and induction of ventricular fibrillation. Programmable automatic scanning pacemakers have been used successfully to treat paroxysmal supraventricular tachycardia and have been used recently in combination with antiarrhythmic agents to control ventricular tachycardia. This report outlines the use of an automatic scanning pacemaker alone for the treatment of symptomatic ventricular tachycardia in a patient who was unable to tolerate conventional antiarrhythmic medications.     

Acute reductions in ventricular myocardial tissue velocities after direct current cardioversion of atrial fibrillation.

BACKGROUND: Cardioversion by direct current (DC) and other methods can cause atrial "stunning." There are case reports of acute pulmonary edema after DC cardioversion, but whether acute ventricular dysfunction is a general consequence of DC cardioversion is unknown. We have investigated whether DC cardioversion acutely affects myocardial velocity assessed by Doppler tissue imaging. METHODS: 40 patients (30 with atrial fibrillation and 10 with atrial flutter) undergoing elective DC cardioversion underwent transthoracic echocardiography with Doppler tissue imaging before and immediately after cardioversion, and after follow-up. Peak systolic velocity was derived for 6 ventricular segments using Doppler tissue imaging. RESULTS: Immediately after DC cardioversion of atrial fibrillation, peak systolic velocity decreased in basal lateral (4.3 +/- 2.0-3.3 +/- 1.7 cm/s, P <.001), mitral annulus-septal (3.8 +/- 1.0-3.5 +/- 0.9, P <.05), mitral annulus-lateral (4.9 +/- 1.6-4.1 +/- 1.7, P <.001), and tricuspid annular (7.8 +/- 2.0-7.0 +/- 1.2, P <.03) segments, even though left ventricular ejection fraction was unchanged. In contrast, for the atrial flutter group there were no significant changes in peak systolic velocity in any segment post-DC cardioversion. Follow up studies were performed after sustained in sinus rhythm in both atrial fibrillation and atrial flutter groups. For both groups, increased peak systolic velocity was found in all 6 segments on follow-up (all P <.05). CONCLUSIONS: DC cardioversion causes subclinical, acute reversible reduction in left ventricular peak systolic velocity in patients with atrial fibrillation. The causes of this reduction in myocardial contractile velocity and the circumstances in which acute dysfunction become clinically significant warrant further investigation.     

Paroxysmal Atrial Fibrillation and High Degree AV Block: Use of Single-Lead VDDR Pacing with Mode Switching

Dual chamber rate responsive pacing incorporating a mode switching option is increasingly listed in patients with chronic paroxysmal atrial fibrillation and high degree AV block. Single-lead VDDR pacemakers have been rarely used for this indication. The purpose of this study was to determine thnir reliability of atrial sensing during atrial fibrillation, the percentage of at rial synchronous ventricular pacing, and the behavior of the sinus rate outside the phases of atrial fibrillation. We studied ten patients with a single-lead VDDR pacemaker implanted for this indication. Follow-up visits were performed at predischarge and after 1, 3, 6, 12. 18, and 24 months. During the mean follow-up period of 18.9 ± 6.9 months, the atrial sensing thresholds in sinus rhythm remained stable. Atrial synchronous ventricular stimulation was achieved in 68,7 ±31.2% (median 82.5%) of the whole follow-up time. All patients showed an adequate atrial rate response during sin us rhfthm. Atrial fibrillation was detected by the pacemakers in 24.0 ± 29.8% of time. In 3 of 10 patients the duration of atrial fibrillation showed a steady increase from visit to visit. The sensed amplitudes of atrial fibrillation ranged from 0.1–1.0 mV. A programmed atrial sensitivity of 0.1 mV was necessary to achieve complete sensing of atrial fibrillation. None of the patients experienced tachycardias with optimized pacemaker programming. Single-lead VDDR pacing incorporating a mode-switching option is useful in patients with high degree AV block and paroxysmal atrial fibrillation, since it provides atrial synchronous ventricular pacing in more than two-thirds of follow-up time. In a subgroup of patients, a progressive increase of the time during atrial fibrillation was demonstrated. A reliable detection of paroxysmal atrial fibrillation requires the programming of the atrial sensitivity to its most sensitive value.     

Induction of Ventricular Tachycardia by Pacemaker Programming

The induction of ventricular tachycardia or ventricular fibrillation by competitive pacing, especially in the setting of acute myocardial ischemia, is well known. A case of ventricular tachycardia induced by a multiprogrammable unipolar cathodal ventricular pacemaker is reported. The arrhythmia was caused by reprogramming, which necessitates a short switch to fixed rate pacing in this model (Spectrax 5985 SX). This potential hazard is not well established in patients with unipolar pacemakers. The use of the magnet as one of the preconditions for reprogramming should be avoided in future pacemakers. (PACE, Vol. 5, July-August 1982)     

Ventricular Tachycardia and Ventricular Fibrillation in Patients with Short P-R Intervals and Narrow QRS Complexes

Eleven patients with short P-R Intervals and narrow QRS complexes had ventricular tachycardia due to organic heart disease: mitral valve prolapse with mitral insufficiency (2 patients); alcoholic (?) cardiomyopathy (2 patients); and coronary artery disease (7 patients). Intracardiac studies showed short A-H intervals during sinus rhythm in all cases. The onset of ventricular fibrillation (which, to our knowledge, has not been observed in patients having short P-R and A-H intervals coexisting with narrow QRS complexes) was documented in 4 cases. Only 1 patient (with quinidine syncope) had been premedicated. In the 3 other patients the episodes of ventricular fibrillation appeared during bouts of atrial fibrillation with rapid ventricular rates which could have been an expression of the “enhanced A-V conduction” that had been manifested in sinus beats by short P-R and A-H intervals. In clinical settings and physiological conditions proven to be hemodynamicaliy unstable (such as transient ischemia or acute myocardial infarction) these rapid ventricular rates could have led to ventricular fibrillation; directly because of the R-on-T phenomenon, and/or indirectly due to decreased coronary perfusion. Ventricular tachycardia and ventricular fibrillation due to organic heart disease probably occur more often than suggested by the few reported cases in the literature. Its significance, however, has to be clarified by further prospective studies     

The role of pacemakers in the management of patients with atrial fibrillation

Pacemakers have an important role in the major strategies for the management of atrial fibrillation, rate control and rhythm control. Of all the current non-pharmacologic therapies for atrial fibrillation, the use of pacemakers impacts the largest number of patients. Pacemakers are used to facilitate medical management of atrial fibrillation with rate control agents and anti-arrhythmic drugs. Atrioventricular junction ablation in conjunction with pacemaker implantation can be an effective therapy for controlling a rapid ventricular rate during atrial fibrillation. The minimization of right ventricular apical pacing in patients with paroxysmal atrial fibrillation is an important objective. Cardiac resynchronization therapy devices are likely to be beneficial in select patients with chronic atrial fibrillation.     

Inappropriate Shocks Delivered by an ICD as a Result of Sensed Potentials from a Transcutaneous Electronic Nerve Stimulation Unit

Although the potential for transcutaneous electronic nerve stimulation (TENS) units to interfere with appropriate function of cardiac pacemakers is well documented, an adverse interaction between a TENS unit and an ICD has never been reported. We describe a patient in whom a TENS unit created an electrical artifact that was interpreted by a transvenous ICD as ventricular fibrillation, leading to the delivery of inappropriate therapy. TENS units should be used with caution in patients with ICDs.     

Electronic Article Surveillance: A Possible Danger for Pacemaker Patients

In order to evaluate if antitheft devices commonly designed as electronic article surveillance (EAS) systems can be dangerous for pacemaker patients, in vitro and in vivo studies were made in close cooperation between a pacemaker center and an EAS designer. Three types of EAS radiation including radiofrequency, magnetic, and pulsed electromagnetic fields were applied to various pacemakers. The in vitro study consisted of exposing to the EAS fields 28 pacemakers connected to unipolar leads. Radiofrequency fields and pulsed electromagnetic fieids evoked minor effects and no prolonged inhibitions. When exposed to magnetic fields, most of the pacemakers switched to "fixed rate" pacing, but inhibitions were observed in 13 pacemakers exposed to 300 Hz, and in 14 pacemakers exposed to a 10-kHz magnetic field when they were moved at cardiac frequencies within the fields. The in vivo study was made on 32 volunteers treated by 26 different pacemakers: 22 single chamber and ten dual chamber. All patients had been monitored in the pacemaker clinic and pacemakers were working well. Radiofrequency and pulsed electromagnetic fields did not affect the pacemaker function. Magnetic interference evoked prolonged inhibition of seven out of the ten dual chamber pacemakers, causing brief asystole in patients being continually paced. None of the dual chamber pacemakers incorporated "safety stimulation intervals" after ventricular bianking. The EAS artifact was sensed after the ventricular blanking causing a cross-talk ECG pattern. No reprogramming was induced by the electromagnetic fields. This experience demonstrates that certain EAS may be dangerous for pacemaker patients. Following this cooperative study a pacemaker safe EAS circuit delivering short bursts of magnetic fields has been designed.     

Electrophysiology studies: precordial thumping patients paced into ventricular tachycardia

The American Heart Association currently recommends the precordial thump as the initial maneuver in the treatment of ventricular tachycardia and monitored ventricular fibrillation. Advocates of the precordial thump maintain that it affords the advantage of immediate availability and might prove lifesaving in cases of ventricular tachycardia. A canine study and a prehospital study have argued that in the cardiac arrest model, thumping ventricular tachycardia causes ventricular fibrillation as often as reversion to a sinus rhythm. We therefore studied the effects of the precordial thump on patients undergoing electrophysiology studies who had been paced into ventricular tachycardia. A total of nine patients received precordial thumps for 11 separate episodes of electrically induced sustained ventricular tachycardia. Our thumps failed on all 11 attempts to convert any of our patients. All 11 were subsequently successfully restored to a supraventricular rhythm with overdrive pacing or countershock. There was no detrimental effect from thumping ventricular tachycardia as has been previously reported. Our results would indicate that countershock is more effective than precordial thumping for converting ventricular tachycardia to a supraventricular rhythm, but previously reported "detrimental effects" of thumping are not confirmed by this study.     

Correlation Between the Ventricular Electrogram Amplitude in Sinus Rhythm and in Ventricular Fibrillation

During testing of implantable defibrillators, ability to sense ventricular fibrillation is assessed by observing electrograms and the emitted ECG interpretation channel during induced ventricular fibrillation. We hypothesized that ventricular electrogram amplitude in sinus rhythm could be used to predict the ventricular electrogram amplitude in ventricular fibrillation and serve as a first approximation of the "safety margin" for sensing ventricular fibrillation. We compared the peak-to-peak epicardial ventricular electrogram during sinus rhythm and ventricular fibrillation in 12 patients undergoing defibrillator implantation. The ventricular electrogram was recorded with an integrated bipolar lead and filtered at 10-50 Hz. Ventricular fibrillation was induced by alternating current and the ventricular electrogram measured from cessation of alternating current to the first countershock. The mean ventricular electrogram amplitude in sinus rhythm was 15.3 +/- 5.4 mV (range 7.1-25.5) and in 37 episodes of ventricular fibrillation was 8.3 +/- 3.6 mV (range 2.1-16.3). There was a significant relationship between the mean ventricular electrogram amplitude in sinus rhythm and in ventricular fibrillation (R = 0.7, P less than 0.001). There was wide variation among individuals in the decrease in the mean ventricular electrogram amplitude during ventricular fibrillation, with the ratio of mean ventricular electrogram in sinus rhythm to mean ventricular electrogram in ventricular fibrillation ranging from 0.29 to 1.05 (mean 0.55 +/- 0.20). This suggests that up to a fourfold decrease may be expected in the mean ventricular electrogram amplitude during ventricular fibrillation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Beyond coronary sinus angiography: the value of coronary arteriography and identification of the pericardiophrenic vein during left ventricular lead placement

OBJECTIVE: The purpose of this study was to define the role coronary arteriography (venous phase) for improving the success of left ventricular (LV) lead implantation and to define the value of identifying the pericardiophrenic vein for optimal LV lead placement in biventricular (bi-v) device implantation. METHODS: Seventy-seven patients underwent bi-v device implantation between July 2002 and October 2003. If the coronary sinus (CS) could not be accessed, then left coronary arteriography was performed during the same procedure. CS access was guided by venous phase images of the coronary arteriogram. The pericardiophrenic vein was identified by selective cannulation or direct visualization. Patients with Cr > 1.5 had gadolinium used as the contrast agent. RESULTS: Seventy-five successful implants were performed (97%). In seven patients (9%) repeated attempts at retrograde cannulation of the CS failed (attempt time 130 +/- 20 minute, mean +/- SD). In these patients, coronary arteriography helped define the location of the CS, which was subsequently successfully cannulated. In six patients the pericardiophrenic vein was identified either during occlusion venography of the CS (postthoracotomy, veno-venous collaterals, n = 2) or during selective cannulation of the pericardiophrenic vein (using a DAIG Csl catheter, n = 4). The vein was directly visualized in three patients who underwent surgical LV lead implantation. LV leads in all these cases were implanted in areas not overlying the preidentified pericardiophrenic vein. During follow-up, none of these patients had evidence of phrenic nerve stimulation. CONCLUSIONS: Intraoperative left coronary arteriography increases the success of CS cannulation. Identification of the pericardiophrenic vein is a useful method to avoid phrenic nerve stimulation.     

Reducing unnecessary right ventricular pacing with the managed ventricular pacing mode in patients with sinus node disease and AV block

BACKGROUND: Frequent and unnecessary right ventricular apical pacing increases the risk of atrial fibrillation or congestive heart failure. We evaluated a new pacing algorithm, managed ventricular pacing (MVP) which automatically changes modes between AAI/R and DDD/R in patients receiving pacemakers for symptomatic bradycardia. METHODS: Patients were randomized to the MVP mode or DDD/R mode for 1 month and then crossed over to the alternate pacing modality for an additional month. On completion of the crossover phase, the pacing mode selected was individualized and patients were followed for an additional 4 months. RESULTS: Of the 129 patients who successfully completed the crossover study, the cumulative percent ventricular pacing was significantly reduced in the MVP mode (median 1.4%) compared to the DDD/R mode (median 89.6%, 94.0% relative reduction; 95% CI 89.3-98.8%, P < 0.001). Patients with sinus node disease (SND, n = 51) when compared to patients with AV block (AVB) (n = 68) experienced a greater reduction in ventricular pacing with the MVP mode compared to the DDD/R mode (median relative reduction 99.1%; 95% CI 97.5-99.9% vs median relative reduction 60.1%; 95% CI 16.7-93.9% P < 0.001). The reduced percent ventricular pacing during MVP was sustained over longer term follow-up. CONCLUSIONS: The majority of patients with a bradycardia indication for cardiac pacing do not require ventricular pacing most of the time. The MVP mode significantly reduces unnecessary right ventricular pacing. This mode benefits even patients with intermittent AVB and is sustained over longer term follow-up.     

Present Day Pacemakers for Pulse Generator Exchange: Is 3.5 V a Sufficient Nominal Setting for the Pulse Amplitude?

Projected pacemaker longevity is calculated according to the nominal setting, which is 3.5 V for pulse amplitude in most present day pacemakers. The aim of this study was to test whether the nominal ventricular output setting of 3.5 V and 0.4 ms provides a 100% safety margin if these pacemakers are connected to implanted ventricular pacing leads. The study included 24 patients undergoing pulse generator exchange. The new pacemaker was either a Thera DR (n = 21) or Them SR (n = 3) device. Ventricular pacing leads were implanted 70 ± 38 months previously. Intraoperative measurements included pacing threshold at 0.5-ms pulse duration, impedance, and R wave amplitude. To achieve a 100% safety margin with 3.5 V, the cut-off pacing threshold is 1.7 V. At discharge it was assessed whether ventricular pulse amplitude remained at > 3.5 V or was programmed to > 3.5 V. At pulse generator exchange, pacing threshold was 1.2 ± 0.5 V, including four patients with pacing thresholds > 1.7 V. Impedance was 587 ± 189 Ω and R wave amplitude was 12.8 ± 4.8 mV. At discharge, ventricular pulse amplitude remained at the nominal setting in 13 patients, including 2 patients with high pacing thresholds at pacemaker exchange, and was programmed to < 3.5 V in 7 patients. Ventricular pulse amplitude was programmed to > 3.5 V in four patients. Two of these patients had high pacing thresholds (> 1.7 V/0.5 ms) at pulse generator exchange; the other two patients were programmed to > 3.5 V, although 3.5 V already provided a 100% safety margin. After pulse generator exchange, 92% of the patients could be paced with a 3.5- V pulse amplitude. Pacemakers were programmed in four patients > 3.5 V, but in only two of them to obtain a sufficient safety margin. High pacing thresholds at pulse generator exchange did not generally predict high pacing thresholds at discharge.     

人本疗法对冠状动脉造影病人焦虑的影响

[目的]探讨人本疗法心理干预对冠状动脉造影病人焦虑的影响。[方法]将80例行冠状动脉造影焦虑的病人随机分为观察组和对照组各40例,对照组行常规健康教育,观察组在此基础上给予人本疗法心理干预,分别于确诊后和冠状动脉介入术前30min采用焦虑自评量表(SAS)进行评分。[结果]观察组冠状动脉造影介入前30min焦虑评分显著低于对照组(P<0.01)。[结论]对冠状动脉造影介入术前病人实施人本疗法心理干预,可减低病人焦虑程度。     

人本疗法对冠状动脉造影病人焦虑的影响

[目的]探讨人本疗法心理干预对冠状动脉造影病人焦虑的影响。[方法]将80例行冠状动脉造影焦虑的病人随机分为观察组和对照组各40倒，对照组行常规健康教育，观察组在此基础上给予人本疗法心理干预，分别于确诊后和冠状动脉介入术前30min采用焦虑自评量表（SAS）进行评分。[结果]观察组冠状动脉造影介入前30min焦虑评分显著低于对照组（P〈0．01）。[结论]对冠状动脉造影介入术前病人实施人本疗法心理干预，可减低病人焦虑程度。