Comparison of Bipolar Atrial Electrogram Amplitude in Sinus Rhythm, Atrial Fibrillation, and Atrial Flutter

Automatic mode switching pacemakers revert to non-atrial tracking modes in response to sensed atrial tachyarrhythmias. It is unclear how atrial electrogram amplitudes in sinus rhythm compare to those during atrial tachyarrhythmias. In this study, peak-to-peak bipolar atrial electrogram amplitudes were measured during sinus rhythm and either atrial fibrillation or atrial flutter in 69 patients. The mean atrial electrogram amplitudes were 1,59 ± 1.36 m V during sinus rhythm and 0.77 ± 0,58 mV during atrial fibrillation (P < 0.0001) for 25 patients with atrial fibrillation and 1.81 ± 2.07 mV during sinus and 1.5 ± 1.81 mV(P < 0.0001) for 44 patients with atrial flutter. The mean electrogram amplitudes during both atrial fibrillation and flutter correlated significantly with amplitudes during sinus rhythm (R = 0.79, R = 0.94. respectively, both P < 0,0001). The coefficient of variance of individual electrogram amplitudes was greater in atrial fibrillation than sinus (P < 0.0001). By comparing 20th percentile electrogram amplitudes in atrial fibrillation and flutter to mean sinus amplitudes, intermittent very low electrogram amplitudes (< 0.3 mV) were more likely during atrial fibrillation and flutter if the mean sinus electrogram amplitudes were < 1.5 mV and < 0.5 mV, respectively (P < 0.01). Eightieth percentile electrogram amplitude values in atrial fibrillation and flutter were equally likely to exceed mean sinus amplitude values in respective patients, in conclusion, mean atrial electrogram amplitudes during atrial fibrillation and flutter are less than but correlated to sinus rhythm electrogram amplitudes. Very low amplitude individual electrograms during these atrial arrhythmias are associated with low mean sinus rhythm electrogram amplitudes. These findings may have implications for the programming of permanent dual chamber pacemakers in patients with paroxysmal atrial fibrillation and flutter.     

Relationship Between Atrial Conduction Defects and Fractionated Atrial Endocardial Electrograms in Patients with Sick Sinus Syndrome

The relationship between abnormal atrial electrograms (AAE) recorded during sinus rhythm by endocardial calheter mapping of the right atrium and the afrial conduction defects of sinus impulses or single atrial extrastimuli was investigated in 44 patients with sick sinus syndrome. The patients were divided into two groups on the basis of the presence (n = 29) or absence (n = 15) of AAE recorded during sinus rhythm. The P wave duration in the AAE (+) Group patients was 137 ± 14 msec, and 125 ± 15 msec in (he AAE (−) Group; P < 0.02. The intraatrial conduction time of sinus impulses in the AAE (+) Group was 54 ± 12 msec, and 39 ± 9 msec in the AAE (−) Group; P < 0.001. The interatrial conduction time in the AAE (+) Group was 101 + 14 msec, and 78 ± 16 msec in the AAE (−) Group; P < 0.001. In the AAE (+) Group, H (38%) patients ha d a sinus node recovery time > 4 seconds, whereas in the AAE (−) Group there was only one (6%) patient; P < 0.03. AAE showed a specificity of 93% and a positive predictive accuracy of 91% in predicting inducibility of atrial fibrillation. The sensitivity was 35% and the negative predictive accuracy was 42%. Sustained atrial fibrillation was induced in ten (35%) patients of the AAE (+) Group, and in one (7%) patient of the AAE (−) Group; P < 0.05. These data suggest that in patients with sick sinus syndrome who possess abnormal endocardial eJectrograms in sinus rhythm within the right atrium have: (1) a significantly longer P wave duration: (2) a significantly longer intraatrial and interafrial conduction time of sinus impulses; and (3) a significantly greater sinus node dysfunction and higher incidence of induction of sustained atriai fibrillation. It is concluded that there are significantly greater atrial conduction defects in patients with sick sinus syndrome who possess AAE within the right atrium during sinus rhythm.     

Amplitude of Atrial Electrical Activity During Sinus Rhythm and During Atrial Flutter-Fibrillation

The onset of atrial flutter or fibrillation in a patient with a DDD pacemaker may result in sensing of the atrial arrhythmia and an inappropriate ventricular pacing response. In order to assess the potential of this problem, we evaluated the amplitude of atrial electrograms recorded from the right atrial appendage during sinus rhythm and during atrial flutter or fibrillation during 19 episodes in 18 patients. in 11 episodes of fibrillation and eight episodes of flutter, there was no difference in amplitude of either unipolar or bipolar atrial electrograms compared to that recorded during sinus rhythm (p > 0.05). In 14 of 19 episodes, the direction of depolarization of the bipolar electrogram did not change appreciably between sinus rhythm and the atrial arrhythmia. In summary, there is insufficient difference between amplitude of atrial depolarizations recorded during sinus rhythm and atrial flutter or fibrillation to be differentiated reliably by DDD pacemakers.     

Atrial Lead Implantation During Atrial Flutter or Fibrillation?

In patients with sinoatrial disease, unexpected atrial flutter (Af) or fibrillation (AF) is a common problem during implantation of atrial-based pacing systems. As an alternative approach to blind atrial lead placement, lead positioning could be optimized by atrial electrogram mapping. It was the object of this study to evaluate if atrial lead implantation according to this approach and during ongoing arrhythmia is reasonable or if it should be postponed until restoration of sinus rhythm (SR). Twenty-nine consecutive patients (group I) with sick sinus syndrome received a dual-chamber pacemaker during an episode of Af (n = 11) or AF (n = 18). All but two atrial leads were of the screw-in type and had bipolar sensing. Atrial lead position was optimized by mapping the electrogram under fluoroscopy to find locations with high potential amplitudes. The patients were followed for 15.1 ± 9.8 months, and atrial sensing threshold (AST), atrial pulse width threshold (PWT) at 2.0 V, the pacing mode programmed, and the clinical outcome (OUT) were recorded. The control group consisted of 30 patients (group II) who equally had a history of AF or Af, but were in SR during implantation. The atrial peak-to-peak potential (APEAK) after final lead placement was lower for AF (median value 2.5 mV, lower-upper quartile: 1.7–3.1 mV) as compared to Af (3.8 mV, 2.7–4.9 mV, P < 0.05) and SR (4.1 mV, 3.3–6.2 mV, P < 0.001). There was a correlation (P < 0.01) between APEAK during Af/AF and the postoperative AST immediately after restoration of SR. No lead in any group had to be corrected due to improper sensing in the postoperative course. Median chronic AST was 2.8 mV (2.0–4.0 mV) in group I and 4.0 mV (2.8–4.0 mV) in group II. Median chronic PWT at 2.0 V was 0.15 ms (0.12–0.26 ms) in group I and 0.15 ms (0.09–0.20 ms) in group II. There was no significant difference in chronic AST and PWT between both groups. All but two patients in group I preserved SR as the basic rhythm. A stable SR was observed in 10 of 29 patients, intermittent Af/AF was documented in 17 of 29 patients, seven of whom were asymptomatic. There was no significant difference in OUT between group I and II. Hence, sinus rhythm is not a prerequisite of atrial lead implantation. Mapping the Af or AF waves appears to be useful to guide lead placement and to achieve sufficient sensing and pacing conditions after conversion to sinus rhythm.     

Concealed Atrial Parasystole Following the Senning Operation

A patient with sick sinus syndrome following the Senning operation was also found to have concealed atrial parasystole during intracardiac electrophysiological study. This atrial parasystolic pattern could he converted to atrial bigeminy by changing the atrial drive rate.     

Effect of Propranolol on Ventricular Rate During Atrial Fibrillation in the Wolff-Parkinson-White Syndrome

Atrial fibrillation was induced during an electrophysiology study in 10 patients with the Wolff-Parkinson-White (WPW) syndrome, after determination of baseline properties of the accessory atrioventricular (AV) connection; intravenous propranolol (0.2 mg/kg) was then administered. Atrial fibrillation terminated during the drug infusion in three patients, allowing determination of propranolol's effects on conduction and refractoriness during sinus rhythm, before atrial fibrillation was reinduced. In these three patients propranolol had no effect on refractoriness or conduction properties of the accessory AV connection during sinus rhythm. The mean ventricular rate during atrial fibrillation was slowed by 15–56 beats/min in six patients, had no effect on the mean rate in three patients, and markedly increased the ventricular rate (203 to 267 beats/min) in one patient. In this patient, 54% of QRS complexes during atrial fibrillation were narrow, compared to 0–25% in the other patients. Propranolol reduced the percentage of QRS complexes that were narrow from 13 ± 16% to 1 ± 2% (mean ± standard deviation, p < 0.05). We conclude that propranolol may slow the ventricular rate during atrial fibrillation in some patients with the WPW syndrome, probably by blockcing the effects of adrenergic activation. However, propranolol should not be used in patients with the WPW syndrome who have atrial fibrillation, if most QRS complexes during atrial fibrillation are preexcited. When a large percentage of QHS complexes are narrow, propranolol may increase the ventricular rate, probably by eliminating concealed retrograde conduction in the accessory AV connection.     

Abnormal right atrial electrograms predict the transition to chronic atrial fibrillation in paced patients with sick sinus syndrome

Although pacing therapy for sick sinus syndrome (SSS) is established, the risk of developing chronic atrial fibrillation (CAF) makes pacing therapy infeasible in some patients. We evaluated whether electrophysiological characteristics of atrial muscle can serve as predictors of the transition to CAF after pacemaker implantation in patients with SSS. Eighty-nine patients with SSS underwent electrophysiological study before pacing therapy. Catheter mapping of 12 right atrial sites was performed during sinus rhythm during electrophysiological. An abnormal atrial electrogram was defined as having a duration of 100 ms or longer, or eight or more fragmented deflections, or both. Right atrial extrastimulation was also performed for atrial vulnerability. After electrophysiological study, all patients underwent pacemaker implantation and were followed up. During the follow-up period of 85 +/- 50 months, development of CAF was observed in 12 patients (group A). The remaining 77 patients remained in sinus rhythm (group B). There were significantly more abnormal atrial electrograms in group A than group B (2.7 +/- 2.3 vs 0.8 +/- 1.2; P < 0.001). The distribution of abnormal atrial electrograms was also greater in group A; patients in group A had more abnormal atrial electrograms than patients in group B in both the high and middle right atrium (P < 0.005 and P < 0.01, respectively). Kaplan-Meier analysis showed that almost 50% of the paced patients with abnormal atrial electrograms (n = 42) developed CAF (P < 0.005). Our data suggest that the existence of abnormal atrial electrograms is predictive of the transition to CAF in paced patients with SSS.     

Preprocedural ventricular rate predicts subsequent sick sinus syndrome after ablation for long-standing persistent atrial fibrillation

Background: Concealed sick sinus syndrome may become manifest after restoration of sinus rhythm by ablation in patients with long-standing persistent atrial fibrillation (AF). The purpose of this study was to investigate the association between the preprocedural ventricular rate during AF and sinus node function in patients with long-standing persistent AF. Methods: Consecutive patients (n = 102) who underwent ablation for long-standing persistent AF were enrolled. We measured the ventricular rate during AF before ablation in the absence of antiarrhythmic drugs. Sinus node function was assessed by electrophysiological study and serial Holter recordings after ablation. Results: Patients in the lowest quartile of ventricular rate during AF had longer corrected sinus node recovery time (1.06 ± 1.39 seconds) than those in the other quartiles (0.54 ± 0.31 seconds; P = 0.006) and lower mean heart rate on 24-hour Holter recording 3 months after ablation (68 ± 9 beats/min vs 75 ± 10 beats/min, P = 0.01). During a mean follow-up of 23 ± 10 months, sick sinus syndrome necessitating permanent pacemaker implantation developed in five (5%) patients, and multivariate analysis revealed that a low ventricular rate during AF rate was an independent risk factor for sick sinus syndrome (odds ratio = 0.90 for a 1 beat/min increase in AF rate, P = 0.04). Conclusions: A low preprocedural ventricular rate during AF indicates the existence of sinus node dysfunction after restoration of sinus rhythm by ablation in patients with long-standing persistent AF. (PACE 2012; 35:1074-1080).     

Atrial Flutter with 1:1 Conduction in Undiagnosed Wolff-Parkinson-White Syndrome

Background

Atrial flutter with 1:1 atrioventricular conduction via an accessory pathway is an uncommon presentation of Wolff-Parkinson-White syndrome not previously reported in the emergency medicine literature. Wolff-Parkinson-White syndrome, a form of ventricular preexcitation sometimes initially seen and diagnosed in the emergency department (ED), can present with varied tachydysrhythmias for which certain treatments are contraindicated. For instance, atrial fibrillation with preexcited conduction needs specific consideration of medication choice to avoid potential degeneration into ventricular fibrillation.

Case Report

We describe an adult female presenting with a very rapid, regular wide complex tachycardia successfully cardioverted in the ED followed by a normal electrocardiogram (ECG). Electrophysiology study confirmed atrial flutter with 1:1 conduction and revealed an accessory pathway consistent with Wolff-Parkinson-White syndrome, despite lack of ECG findings of preexcitation during sinus rhythm.Why should an emergency physician be aware of this? Ventricular tachycardia must be the first consideration in patients with regular wide complex tachycardia. However, clinicians should consider atrial flutter with 1:1 conduction related to an accessory pathway when treating patients with the triad of very rapid rate (>250 beats/min), wide QRS complex, and regular rhythm, especially when considering pharmacologic treatment. Emergency physicians also should be aware of electrocardiographically concealed accessory pathways, and that lack of delta waves does not rule out preexcitation syndromes such as Wolff-Parkinson-White syndrome.     

Diagnostic implications of atrial vulnerability.

Extrastimulation in the atrial vulnerable zone may result in atrial fibrillation or flutter (AFF), especially with stimulation of multiple atrial sites. However, the clinical relevance of such vulnerability to AFF is unknown. Therefore, single twice-threshold extrastimuli were applied at three disparate right atrial sites in 45 consecutive unmedicated patients without overt heart failure. Group I consisted of 12 patients with documented spontaneous paroxysms of AFF. AFF was duplicated in 9 to 12 patients using extrastimulation in the vulnerable zone (5 in sinus rhythm, 4 requiring atrial pacing at 120 beats/min). Group II consisted of 33 patients without documented AFF dispite monitoring. Vulnerability to AFF was found in 12 of 33 patients (4 in sinus rhythm, 8 requiring atrial pacing). The duration of induced AFF did not discriminate between the two groups. Among the 12 Group II patients vulnerable to AFF, 3 had rapid palpitations, 2 had undiagnosed rapid tachycardias, 1 had atrial tachycardias and 1 junctional tachycardias. In vulnerable patients, the pause after AFF correlated with the pause after atrial pacing, but only 1 of 11 Group II patients with sick sinus syndrome was vulnerable. Thus, paroxysmal AFF may be duplicated with the extrastimulus technique if sufficient arial sites are stimulated, providing a model for evaluation of these arrhythmias. But atrial vulnerability, even to extrastimulation at normal heart rates, may be seen in patients suspected of atrial tachyarrhythmia in the absence of documented AFF, and does not contribute to the diagnosis of sinoatrial dysfunction.     

Electrophysiological Abnormalities of the Atrial Muscle in Patients with Manifest Wolff-Parkinson-White Syndrome Associated with Paroxysmal Atrial Fibrillation

We investigated the electrophysiological properties of the atrial muscle in 33 patients with manifest Wolff-Parkinson-White syndrome. Group I consisted of 13 patients with paroxysmal atrial fibrillation and group II consisted of 20 patients without paroxysmal atrial fibrillation. The anterograde and retrograde effective refractory periods of the accessory pathway and the inducibility of atrioventricular reciprocating tachycardia were not significantly different between the two groups. Endocardial electrograms, obtained by right atrial catheter mapping, were recorded during sinus rhythm from 12 sites of the right atrium in 12 of the 13 group I patients and in all group II patients. An abnormal atrial electrogram was defined as 100 msec or longer in duration, and/or the occurrence of eight or more deflections. Ten (83%) of the 12 group I patients had abnormal atrial electrograms, while only two (10%) of the 20 group II patients had abnormal atrial electrograms, and the difference was significant (P less than 0.01). Thirty-six (26%) of the total 139 electrograms obtained from 12 group I patients and two (1%) of the total 199 electrograms obtained from 20 group II patients fulfilled the criteria for an abnormal atrial electrogram, and the difference was significant (P less than 0.01). The fragmented atrial activity zone, interatrial conduction delay zone, and repetitive atrial firing zone obtained by right atrial extrastimulation were significantly wider in group I than in group II, respectively. It was concluded that electrical abnormalities of the atrial muscle may play an important role in the occurrence of paroxysmal atrial fibrillation in patients with Wolff-Parkinson-White syndrome.     

Relationship between P-wave duration and atrial electromechanical delay assessed by tissue Doppler echocardiography

Background: The aim of the study was to assess the relationship between P‐wave duration on the surface electrocardiogram (ECG) and echocardiographic parameters of atrial electromechanical delay (EMD), as well as contraction synchrony during different atrial pacing modalities. Methods: In 57 patients with sinus node disease and prolonged sinus P‐wave duration treated with multisite atrial pacing (MSAp), the EMD was measured by tissue Doppler in several left and right atrial sites during sinus rhythm, MSAp, and single‐site pacing at right atrial appendage (RAAp), Bachmann's bundle (BBp) region, and coronary sinus (CSp) ostium. Regional atrial synchrony was calculated on the basis of EMD. Results: P‐wave duration was 141 ± 16, 120 ± 17, 138 ± 17, 144 ± 16, and 160 ± 19 ms during sinus rhythm, MSAp, BBp, CSp, and RAAp, respectively (P < 0.001 RAAp and MSAp vs other). P‐wave duration correlated with all atrial EMDs as well as interatrial and intraleft atrial parameters of dyssynchrony. In multivariate analysis, the EMD in lateral left atrial wall was the strongest predictor of P‐wave duration (β 0.41; P < 0.001). The relationship between P‐wave duration and the atrial EMDs was most prominent during RAAp (all left atrial walls r > 0.51; P < 0.01) and BBp (all atrial walls r > 0.42; P < 0.05), while during sinus rhythm and CSp, only weak correlation between echo and ECG was found. Neither of the tissue Doppler parameters correlated with P‐wave duration during MSAp. Interatrial dyssynchrony correlated with P‐wave duration during sinus rhythm and RAAp and intraleft atrial dyssynchrony only during sinus rhythm. Conclusions: P‐wave duration of the surface ECG is highly correlated with the atrial EMD, the relationship is specific for each pacing modality. (PACE 2011; 23–31)     

A New Defibrillator Discrimination Algorithm Utilizing Electrogram Morphology Analysis

Inappropriate therapies delivered by implantable cardioverter defibrillators (ICDs) for supraventricular arrhythmias remain a common problem, particularly in the event of rapidly conducted atrial fibrillation or marked sinus tachycardia. The ability to differentiate between ventricular tachycardia and supraventricular arrhythmias is the major goal of discrimination algorithms. Therefore, we developed a new algorithm, SimDis, utilizing morphological features of the shocking electrograms. This algorithm was developed from electrogram data obtained from 36 patients undergoing ICD implantation. An independent test set was evaluated in 25 patients. Recordings were made in sinus rhythm, sinus tachycardia, and following the induction of ventricular tachycardia and atrial fibrillation. The arrhythmia complex is defined as wide if the duration is at least 30% greater than the template in sinus rhythm. For narrow complexes, four maximum and minimum values were measured to form a 4-element feature vector, which was compared with a representative feature vector during normal sinus rhythm. For each rhythm, any wide complex was classified as ventricular tachycardia. For narrow complexes, the second step of the algorithm compared the electrogram with the template, computing similarity and dissimilarity values. These values were then mapped to determine if they fell within a previously established discrimination boundary. On the independent test set, the SimDis algorithm correctly classified 100% of ventricular tachycardias (27/27), 98% of sinus tachycardias (54/55), and 100% of episodes of atrial fibrillation (37/37). We conclude that the SimDis algorithm yields high sensitivity (100%) and specificity (99%) for arrhythmia discrimination, using the computational capabilities of an ICD system.     

Use of a Dual Chamber Pacemaker with a Novel Fallback Algorithm as an Effective Treatment for Sick Sinus Syndrome Associated with Transient Supraventricular Tachyarrhythmia

A dual chamber pacemaker having a fallback (FB) mode was utilized in nine patients with sick sinus syndrome (SSS) associated with transient supraventricular tachyarrhythmia (atrial fibrillation [Af] in three patients, atrial flutter [AF] in two, and paroxysmal atrial tachyarrhythmia [PAT] in four). Various degrees of abnormality of atrioventricular (AV) conduction were observed at the time of pacemaker implantation in five patients. In this pacemaker, a DDD mode was active during sinus rhythm, but the mode changed, through a given cycle of high rale tracking at an upper rate limit (VRL), to VDI only during intrinsic atrial rate increases that were either normally or abnormally above the URL. The VDI mode automatically returned to DDD when the atrial rate fell below the URL. At follow-up periods of 7–12 months, this pacemaker appeared to be especially effective in those SSS patients with transient Af or AF. In the SSS patients with PAT, however, the FB mode was not active because the PAT rhythm was conducted to the ventricle without block (1:1 conduction) and thus the given cycles of ventricular tracking at the URL did not occur. From the repetitive FB starting tests that were performed during an Af period in one patient with transient Af, a 2:1 point setting of a given URL plus 30–50 ppm was required to quickly start the FB algorithm. Moreover, an atrial sensitivity setting that was less than half of the P wave amplitude was desirable. These results suggest that, when properly set, the DDD plus FB mode is useful in a SSS patient with transient supraventricular tachyarrhythmia when a significant degree of AV block is present.     

Limitations to Activation of the Antitachycardia Burst Pacing Function of the Symbios 7008 Pacemaker in the Universal (DDD) Mode

The Symbios 7008 antitachycardia pacemaker was implanted in five patients for control of supraventricular tachycardia. Shortly after implantation in the first two patients, it was noted that the burst pacing sequence was not automatically activated by tachycardia when the pacemaker was in the DDD mode. Data from these two and the subsequent three patients were evaluated to explain this observation. The problem was primarily related to the operation of the device during the postventricular atrial refractory period. In all patients, the atrial electrogram encroached upon the programmed postventricular atrial refractory period because VA conduction during SVT was less than the lowest programmable interval (155 ms). Atrial events occurring during this interval will not trigger the tachycardia termination sequence. In all five patients, the size of the atrial electrogram decreased substantially (48 +/- 10%; mean +/- SD) during supraventricular tachycardia compared to sinus rhythm. In at least two of the five patients, decreased atrial size during supraventricular tachycardia may also have resulted in intermittent failure of atrial sensing during tachycardia, even at the most sensitive setting (0.6 mV). The latter may remain a problem even if the technical fault in SVT detection in the DDD mode were corrected. Two related problems were noted in the DDD mode: ventricular events during rapid SVT do not reset the low rate interval, resulting in random low rate pacing; and, automatic prolongation of atrial refractory period by two successive ventricular events without an intervening atrial sensed event compounds problems of atrial sensing. All of these problems were easily circumvented in all patients by noninvasive reprogramming to the DVI mode in which supraventricular tachycardia detection is based on ventricular sensing. These findings have implications for the future design of such devices.     

Novel Form of Atrial Tachycardia Originating at the Atrioventricular Annulus

We report two patients with reentrant atrial tachycardia that originated at the AV annulus. Atrial tachycardia originated in the posterior portion of mitral annulus in one patient (case 1) and the posterolateral portion of tricuspid annulus in one patient (case 2). Tachycardia was successfully eliminated by RF catheter ablation in both patients, with the catheter placed underneath the mitral valve in case 1 and on the tricuspid annulus in case 2. Spiky potentials were recorded in the diastolic phase of the atrium during tachycardia at the sites of successful ablation. Spiky potentials were also recorded after atrial electrogram during sinus rhythm, and showed decremental properties during atrial pacing. An accelerated atrial rhythm was observed during RF application, and tachycardia could not be induced after ablation in either patient. Tachycardia in these patients seemed to be due to reentrant tachycardia originating in the accessory AV node (Mahaim fiber) without ventricular connection.     

Continuous Holter telemetry of atrial electrograms and marker annotations using a common Holter recording system: impact on Holter electrocardiogram interpretation in patients with dual chamber pacemakers

The impact of continuous telemetry of atrial electrogram and marker annotations on Holter ECG interpretation was assessed in 98 patients with bipolar dual chamber pacemakers (VDD pacemakers n = 29, DDD(R) systems n = 69). Atrial electrogram and marker annotations were continuously sampled by a telemetry coil that was externally positioned on the pacemaker pocket, amplified, and transduced to a three-channel Holter ECG recorder in addition to an ECG recording. Holter tapes were analyzed by two experienced investigators for quality of P wave recognition and episodes suspicious of pacemaker dysfunction. Initially, only the ECG channel was analyzed. Thereafter, results were compared to those achieved on the basis of the complete recording including atrial electrogram and marker annotations. Recognition of atrial rhythm was markedly improved by Holter telemetry. During 99.3% of recording time telemetry showed a satisfying quality, whereas ECG alone allowed a reliable P wave recognition only during 84.4% of recording time (P < 0.001). One hundred twenty-nine episodes suspicious of pacemaker malfunction occurred in 17 of 98 patients. By analysis of ECG, only 78.3% of episodes were concordantly classified by the investigators. However, 98.4% of all episodes were properly identified when atrial electrogram and marker annotations were added to the analysis (P < 0.001). In particular, discrimination between atrial undersensing, sinus bradycardia, and atrial sensed events within the refractory periods was facilitated. Holter telemetry of atrial electrogram and marker annotations facilitates the analysis of Holter ECGs in pacemaker recipients and improves the detection of pacemaker dysfunctions.     

Wavelength and Atrial Vulnerability: an Endocavitary Approach in Humans

If atrial vulnerability parameters are well defined, wavelength (WL) measurement (conduction velocity x refractory period), has never been assessed through an endocavitary electrophysiological exam.
We investigated 30 patients (14 female, mean age 63.4 ± 13 y.o.), 10 with paroxysmal atrial fibrillation (PAF group), 10 with ischemic cerebral injury (ICI group) by comparison with 10 controls (C group).
The upper to lower right atrium conduction time and velocity were measured in the right atrium with a decapolar electrode catheter applied along the free wall. Others parameters correlated to atrial excitability were also taken into account: effective (ERP) and functional refractory periods (FRP); spontaneous or paced atrial electrogram (AI) or extrastimulated atrial electrogram (A2) widths, ERP/ A2 ratio, provocative atrial testing. Measurements were taken in sinus rhythm and in 600 – 460 ms paced cycle lengths. If ERP, FRP, Al widths are the same in the 3 groups, PAF and ICI groups have a significant increased conduction time and lower conduction velocity, leading to a shorter A1 WL during 600 and 460 ms paced rhythms (p 0.05) and A 2 WL during 460 ms paced rhythm. The provocative testing was positive in 60% of PAF and ICI groups, and there is a significant correlation between arrhythmia induction and 600 ms A1 WL or 460 ms A2 WL.
This electrophysiological study suggests the possibility of an approach in humans of wavelength concept and proves the presence of correlation between a short wavelength and atrial spontaneous or induced arrhythmias. A no-arrhythmia band (A1 WL > 17 cm during 600 ms paced rhythm, Al WL > 16 cm or A2 WL > 12cm during 460 ms paced rhythm) and a fibrillation-band (A1 WL < 12 cm during 600 and 460 ms pacing, A 2 WL < 7 cm during 460 ms pacing) can be defined. Therefore, the ICI group has the same atrial pattern as the AF group.     

Precipitation of ventricular fibrillation by intravenous diltiazem and metoprolol in a young patient with occult Wolff-Parkinson-White syndrome

We report the case of a young man who presented with a rapid, narrow-complex atrial fibrillation. A few hours after being administered intravenous metoprolol and diltiazem for rate control, he developed intermittent ventricular preexcitation on the electrocardiogram (ECG) and experienced ventricular fibrillation, from which he was successfully defibrillated. A subsequent electrocardiogram in sinus rhythm demonstrated previously unknown Wolff-Parkinson-White pattern. A left lateral accessory pathway was successfully ablated. Wolff-Parkinson-White syndrome should be included in the differential diagnosis when a young patient presents with atrial fibrillation, even if the ventricular complexes on the ECG are not preexcited.     

Discrimination of Retrograde from Anterograde Atrial Activation Using Intracardiac Electrogram Waveform Analysis

The prevention of pacemaker-mediated tachycardias requires a safe, reliable method for distinguishing retrograde from anterograde atrial activation by dual chamber pacemakers. In this study, a technique was developed to detect the morphological change that occurs in the waveform of the intra-atrial electrogram during retrograde atrial activation. The method employed for waveform analysis is based upon statistical correlation. In 19 patients undergoing electrophysiological studies, atrial electrograms were recorded from bipolar endocardial electrodes during sinus rhythm and 1:1 retrograde atrial depolarization while undergoing right ventricular pacing. Data were digitally sampled at 750, 1,000, and 1,500 Hz. Templates of anterograde atrial depolarization were constructed by signal averaging waveforms from an initial sinus rhythm passage. These were used for analysis of anterograde depolarizations from a subsequent passage of sinus rhythm and a passage of known retrograde atrial depolarization. In all 19 cases, a patient-specific threshold could be derived to separate anterograde from retrograde atrial depolarizations using 1,000 Hz and 1,500 Hz sampling rates. However, at a sampling rate of 750 Hz, separation of anterograde from retrograde atrial activation was possible in only 16/19 patients (84%). We conclude that correlation waveform analysis of a suitably sampled atrial electrogram is a reliable method of discriminating retrograde atrial depolarization from anterograde atrial depolarization in intracardiac electrograms.