Transesophageal Atrial Pacing Complications in Patients Suspected of Tachy-Brady Syndrome

RACZAK, G., ET AL.: Transesophageal Atrial Pacing Complications in Patients Suspected of Tachy-Brady Syndrome. The clinical effects of transesophageal atrial pacing (TAP) were assessed in 308 patients. Indications for TAP included evaluation for pacemaker implantation in patients suspected of sinus node dysfunction and determination of the suitable type of pacemaker. Most patients underwent program stimulation including rapid as well as burst stimulation. In one patient, following the study, cerebral arterial embolism occurred, most likely secondary to an induced arrhythmia. That was the only single case of permanent consequences following TAP. Additionally, one patient was accidentally stimulated in the ventricle using low voltage electric current that induced ventricular fibrillation. This was promptly reversed with defibrillation. Twenty-six patients in whom an arrhythmia was previously induced, required medical therapy, two of whom required cardioversion, and 24 required drug therapy, subsequent to clinical intolerance of the arrhythmia. No lethal complications occurred.     

Anomalous "VVI" Pacing of a Dual Chamber Pacemaker When Programmed in DDI(R) Mode

We describe the case of a dual chamber rate responsive pacemaker (Relay, model 294-03, Intermedics, Angleton, TX, USA) implanted in a 68-year-old male for sick sinus syndrome, which was not working properly when programmed in the DDIR mode, thus determining occasionally a sort of "VVI" pacing. However, the pacemaker performed well when programmed in the DDDR mode. We discovered that this was not a malfunction of a single device but rather a general behavior of this family of Intermedics dual chamber pacemakers (also not rate responsive), caused by a software problem.     

Ventricular Pacing from the Atrial Channel of a DDD Pacemaker: A Consequence of Pacemaker Twiddling?

ANDERSON, M.H., ET AL.: Ventricular Pacing from the Atrial Channel of a DDD Pacemaker: A Consequence of Pacemaker Twiddling? The breakdown of pacemaker lead insulation under conditions of mechanical stress leading to failure of pacing is well recognized. We present a case where adjacent breakdown of insulation in two unipolar pacing leads resulted in inappropriate ventricular pacing. Replacement of the leads rectified the problem. [PACE, Vol. 13, December, Part I 1990)     

Pacemaker Syndrome Induced by the Mode Switching Algorithm of a DDDR Pacemaker

A patient with marked first-degree AV block and a DDDR pacemaker presented with a history of paroxysmal narrow QRS tachycardia, subsequently identified as sinus tachycardia (with a very long PR interval), causing a clinical problem similar to pacemaker syndrome because of loss of AV synchrony. The latter resulted from an excessively long postventricular atrial refractory period (PVARP) that prevented sensing of sinus P waves. The unfavorable hemodynamics caused reflex sinus tachycardia. The long PVARP was mandated by the mode switching algorithm of this particular device and was automatically set according to the selected tachycardia detection rate. The patient became asymptomatic when the mode switching function was turned off and the PVARP shortened.     

Hemodynamic Findings During Sinus Rhythm, Atrial and AV Sequential Pacing Compared to Ventricular Pacing In a Dog Model

The hemodynamic responses of atrial lAF], atrioventricu-lar sequential (AVP) and ventricuJar pacing (VP) were compared to sinus rhythm (SfiJ in seventeen anesthetized dogs with intact AV conduction. The atrium and/or ventricle were paced at fixed rates above the control sinus rate. An AV interval shorter than normal conduction was selected to capture the ventricle. The changes of pulmonary capillary wedge pressure (PCWP, mmHg). mean aortic pressure (MAP, mmHg), cardiac output (CO, L/min), systemic vascular resistance (SVR, dynes/s/cm⁻⁵), left ventricular stroke work index (SWI) and mean systolic ejection rate (MSER, ml/s) during sinus rhythm, atrial pacing and atrio-ventricular sequential pacing (expressed in percentages of the individual values during ventricular pacing) were:
The importance of atrial systole for cardiac performance was clearly demonstrated in dogs with normally compliant hearts. In both atrial and atrioventricular sequential pacing compared to ventricular pacing there was a reduction of pulmonary capillary wedge pressure (PCWP) (p < 0.01) and systemic vascular resistance (SVR) (p < 0.01) despite an increase in cardiac output (CO). The lesser mean systolic ejection rate (MSER) found during atrioventricular sequential pacing compared to sinus rhythm and atrial pacing may be explained by the abnormal ventricular depolarization in this pacing mode; nevertheless, the mean systolic ejection rate was still greater than that found during ventricular pacing (p < 0.05).     

Pacemaker Electrocardiography of Rate Smoothing During DDD Pacing

A rate smoothing option is available in a new bipolar AV universal (DDD) pacemaker. In three patients, two with intact retrograde conduction and one with retrograde block, rate smoothing values of 3% and 6% were programmed. Irregular pacemaker-mediated tachycardia occurred in one patient and AV synchrony was temporarily lost in the other two patients. In this report, we describe the pacemaker electrocardiography of rate smoothing during DDD pacing.     

Myopotential Interference Inducing Pacemaker Tachycardia in a DVI Programmed Pacemaker

A 67-year-old male, suffering from ventricular tachycardia unresponsive to drug therapy, received a universal AV sequential pacemaker (DDD,M). Tim pacemaker was programmed in the DVI mode, pacing role 100 bpm, AV interval 250 ms. After implantation, the patient experiences two episodes of tachycardia that proved to be pacemaker tachycardia with a rate of 150 bpm. The first period was self-terminating, and the second had to be stopped by reprogramming the pulse generator. Pacemaker tachycardia could easily be provoked by instructing the patient to contract the pectoral muscle adjacent to the pulse generator. To our knowledge, this is the first report to pacemaker tachycardia provoked by myopotentials in a pulse generator programmed in the DVI mode.     

A Case of Ventricular Undersensing in the DDI Mode: Cause and Correction

A case is presented that demonstrates a confusing problem of ventricular undersensing in the DDI pacing mode. Electrocardiographic monitoring of the patient after pacemaker implantation revealed intermittent ventricular channel outputs which appeared to be inappropriate. These occurred a period of time after the intrinsic R wave, equal to the programmed AV interval. This problem was caused by ventricular lead undersensing, which resulted when the patient's intrinsic rate was such that the intrinsic ventricular complex occurred during the ventricular blanking period. The problem was corrected by reprogramming the blanking period.     

Assessment of VVI Diagnostic Pacing Mode in Patients with Cardioinhibitory Carotid Sinus Syndrome

In this study, we used Holter pacemakers in a group of 13 patients affected by severe carotid sinus syndrome in order to evaluate its evolution. All the patients had one to three syncopal episodes and frequent other symptoms such as fainting, dizziness, lightheadedness and pre-syncope interferring with their daily activity so that pacemaker therapy was considered necessary. Patient selection criteria were: presence of the isolated cardioinhibitory type, absence of associated sinus dysfunction and absence of symptomatic WI pacemaker effect. All the patients received a Micropacer 1 device; among special functions, bradycardia events counter was activated and programmed so that each sequence of three consecutives beats at a cycle length 1.5 sec (i.e., 4.5 sec total interval) could he recognized and stored in its memory. The follow-up lasted 13±7 months. Brady events occurred in eight out of 13 patients (62%), during this period. Syncope and major symptoms disappeared in ail the patients; mild dizziness recurred rarely in two patients and were not linked to brady-events recording. In conclusion, disappearance of severe symptoms observed after pacemaker implant in cardioinhibitory carotid sinus syndrome seems to depend from pacing therapy, in most cases, yet from the benign natural course of the disease in some other cases.     

Clinical Experience with a New Multiprogrammable Dual Chamber Pacemaker

We evaluated the clinical performance of a new dual chamber pacemaker, ELA Chorus(tm), in 35 patients. This device incorporates linear rate adaptive AV delay (AVDR), rate smoothing, fallback, impedance telemetry, pacemaker mediated tachycardia (PMT) recognition and reprogramming software, intracardiac electrogram displays, aufothreshold testing, diagnostic data, battery depletion curves, and laptop computer programming. Mean patient age was 68 years; 18 patients had AV block, six had sinus node dysfunction (one with AV block), nine had carotid sinus hypersensitivity (three with AV block), and two had vagally mediated syncope. At hospital discharge, programming was DDD with a mean low rate of 60 (50–70) beats/min, mean high rate of 126 (120–154) beats/mm; AVDR was ON in 21 patients, rate smoothing ON in six patients, fallback ON in six patients, and PMT reprogramming algorithm ON in 27 patients, Pacemaker follow-up involved 500 clinic visits over 14.3 months (1–36). Three patients developed atrial fibrillation, reprogrammed to DDI mode (two patients) or fallback (one patient). Fallback was used 617 times. PMT occurred 427 times in six patients; the PMT algorithm reprogrammed AV delay and postventricular atrial refractory period (PVARPJ automatically, a function unique to the Chorus(tm). Intracardiac electrograms and autothreshold testing improved follow-up efficiency. This new dual chamber pacemaker enhances programming flexibility and improves diagnostic accuracy at follow-up.     

Pacemaker Syndrome in the Young:

The aim of this study was to determine if single chamber rate responsive ventricular pacing (VVIR) predisposes growing children to develop pacemaker syndrome (PS), and if so, what are determining factors and/or clinically useful predictors. PS is a constellation of symptoms that result from the lack of consistent AV sequential filling due to atrial contraction against closed AV valves. PS has not been commonly reported in the young. Data from all patients with pacemakers with congenital complete atrioventricular block (CAVB) with normal anatomy, and those with congenital heart disease (CHD), and surgically acquired CAVB were reviewed. Inclusion criteria were normal ventricular function by cardiac ultrasound and 100% VVIR pacing. Of 89 patients with VVIR pacemaker implants, 33 met these criteria. Of these, 19 developed PS. For statistical analysis, chi-square and independent samples t-test was used with significance defined at P < or = 0.05. No consistent association was found between cardiac anatomy, type of CAVB, or age at implant with development of PS. However, PS did correlate with duration of pacing (P = 0.02). The exercise stress test showed significant differences between 100% VVIR-paced patients with and without PS, in terms of work rate (P = 0.002) and measured oxygen consumption (P = 0.01). This study shows that PS appears to be a time related event in younger children with normal ventricular function who are 100% ventricular paced. Thus, this supports VVIR pacing as an adequate and cost-effective initial therapy for symptomatic bradycardia due to CAVB.     

Pacemaker Syndrome with AAI Rate Variable Pacing: Importance of Atrioventricular Conduction Properties, Medication, and Pacemaker Programmability

A patient who received an AAI Activitrax rate variable pacemaker for treatment of symptomatic sinus bradycardia is described. disopyramide prolonged the anterograde effective refractory period of the fast conducting atrioventricular (AV) nodal pathway to such an extent, that conduction switched to the slow AV nodal pathway at low atrial pacing rates. This gave rise to symptoms of the pacemaker syndrome during moderate exercise because the paced atrial event was conducted with a long, spike to Q interval with occurrence of the paced atrial event just after the preceding QRS complex. A change of medication solved this problem. Programming a bipolar electrode configuration avoided sensing of far-field QRS signals with the associated problems of resetting the basic pacing interval as well as the upper rate interval. AAI rate variable pacing requires careful evaluation of AV conduction properties, AV conduction intervals as well as the influence of medication to be given. The use of multiprogrammable pacemakers with marker channel capability will significantly facilitate the understanding and resolution of anomalous behavior.     

Erosion of an Epicardial Pacemaker Secondary to Postpericardiotomy Syndrome

This report describes an unusual case of postpericardiotomy syndrome and pulse generator erosion following subxiphoid insertion of an epicardial pacemaker.     

Irregular Ventricular Stimulation in the DDI Mode of a Dual Chamber Pacemaker With Atrial-Based Lower Rate Timing

This report describes two patients with atrial fibrillation in whom an implanted CHORUS DDD pacemaker programmed to the DDI mode produced an irregular ventricular stimulation rate. The lower rate timing of these devices is atrial-based only when an atrial event opens an AV interval shorter than the programmed AV delay. In the DDI mode, if Api represents the time when an atrial paced event (Ap) would have occurred if it had not been inhibited by a previous atrial sensed event (As), then Api-Vp constitutes the implied AV interval where Vp is a paced ventricular event. Although the As-Vp interval (As-Api+Api-Vp) generates an atrial refractory period during its entire duration, the pacemaker can sense an atrial event (A r ) during the implied AV interval. A r cannot start another AV delay, but it can initiate the atrial-based lower rate interval. This timing mechanism can cause irregular prolongation of Vp-Vp intervals to a value longer than the programmed lower interval with a maximal extension equal to the programmed AV delay. Such behavior of the CHORUS pacemaker should not be interpreted as malfunction.     

Pacemaker Induced Mitral Regurgitation: An Alternative Form of Pacemaker Syndrome

A patient in atrial fibrillation was referred for mitral valve replacement due to severe mitral regurgitation. A cardiac pacemaker had previously been implanted. Cardiac catheterization demonstrated large V waves in the wedge pressure tracing during ventricular pacing, which were not present during native conduction. A left ventriculogram demonstrated severe mitral regurgitation during ventricular pacing, but not during native conduction. This patient, in atrial fibrillation, had severe mitral regurgitation induced by ventricular pacing and not by native conduction. Pacemaker syndrome may be caused by mitral regurgitation that is probably not secondary to AV dissociation, but rather the result of dyssyn-chronous ventricular contraction.     

Noninvasive Beat-to-Beat Arterial Blood Pressure Measurement During VVI and DDD Pacing: Relationship to Symptomatic Benefit from DDD Pacing

To noninvasively assess the hemodynamic effects of VVI and DDD pacing modes we measured beat-to-beat arterial blood pressure during VVI and DDD pacing in 30 patients with complete heart block (CHB), using fingertip photoplethysmography. Of these patients, 15 undertook a double-blind cross-over comparison of the symptomatic effects of VVI versus DDD pacing to determine the relationship between blood pressure changes and the occurrence of symptoms suggestive of the pacemaker syndrome during ventricular pacing. Mean (SD) systolic blood pressure was 11.7 (15.4) mmHg lower during VVI pacing compared to DDD pacing (P < 0.0005). The mean (SD) beat-to-beat variability of systolic blood pressure was 5.20 (2.87%) in VVI mode versus 2.12 (1.07%) in DDD mode (P < 0.0000005). In comparison with DDD pacing, the excess of symptoms experienced by patients during VVI pacing did not correlate with the change in mean systolic blood pressure, but was significantly correlated with the increase in beat-to-beat systolic blood pressure variation during VVI pacing (r = 0.58, P = 0.024). We conclude that noninvasive measurement of fingertip arterial beat-to-beat blood pressure is a rapid and simple method of assessing the hemodynamic effect of VVI pacing. Beat-to-beat blood pressure variability was related to symptomatic intolerance of VVI pacing and may have potential utility as an aid to diagnosis or as a predictor of pacemaker syndrome.     

Variability of Left Atrial Bloodflow Predicts Intolerance of Ventricular Demand Pacing and May Cause Pacemaker Syndrome

Variability of left and right atrial and left ventncular bloodflow was studied using transthoracic and transesophageal Doppler echocardiography and related to pacemaker mode preference during everyday activity. Bloodflow variability was less at all sites during dual chamber pacing compared to single chamber pacing. However, in patients suffering from pacemaker syndrome and whom prefer DDDR pacing, significantly increased variability of left atrial antegrade (but not retrograde) bloodflow during VVIR pacing compared to DDDR pacing was noted, which was not evident in patients tolerating VVIR mode pacing. This effect was not detected at any other site and suggests that adverse left atrial hemodynamics may result in intolerence to VVI/R mode pacing and might cause pacemaker syndrome.     

Pacemaker Syndrome in a Patient with DDD Pacemaker for Long QT Syndrome

A patient with long QT syndrome was treated with beta blockers and had a permanent DDD pacemaker implanted. The lower rate was set to 85 beats/min because this provided the best shortening of QT interval at the lowest paced heart rate. The atrioventricular (AV) delay was programmed to 250 msec to allow native AV conduction. Patient returned complaining of symptoms suggestive of pacemaker syndrome. ECG during one of these episodes showed AV sequential pacing. Doppler echocardiography of hepatic vein flow suggested atrial contraction against a closed tricuspid valve. Endocardial electrogram telemetry demonstrated ventriculoatrial (VA) conduction with the retrograde atrial electrogram falling within the atrial refractory period and thus was not sensed. The following atrial stimulus did not capture because of the atrial refractoriness. Ventricular pacing proceeded after the programmed AV delay. Reprogramming the AV delay to 200 msec restored AV synchrony by allowing the atrial stimulus to capture by placing it outside of the refractory period of the atrium. No further symptoms reported during six months of follow-up.