Pacemaker Stimulus Research Articles

B-PO03-193 THE MISSING LINK- TIME TO MAXIMAL RATE OF LEFT VENTRICULAR PRESSURE RISE REFLECTS RESYNCHRONIZATION WITH BIVENTRICULAR PACING IN PATIENTS WITH HEART FAILURE AND LEFT BUNDLE BRANCH BLOCK

No measures exist that specifically quantifies myocardial resynchronization. We compared the acute differences between BIVP and LVP with regards to the preload dependent maximum rate of the LV pressure rise (dP/dtmax), and time to peak dP/dt (Td) to determine which better reflect dyssynchrony and resynchronization. Twenty-nine patients in heart failure with LBBB underwent CRT implantation with continuous LV pressure registration. The LV lead was first placed in either apical or anterior position followed by a permanent placement in a lateral position. Sequential LVP and BIVP pacing were performed for one minute, at a rate 10% above intrinsic heart rate, before dP/dtmax measurements were recorded. For LVP, BIVP and RVP a patient specific AV delay was used to avoid fusion with intrinsic conduction. Td was defined as the time from pacemaker stimuli to peak dP/dt. Mixed linear models were used for statistics, numbers are estimated marginal means±SEM and are only reported when with significance set at p<0.05. We found no differences in dP/dtmax between BIVP (899±37mmHg/s) and LVP (910±37mmHg/s), while RVP (799±37mmHg/s) was lower. Myocardial synergy was demonstrated as Td was lower with BIVP (165±4ms) than LVP (178±4ms) and RVP (184±4ms). We found no differences in dP/dtmax between lateral (890±35mmHg/s) and anterior (874±38mmHg/s) while apical (824±38mmHg/s) was lower. Td was lower in lateral (171±4ms) than in anterior (179±4ms) and apical (182±4ms) positions. BIVP in lateral position (158±4ms) was lower than any other pacingmode*position, with BIVP*anterior at 173±4ms) and LVP*lateral at 170±2ms. No difference was seen in dP/dtmax between (BIVP+LVP)*(lateral+anterior) that was higher than all other pacingmode*positions. Resynchronization with biventricular pacing translates into a shorter Td and hence links electrical and mechanical events. Td could be the missing link between electrical and mechanical dyssynchrony and may serve as a biomarker for cardiac resynchronization therapy to demonstrate biventricular synergy.

Impact of homeometric autoregulation using a stepwise change in heart rate on dP/dtmax and time to peak dP/dt with resynchronization therapy

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Norwegian South East heath Authorities Background We investigated the homeometric autoregulation utilizing a stepwise change in heart rate on dP/dtmax and time to peak dP/dt (Td) with biventricular pacing (BIVP) and the LV lead positioned in the apical, anterior and lateral positions. Pacing at low HR (LHR) and high heart rates (HHR) changes contractility through homeometric autoregulation (Bowditch effect) without changing the resynchronization itself. Purpose To determine the effect of a change in contractility through homeometric autoregulation on two different effect measures of resynchronization therapy. Methods Twenty-nine patients in heart failure with LBBB underwent CRT implantation with continuous LV pressure registration. The LV lead was first placed in either apical or anterior position followed by a permanent placement in a lateral position. Sequential BIVP pacing was performed for one minute, at a rate 10% above intrinsic heart rate (LHR = 75 ± 9bpm), before dP/dtmax measurements were recorded, and the sequence was repeated with pacing rate increased by 30% (HHR = 98 ± 11bpm). Td was defined as the time from pacemaker stimuli to peak dP/dt. Mixed linear models were used for statistics, numbers are estimated marginal means ± SEM. Significance was set at p &amp;lt; 0.05. Results DP/dtmax was higher with HHR in lateral position (1036 ± 41mmHg/s) than with LHR (933mmHg/s). The same was observed for all other lead positions. However, there was no difference between lateral position with LHR and apical position with HHR (930 ± 44mmHg/s). There were no differences in Td between LHR and HHR, but Td was shorter with BIVP in lateral position at pacing LHR (158 ± 4ms) and HHR (155 ± 4ms) than in all other positions. Overall dP/dtmax increased by 10% from LHR to HHR (888 ± 41mmHg/s vs. 980 ± 41 mmHg/s), while overall Td decreased by 2.4% from 168 ± 4ms to 164 ± 4ms. We found a linear relationship between Td and dP/dtmax (R = 0.7) with β=-0.07 that would indicate a 6ms reduction in Td going from LHR to HHR. The overall change in Td from LHR to HHR could therefore be attributed to the change in dP/dtmax. Conclusion Homeometric regulation does not influence Td, but Td is sensitive to changes in resynchronization and pacing lead position. Td is shorter with BIVP in lateral position at both high and low HR as would be expected from a biomarker of resynchronization. HR influences dP/dtmax so distinction between optimal and non-optimal positions using dP/dtmax may be difficult without knowledge of homeometric state.

The missing link- time to maximal rate of left ventricular pressure rise reflects resynchronization with biventricular pacing in patients with heart failure and left bundle branch block

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Norwegian South East Health Authorities Introduction Resynchronization therapy effectively restores myocardial function. No measures exist that specifically quantifies resynchronization. A parameter that quantifies resynchronization should be able to detect effective resynchronization and should not respond to changes in contractility caused by heterometric regulation. Left ventricular pacing (LVP) is associated with dyssynchronous contraction patterns, while biventricular pacing (BIVP) promotes resynchronization dependent on the pacing position of the LV electrode. Purpose We compared the acute differences between BIVP and LVP with regards to the preload dependent maximum rate of the LV pressure rise (dP/dtmax), and time to peak dP/dt (Td) to determine which better reflect dyssynchrony and resynchronization. Methods Twenty nine patients in heart failure with LBBB underwent CRT implantation with continuous LV pressure registration. The LV lead was first placed in either apical or anterior position followed by a permanent placement in a lateral position. Sequential LVP and BIVP pacing were performed for one minute, at a rate 10% above intrinsic heart rate, before dP/dtmax measurements were recorded. For LVP, BIVP and RVP a patient specific AV delay was used to avoid fusion with intrinsic conduction. Td was defined as the time from pacemaker stimuli to peak dP/dt. Mixed linear models were used for statistics, numbers are estimated marginal means ± SEM and are only reported when with significance set at p &amp;lt; 0.05. Results We found no differences in dP/dtmax between BIVP (899 ± 37mmHg/s) and LVP (910 ± 37mmHg/s), while RVP (799 ± 37mmHg/s) was lower. Td was lower with BIVP (165 ± 4ms) than LVP (178 ± 4ms) and RVP (184 ± 4ms). We found no differences in dP/dtmax between lateral (890 ± 35mmHg/s) and anterior (874 ± 38mmHg/s) while apical (824 ± 38mmHg/s) was lower. Td was lower in lateral (171 ± 4ms) than in anterior (179 ± 4ms) and apical (182 ± 4ms) positions. BIVP in lateral position (158 ± 4ms) was lower than any other pacingmode*position, with BIVP*anterior at 173 ± 4ms) and LVP*lateral at 170 ± 2ms. No difference was seen in dP/dtmax between (BIVP + LVP)*(lateral + anterior) that was higher than all other pacingmode*positions. Conclusion Td shortens with BIVP and lateral position, and even more so with BIVP in lateral position and thus reflects resynchronization compared to all other combinations tested. DP/dtmax did not reflect resynchronization as BIVP/LVP and lateral/anterior performs equally good. There are no differences between dP/dtmax with any combination of pacing mode (BIVP + LVP) with position (anterior + lateral). This suggests that Td reflects resynchronization while dP/dtmax does not. Resynchronization with biventricular pacing in lateral position translates into a shorter Td and hence links electrical and mechanical events. Td could be the missing link between electrical and mechanical dyssynchrony and may serve as a biomarker for cardiac resynchronization therapy.

Navigating the 7 cs of certified practice.

Navigating the 7 cs of certified practice.

Understanding the Timing Cycles of a Cardiac Resynchronization Device Designed with Left Ventricular Sensing

Some devices used for cardiac resynchronization therapy (CRT) can sense from the left ventricular (LV) lead as in Biotronik CRT devices (Biotronik GmbH, Berlin, Germany), whose special LV timing cycles form the basis of this report. LV sensing (LVs) was designed to prevent competitive pacing outside the LV myocardial absolute refractory period. LVs works by inhibiting the release of an LV pacemaker stimulus (LVp) in the vulnerable period of the LV during a programmable period. LVs with stored LV electrograms may also provide recordings of diagnostic value in tachyarrhythmias. LVs has added a new dimension to the evaluation of the function of CRT devices, because it is manifested by unfamiliar timing cycles. In this respect, Biotronik devices can initiate an LV upper rate interval (URI) upon sensing a right-sided event when LVs is turned off. An inhibited LVp can also initiate an LVURI. The LVURI should generally be programmed to a relatively short duration and shorter than the right ventricular URI to prevent a special form of desynchronization arrhythmia sustained by LVs. This arrhythmia is characterized by recurring delayed LVs events in sequences associated with RV pacing followed by LVs events with loss of LVp.

The effect of hyperkalaemia on cardiac rhythm devices

In patients with pacemakers, hyperkalaemia causes three important abnormalities that usually become manifest when the K level exceeds 7 mEq/L: (i) widening of the paced QRS complex from delayed intraventricular conduction velocity, (ii) Increased atrial and ventricular pacing thresholds that may cause failure to capture. In this respect, the atria are more susceptible to loss of capture than the ventricles, and (iii) Increased latency (usually with ventricular pacing) manifested by a greater delay of the interval from the pacemaker stimulus to the onset of depolarization. First-degree ventricular pacemaker exit block may progress to second-degree Wenckebach (type I) exit block characterized by gradual prolongation of the interval from the pacemaker stimulus to the onset of the paced QRS complex ultimately resulting in an ineffectual stimulus. The disturbance may then progress to 2 : 1, 3 : 1 pacemaker exit block, etc., and eventually to complete exit block with total lack of capture. Ventricular undersensing is uncommonly observed because of frequent antibradycardia pacing. During managed ventricular pacing, hyperkalaemia-induced marked first-degree atrioventricular block may induce a pacemaker syndrome. With implantable cardioverter-defibrillators (ICDs) oversensing of the paced or spontaneous T-wave may occur. The latter may cause inappropriate shocks. A raised impedance from the right ventricular coil to the superior vena cava coil may become an important sign of hyperkalaemia in the asymptomatic or the minimally symptomatic ICD patient.

Recognition of ventricular fibrillation concomitant with pacing artifacts

Introduction. In pre-hospital settings recognition of underlying rhythm in patients with ventricular stimulation can be difficult especially when a 3-lead electrocardiogram (ECG) is analyzed. This fact is particularly important in patients with life-threa-tening cardiac dysrhythmias. The pacing spikes in the ECG of a patient with cardiac arrest due to ventricular fibrillation may be misdiagnosed as QRS complexes.&nbsp;Aim of the study. The aim of this study was to assess emergency medical care students’ accuracy in recognizing ventricular fibrillation when pacing spikes are present.Material and methods. The study group consisted of 39 emergency medical care students, 16 males and 23 females, aged 21 - 23. Subjects were at the midpoint of their 3-year university healthcare professional education. Subjects were asked to interpret electrocardiograms presenting ventricular fibrillation with concomitant pacing artifacts, ventricular fibrillation and atrial fibrillation with ventricular pacing, respectively. Students were trained in recognition of ECG tracings presenting ven-tricular stimulation, atrial fibrillation and ventricular fibrillation. They were instructed that the duration of the QRS complex in adults is at least 0.06s and that pacemaker stimuli are shorter. Prior to the examination, an electrocardiogram similar to the abovementioned, with ventricular fibrillation and pacemaker stimuli, was not presented.Results. Only one student (out of 39) recognized ventricular fibrillation with pacemaker stimuli present; the majority of stu-dents (92%) incorrectly interpreted the rhythm as atrial fibrillation or atrial flutter. The ECG with isolated ventricular fibrillation was correctly interpreted by all but two students who recognized polymorphic ventricular tachycardia and 62% of students correctly recognized ventricular pacing whereas none of them recognized atrial fibrillation.Conclusions. 1. The skills of recognizing ventricular fibrillation in patients with concomitant ventricular pacing are poor among emergency medical care students.2. The ECG tracing showing concomitant ventricular fibrillation and pacing stimuli should be included in teaching programs for emergency medical care students. An ongoing quality improvement program may reduce the rate of mistakes in ECG analysis in rare cases with life-threatening emergencies.

Establishing a New Electrical Conduction Pathway by Anastomosis of the Right Auricle and Right Ventricle Assisted by Mesenchymal Stem Cells in a Canine Model

Background Electronic pacemakers are the primary treatment of complete atrioventricular (AV) block, but their use is associated with many complications. The aim of the present study was to create an alternative treatment for these patients. Materials and Methods Mesenchymal stem cells (MSCs) isolated from the bone marrow of a 3-month-old dog were cultured in vitro. The MSCs were labeled with 4′, 6-diamidino-2-phenylindole (DAPI) before transplantation. We anastomosed the right auricle and right ventricle in 24 dogs, and transplanted labelled MSCs into the anastomotic area of 8 dog hearts. Using immunostaining we assessed survival and differentiation of the implanted cells at 8 weeks posttransplantation. Electrocardiography confirmed the secondary electrical conduction pathway. Results The ventricular current was captured by the electronic pacemaker in 21 dogs. Compared with the control group (surgery alone), pacemaker stimulus current was significantly less in the MSC group (surgery + MSCs). Conclusions Anastomoşis of the right auricle and right ventricle assisted by MSCs may be a new treatment for patients with complete AV block in the future.

Usefulness of the 12-lead electrocardiogram in the follow-up of patients with cardiac resynchronization devices. Part II

The interval from the pacemaker stimulus to the onset of the earliest paced QRS complex (latency) may be prolonged during left ventricular (LV) pacing. Marked latency is more common with LV than right ventricular (RV) pacing because of indirect stimulation through a coronary vein and higher incidence of LV pathology including scars. During simultaneous biventricular (BiV) pacing a prolonged latency interval may give rise to an ECG dominated by the pattern of RV pacing with a left bundle branch block configuration and commonly a QS complex in lead V1. With marked latency programming the V-V interval (LV before RV) often restore the dominant R wave in lead V1 representing the visible contribution of the LV to overall myocardial depolarization. When faced with a negative QRS complex in lead V1 during simultaneous BiV pacing especially in setting of a relatively short PR interval, the most likely diagnosis is ventricular fusion with the intrinsic rhythm. Fusion may cause misinterpretation of the ECG because narrowing of the paced QRS complex simulates appropriate BiV capture. The diagnosis of fusion depends on temporary reprogramming a very short atrio-ventricular delay or an asynchronous BiV pacing mode. Sequential programming of various interventricular (V-V) delays may bring out a diagnostic dominant QRS complex in lead V1 that was previously negative with simultaneous LV and RV apical pacing even in the absence of an obvious latency problem. The emergence of a dominant R wave by V-V programming strongly indicates that the LV lead captures the LV from the posterior or the posterolateral coronary vein and therefore rules out pacing from the middle or anterior coronary vein. In some cardiac resynchronization systems LV pacing is achieved with the tip electrode of the LV lead as the cathode and the proximal electrode of the bipolar RV as the anode. This arrangement creates a common anode for both RV and LV pacing. RV anodal capture can occur at a high LV output during BiV pacing when it may cause slight ECG changes. During LV only pacing (RV channel turned off) RV anodal pacing may also occur in a more obvious form so that the ECG looks precisely like that during BiV pacing. RV anodal stimulation may complicate threshold testing and ECG interpretation and should not be misinterpreted as pacemaker malfunction. Programming the V-V interval (LV before RV) in the setting of RV anodal stimulation cancels the V-V timing to zero.

Modern pacemaker stimuli as viewed from a 12-lead electrocardiogram

Modern pacemaker stimuli as viewed from a 12-lead electrocardiogram

Acute hyperkalemia and failure of pacemaker stimulus

Acute hyperkalemia may induce well-known serious cardiac arrhythmia. However, ventricular aberration including concealed conduction may also occur. We report the case of a 35-year-old woman who had a previous history of late-operated ventricular septal defect communication and DDD pacemaker was admitted for dyspnea. During hospitalization, an acute hyperkalemia induced sinoatrial block despite correct pacemaker programming. Sodium bicarbonate allowed to restore sinus rhythm. Our report highlights that acute hyperkalemia may increase thresholds of pacemaker stimulus and physicians should be aware that complete block of conduction may occur despite correct pacemaker programming.

Pseudo Pacemaker Stimuli

Current electrocardiographic technology is limited in its ability to detect pacemaker stimuli secondary to the use of 150 Hz low-pass bandwidth filters designed to block high-frequency interference. Software solutions to improve the sensitivity of pacemaker stimulus detection are associated with imperfect specificity. The following case reports include three patients who do not have a pacing device, but were identified by a computer-based preliminary interpretation of a routine 12-lead surface electrocardiogram (ECG) as having a paced rhythm.

Cardiac Resynchronization Therapy and phase resetting of the sinoatrial node: A conjecture

Congestive heart failure is a severe chronic disease often associated with disorders that alter the mechanisms of excitation-contraction coupling that may result in an asynchronous left ventricular motion which may further impair the ability of the failing heart to eject blood. In recent years a therapeutic approach to resynchronize the ventricles (cardiac resynchronization therapy, CRT) has been performed through the use of a pacemaker device able to provide atrial-based biventricular stimulation. Atrial lead senses the spontaneous occurrence of cells depolarization and sends the information to the generator which, in turn, after a settled delay [atrioventricular (AV) delay], sends electrical impulses to both ventricles to stimulate their synchronous contraction. Recent studies performed on heart rate behavior of chronically implanted patients at different epochs after implantation have shown that CRT can lead to sustained overall improvement of heart function with a reduction in morbidity and mortality. At this moment, however, there are no studies about CRT effects on spontaneous heart activity of chronically implanted patients. We performed an experimental study in which the electrocardiographic signal of five subjects under chronic CRT was recorded during the activity of the pacemaker programmed at different AV delays and under spontaneous cardiac activity after pacemaker deactivation. The different behavior of heart rate variability during pacemaker activity and after pacemaker deactivation suggested the hypothesis of a phase resetting mechanism induced by the pacemaker stimulus on the sinoatrial (SA) node, a phenomenon already known in literature for aggregate of cardiac cells, but still unexplored in vivo. The constraints imposed by the nature of our study (in vivo tests) made it impossible to plan an experiment to prove our hypothesis directly. We therefore considered the best attainable result would be to prove the accordance of our data to the conjecture through the use of models and physical considerations. We first used the data of literature on far-field effects of cardiac defibrillators to prove that the pacemaker impulses delivered to the two ventricles were able to induce modifications in membrane voltage at the level of the SA node. To simulate a phase resetting mechanism of the SA node, we used a Van der Pol modified model to allow the possibility of changing the refractory period and the firing frequency of the cells separately. With appropriate parameters of the model we reproduced phase response curves that can account for our experimental data. Furthermore, the simulated curves closely resemble the functional form proposed in literature for perturbed aggregate of cardiac cells. Despite the small sample of subjects investigated and the limited number of ECG recordings at different AV delays, we think we have proved the plausibility of the proposed conjecture.

Impact of automatic threshold capture on pulse generator longevity

The automatic, threshold tracking, pacing algorithm developed by St. Jude Medical, verifies ventricular capture beat by beat by recognizing the evoked response following each pacemaker stimulus. This function was assumed to be not only energy saving but safe. This study estimated the extension in longevity obtained by AutoCapture (AC) compared with pacemakers programmed to manually optimized, nominal output. Thirty-four patients who received the St. Jude Affinity series pacemaker were included in the study. The following measurements were taken: stimulation and sensing threshold, impedance of leads, evoked response and polarization signals by 3501 programmer during followup, battery current and battery impedance under different conditions. For longevity comparison, ventricular output was programmed under three different conditions: (1) AC on; (2) AC off with nominal output, and (3) AC off with pacing output set at twice the pacing threshold with a minimum of 2.0 V. Patients were divided into two groups: chronic threshold is higher or lower than 1 V. The efficacy of AC was evaluated. Current drain in the AC on group, AC off with optimized programming or nominal output was (14.33 +/- 2.84) mA, (16.74 +/- 2.75) mA and (18.4 +/- 2.44) mA, respectively (AC on or AC off with optimized programming vs. nominal output, P < 0.01). Estimated longevity was significantly extended by AC on when compared with nominal setting [(103 +/- 27) months, (80 +/- 24) months, P < 0.01). Furthermore, compared with the optimized programming, AC extends the longevity when the pacing threshold is higher than 1 V. AC could significantly prolong pacemaker longevity; especially in the patient with high pacing threshold.

Clinical experience with an automatic threshold tracking algorithm study.

The automatic threshold tracking pacing system algorithm developed by St. Jude Medical, verifies ventricular capture beat by beat by recognizing the evoked response (ER) following each pacemaker stimulus. The present automatic threshold tracking function requires a bipolar ventricular lead with low polarization. The aim of this study was to evaluate a new algorithm developed to use with unipolar leads with different levels of polarization. An external pacemaker with the ability to sense intrinsic R waves and measure ER signals, as well as deliver stimulus, was used. An algorithm for detecting the true ER in a unipolar sensing configuration (tip-case) was developed. Based on the assumption that the true evoked R wave amplitude is independent of the stimulation amplitude, the algorithm calculates and subtracts the polarization present at any pacing stimulus from the measured ER. The resulting signal is analyzed to verify capture. This study comprises 35 patients of which 26 were new implants and 9 had chronic leads. The automatic threshold-tracking algorithm was calibrated for each patient and pacing was performed at different pulse amplitudes and pulse duration. Capture was verified for each paced beat. The recordings were stored for later comparison with the tape-recorded intracardiac heart signals. The new algorithm correctly verified capture or loss of capture for every single analyzed beat at the different pacing outputs in every individual patient. The results from this initial study suggests that the new ER detection principle will allow automatic threshold tracking to be used not only with low polarization bipolar leads but with most leads.

A stepwise testing protocol for modern implantable cardioverter-defibrillator systems to prevent pacemaker-implantable cardioverter- defibrillator interactions

Current use of newer implantable cardioverter-defibrillators (ICDs) has changed the spectrum of pacemaker–ICD interactions and provided new tools for testing and understanding those interactions. Testing for pacemaker–ICD interactions was performed in 31 procedures involving 22 patients. The protocol included: (1) evaluation of pacemaker stimulus artifact amplitude and its ratio to that of the evoked ventricular electrogram, (2) testing for inhibition of ventricular fibrillation (VF) detection by the ICD during asynchronous pacing at maximum output, (3) evaluation by pacemaker event marker recordings of pacemaker sensing behavior while programmed to nonasynchronous mode during ventricular tachycardia (VT) or VF, and (4) evaluation of postshock interactions. Inhibition of detection of VT/VF was found in 6 of 22 patients (27.2%). Large stimulus artifact amplitude (>2 mV) or stimulus artifact:evoked QRS ratio >1/3 had a positive predictive accuracy of 18% and 14.4%, respectively, and a negative predictive accuracy of 100% and 92.3%, respectively, for clinically significant interaction. Asynchronous pacing occurred in 16 of 31 procedures (51.6%), and was due to underdetection by the pacemaker in 4 of 16 (25%) and noise reversion in 12 of 16 (75%). Postshock phenomena occurred in 6 cases, 3 of which were clinically significant. Overall, 11 of 22 patients (50%) had clinically significant interactions discovered by this protocol, which led to system revisions in 6 and to pacemaker output reprogramming in 5. Thus, pacemaker–ICD interactions are frequently detected using a thorough and systematic protocol. Most cases can be managed by system revision or pacemaker reprogramming.

Usefulness of Holter Recordings in the Evaluation of Pacemaker Function: Standard Techniques and Intracardiac Recordings

A dedicated pacemaker Holter system facilitates recognition of the pacemaker stimulus by amplifying and displaying it in an ECG channel without any other data. Such a Holter pacemaker channel may occasionally generate electrostatic charges that produce deflections resembling pacemaker stimuli (pseudopacemaker spikes) arising from a loose ECG electrode, crushed tape, or a dirty recording head. False‐positive spikes or spurious marker deflections in Holter pacemaker channels and occasional failure to detect tiny bipolar stimuli can present challenging problems in the interpretation of pacemaker function. In multiple‐channel recorders, skewing of the recording heads may lead to timing errors and puzzling recordings when one of the ECG or pacemaker channels lags behind others producing asynchrony or malalignment in simultaneously recorded tracings.The interpretation of Holter recordings from contemporary complex pacemakers requires knowledge of pacemaker timing cycles and their interrelationships, a large variety of programmable parameters or functions, behavior of the nonatrial sensor or sensors in rate‐adaptive systems, device‐specific responses to protect the system from a variety of undesirable situations, and an appreciation of pacemaker eccentricities.There are a few prospective studies on the value of routine Holter recordings in pacemaker patients. The real value of Holter recordings lies with symptomatic patients when symptoms occur during the recording period. Correlation between symptoms and occasional abnormality of pacemaker function during Holter monitoring remains poorly characterized. The cause of the symptoms is frequently unrelated to the pacemaker system and may not be related to coexisting arrhythmias. In asymptomatic patients, Holter recordings are particularly useful to uncover a lead problem after an unrevealing thorough investigation in the pacemaker clinic.Special instrumentation was recently developed to register telemetry data from implanted pacemakers simultaneously with ambulatory electrocardiography. In this way, diagnostic marker signals and/or intracardiac electrograms transmitted from the pacemaker can be recorded continuously for 24 hours by a Holter recorder. Advanced technology involving the memory capability of pacemakers will transform the pacemaker itself into a 24‐hour Holter recorder, probably in 4 to 5 years. At present, the memory for storage of intracardiac electrograms is limited from a few seconds to less than a minute according to the manufacturer, but even such mini‐Holter recordings can be diagnostically important.

Intramyocardial electrograms for non-invasive rejection monitoring: initial experience with an infection-specific parameter

Non-invasive rejection monitoring based on the analysis of paced intramyocardial electrograms enables repeated or even daily graft surveillance. The rejection-sensitive parameter is calculated from the maximum slope of the descending part of the t wave. Biopsy-proven rejection grade 2 or higher (ISHLT classification) can safely be detected. Nevertheless, infection influences the rejection-sensitive parameter in the same manner as does rejection (99% negative predictive value for rejection grade 2 or higher, 17% positive predictive value). We defined the infection-specific parameter as the time on the O line between the pacemaker stimulus and the crossover with the maximum slope of the descending part of the t wave. Patients were classified prospectively according to infection status: patients without infection and those with clinically apparent infection. Patients with clinically apparent infections had a significantly longer infection-specific parameter. A simultaneous decrease of the rejection-sensitive parameter and an increase in the infection-specific parameter was observed during clinical infection: a decrease in the rejection-sensitive parameter and no changes in the infection-specific parameter were observed during rejection. This preliminary analysis revealed that discrimination of rejection and infection might be possible by the analysis of intramyocardial electrograms.

Intramyocardial electrograms for non-invasive rejection monitoring: initial experience with an infection-specific parameter

Abstract Non-invasive rejection monitoring based on the analysis of paced intramyocardial electrograms enables repeated or even daily graft surveillance. The rejection-sensitive parameter is calculated from the maximum slope of the descending part of the t wave. Biopsy-proven rejection grade 2 or higher (ISHLT classification) can safely be detected. Nevertheless, infection influences the rejection-sensitive parameter in the same manner as does rejection (99% negative predictive value for rejection grade 2 or higher, 17 % positive predictive value). We defined the infection-specific parameter as the time on the O line between the pacemaker stimulus and the crossover with the maximum slope of the descending part of the t wave. Patients were classified prospectively according to infection status: patients without infection and those with clinically apparent infection. Patients with clinically apparent infections had a significantly longer infection-specific parameter. A simultaneous decrease of the rejection-sensitive parameter and an increase in the infection-specific parameter was observed during clinical infection; a decrease in the rejection-sensitive parameter and no changes in the infection-specific parameter were observed during rejection. This preliminary analysis revealed that discrimination of rejection and infection might be possible by the analysis of intramyocardial electrograms.

Update: Approach to the Patient with Suspected Implantable Cardioverter-Defibrillator System Malfunction

T he evolution of technology has been described as either revolutionary or evolutionary. The former refers to advances in therapy that are dramatic. The latter describes advances in therapy that are more incremental. The changes in implantable cardioverter-defibrillator (ICD) technology over the last two years fall into the latter category. ICD system malfunction was reviewed in 1998 and the general concepts remain unchanged [1]. ICDs may deliver therapies in response to the either atrial or ventricular arrhythmias, or they may fail to delivery therapy. Furthermore, they may fail to successfully treat a tachycardia because of either failure to detect the arrhythmia (non-detection) or frank failure of the therapy itself (non-conversion). The problems of multiple defibrillator shocks and arrhythmia detection failure are discussed elsewhere in this monograph (see also, this issue pp. 122–128). Non-detection may occur because of improper or phantom programming, ventricular tachycardia occurring below the detection rate of the ICD, detection enhancements preventing satisfaction of detection criteria, undersensing, and oversensing of pacemaker stimulus artifacts (detection inhibition). Furthermore, there can be nonconversion of ventricular arrhythmias due to problems with the arrhythmia therapy prescription, incessant tachycardias, and changes in the defibrillation threshold. Finally, there may be problems with pacing due to altered pacing thresholds, Twave sensing that inhibits pacing, and lead system failure.