Clinical utility of intraatrial pacemaker stored electrograms to diagnose atrial fibrillation and flutter.

The purpose of this study was to determine if intraatrial electrograms (EGMs) are required to diagnose specific types of atrial tachyarrhythmias detected by pacemaker diagnostics. DDD pacemakers in 56 patients were programmed to store episodes of atrial tachyarrhythmias. Some episodes had a stored atrial EGM snapshot of the atrial tachyarrhythmia. The EGMs were analyzed to confirm whether the stored episodes were true atrial tachyarrhythmias or other pacemaker-sensed events. EGM confirmation of atrial tachyarrhythmias correlated with increasing duration and rate of episodes. In particular, using EGMs, 8 (18%) of 44 episodes < 10 seconds in duration confirmed atrial tachyarrhythmias compared to 16 (89%) of 18 episodes > 5 minutes in duration (P < 0.001). Only 10 (18%) of 56 detected atrial arrhythmia episodes at rates < 250 complexes per minute were confirmed by the atrial EGM as true arrhythmias compared to 33 (57%) of 58 detected episodes at rates > 250/min (P < 0.001) Twenty-nine (91%) of 32 EGM confirmed episodes of atrial fibrillation/flutter had an atrial rate > 250 complexes per minute and were a minimum of 10 seconds in duration. Fifteen (88%) of 17 episodes meeting the combined stored data criteria of > 250 complexes per minute and duration > 5 minutes were confirmed as atrial fibrillation or flutter by stored EGMs. Atrial EGMs identified that 71 (62%) of 114 stored high atrial rate (HAR) episodes were events other than true atrial tachyarrhythmias. Pacemaker diagnostic data with intraatrial EGMs can diagnose specific atrial tachyarrhythmias and identify other pacemaker-sensed events. Stored episodes > 250 complexes per minute and > 5 minutes in duration had a high correlation with atrial fibrillation and flutter.

Dynamics of the uncorrected QT interval during vagal-induced lengthening of RR intervals.

Analysis of 21 episodes of vagal-induced atrioventricular block showed that the uncorrected QT intervals at the end of the corresponding RR pauses were not prolonged, in reference to the pre-block QT intervals, with pauses shorter than 1,280 ms. Subsequently, they gradually lengthened as the RR pauses progressively increased to 13,710 ms. This dynamic behavior of the QT interval in subjects without structural heart disease could have resulted from a complex interaction between the cumulative effects of previous cycle lengths (memory effect?) and the autonomic nervous system.

An innovative application of anatomic electromagnetic voltage mapping in a patient with Ebstein's anomaly undergoing permanent pacemaker implantation.

A novel application of the Biosense CARTO System anatomic electromagnetic voltage mapping is presented, utilized as a guide for permanent pacemaker placement. The technique is illustrated in the successful implantation of an atrial lead in a patient with Ebstein's anomaly characterized by a severely dilated right atrium and extremely low-amplitude voltage signals, requiring a DDD pacemaker. Electromagnetic voltage mapping can be used in selected patients with structural heart disease to determine the optimal site for permanent pacemaker lead placement.

Muscarinic receptor stimulation with edrophonium hydrochloride does not elevate ventricular fibrillation thresholds in humans.

INTRODUCTION: Although decreased vagal tone, as measured by heart rate variability is a risk factor for ventricular fibrillation (VF) and sudden cardiac death, it is unknown whether increasing vagal tone has an antiarrhythmic effect. The purpose of this study was to determine whether edrophonium hydrochloride (HCI), a vagomimetic agent, increases VF threshold. METHODS AND RESULTS: Twenty-eight consecutive patients with previously implanted defibrillators had two inductions of VF by monophasic direct-current shocks delivered at 10 to 30 msec after the T wave peak, escalating energies (0.4, 1, then 3 J) until VF was induced. If VF was not induced, this protocol was repeated at the T wave peak and then at 10 to 30 msec before the T wave until VF was induced. Patients were randomized to receive edrophonium HCl (12 to 18 mg) or no drug before repeating the protocol for the second VF induction. The mean sinus cycle length increased from 782 to 872 msec in the group receiving edrophonium HCI (P = 0.006 ). In the control group, the mean sinus cycle length remained unchanged (838 vs 858 msec). The mean energy to induce VF, coupling interval relative to the T wave, and the number of attempts to induce VF were not different between VF induction attempts 1 and 2, and they were not different between the group receiving edrophonium HCl and the control group. CONCLUSION: In a sedated patient population with implantable defibrillators, edrophonium HCI infusion prolongs sinus cycle length but does not change inducibility of VF using T wave shocks.

Cycling of inducibility of paroxysmal supraventricular tachycardia in women and its implications for timing of electrophysiologic procedures.

Arrhythmias in women may be affected by phases of the menstrual cycle. This study was designed to determine the prevalence of perimenstrual clustering of spontaneous episodes of paroxysmal supraventricular tachycardia (SVT) in women. It also tested the hypothesis that women with this temporal pattern of events have an altered probability of induction of paroxysmal SVT during electrophysiologic testing at higher estrogen states (midcycle or with estrogen replacement therapy) than at low estrogen states (perimenstrual or without estrogen replacement). A structured history of the relation of spontaneous paroxysmal SVTs to phases of the menstrual cycle was obtained prospectively among 42 women referred during a 3-year period. Patients with cyclical patterns of spontaneous tachycardias, who had had negative electrophysiologic studies at midcycle or while receiving estrogen replacement therapy, had repeat procedures (1) when premenstrual or at the onset of menses, or (2) after stopping estrogen replacement therapy. Seventeen of 42 consecutive female patients (40%) had histories of perimenstrual clustering of arrhythmias. Six women (4 with normal menstrual cycles, 2 on estrogen replacement therapy), who qualified for paired electrophysiologic studies because of a negative initial electrophysiologic study that included provocation with isoproterenol, had inducibility into SVTs during the second study. All 6 had dual atrioventricular (AV) nodal pathway physiology, 4 had AV nodal reentrant tachycardia (AVNRT) induced, 1 had both AVNRT and reciprocating AV tachycardias, and 1 had nonsustained AVNRT and an atrial tachycardia induced. Successful ablation procedures were performed in 5 of the 6 patients. Thus, among women with a history of perimenstrual clustering of paroxysmal SVT and among those receiving estrogen replacement therapy, scheduling of elective electrophysiologic procedures at times of low estrogen levels (premenstrual or off estrogen replacement therapy) may facilitate the probability of a successful procedure.

Analysis of charges and complications of permanent pacemaker implantation in the cardiac catheterization laboratory versus the operating room.

During the last two decades, an increasing number of permanent pacemakers have been implanted outside of the operating room (OR) by nonsurgeons. Previous investigators have demonstrated that pacemakers can be safely implanted in the cardiac catheterization laboratory with no increase in complications or infections. This is the first study of its kind to simultaneously evaluate cost, length of hospitalization, and complications between pacemakers implanted in the OR by surgeons with those implanted in the catheterization laboratory by an electrophysiologist. A total of 254 consecutive pacemaker implants were analyzed over a 2-year period. The OR group consisted of 122 patients with a mean age of 64 +/- 21 years versus 132 patients in the catheterization laboratory group with a mean age of 65 +/- 17 years. The indication and type of pacemaker implanted were similar among both groups with 78% of OR patients and 73% of catheterization laboratory patients receiving dual chamber devices. The average cost for pacemaker implantation in our study was significantly higher in the OR group $5,464 +/- $1,670 versus $2,682 +/- $8 for the catheterization laboratory group (P < 0.001). There was a reduction in preimplant days in the catheterization laboratory group 3.16 +/- 12.40 days versus 5.65 +/- 9.54 days in the OR group (P < 0.05). Complications were minimal and there were no significant differences between the two groups. This study confirms that pacemakers can be safely implanted in the catheterization laboratory by nonsurgeons with no increase in complications and a significant reduction in hospital costs.

Sudden Wenckebach periods and their relationship to neurocardiogenic syncope.

Throughout a 9-month period during which 1,125 Holter tapes were reviewed prospectively we identified 13 nonmedicated patients with an arrhythmia, which for the purposes of this presentation was categorized, because of their mode of initiation, as sudden Wenckebach periods (WP). The episodes emerged abruptly from a normal (< or = 200 ms) PR interval with sudden prolongation of PR and PP intervals (and reversed PR-RP relationship) that took place over 1-8 cycles. The postpaced PR interval was shorter than that of the last conducted beat. The episodes were separated into two groups. Group I included 11 patients with symptoms other than syncope and Group II included 2 patients with syncope. There were 26 episodes of sudden WP in Group I. Twenty-five terminated in a single (and one in double) blocked P waves. Most episodes occurred between 10 PM and 7 AM. Symptoms did not correlate with the episodes. Mean 24-hour rates were < 90. In Group II there were 22 episodes, all occurring between 6 AM and 10 PM. The mean sinus cycle lengths before the phenomenon started to occur in Group I (861 +/- 185 ms) as well as the cycle lengths at the onset of block (1,096 +/- 215 ms) were statistically longer than those in Group II (591 +/- 40 ms and 747 +/- 63 ms, respectively, P < 0.0001). Although the mode of onset in the episodes in Group II was similar to Group I, 16 episodes terminated in 2-6 blocked P waves. Thus, the entire number of episodes could be categorized as an unusual type (because of the PR prolongation) of paroxysmal, or advanced second degree AV block. Because these patients had negative electrophysiological studies, positive tilt tests, and absent syncope after oral propranolol therapy, they were considered as having neurocardiogenic syncope. In addition, the faster than normal (> 100) mean 24-hour rates) suggested that they also had so-called inappropriate sinus tachycardia. In summary, Group I consisted of patients with a normal, benign, vagal-induced second-degree AV block, whereas the Holter findings in Group II appeared to reflect unusual (but natural, i.e., nonprovoked) electrocardiographic manifestations of certain patients with neurocardiogenic syncope.

Reverse alternating Wenckebach periods and other modes of regression of > or = 8:1 to 2:1 atrioventricular block.

The modes of regression of very high degrees of atrioventricular nodal block (> or = 8:1) were studied in patients with atrial flutter and a specific variant of the tachycardia-bradycardia syndrome. The occurrence of reverse alternating Wenckebach periods, previously reported only in 2:1 atrioventricular block, emphasizes the complexities of multilevel block.

Frequency of sudden cardiac death and profiles of risk.

The epidemiology of ventricular tachycardia/fibrillation (VT/VF) and sudden cardiac death (SCD) must be explored from multiple aspects, each of which contributes insights into the problem and no one of which exerts exclusive dominance for preventive or therapeutic strategies. These include: (1) population dynamics, using conventional epidemiologic approaches; (2) risk as a function of time from an index event; (3) conditioning risk factors, based on the presence of underlying disease states; (4) transient risk factors that are dynamic and trigger a potentially fatal event at a specific point in time; and (5) "response risk," which refers to individual susceptibility (possibly determined genetically) to the adverse effects of longitudinal and/or dynamic risk factors. Major inroads into profiling individual or population risk of SCD will require better understanding of each of these epidemiologic-clinical-physiologic interactions. The disciplines range from epidemiology, through clinical medicine, to membrane channel physiology, genetic determinants, and molecular biology.

Dynamics of, and alternating Wenckebach periods during, 4:1 and 6:1 atrioventricular block.

In summary, the irregular dynamics of progression of 4:1 AV block in atrial flutter, presumably different from those observed in similar degrees of rate-dependent block, most likely reflected the complex electrophysiologic mechanisms operating during the highest degrees of AV nodal block. Occurrence of previously undescribed arrhythmias, namely Wenckebach periods during 4:1 and 6:1 block, tends to support the multilevel block hypothesis.

A different approach to the analysis of pure ventricular parasystole.

Until recently, it had not been recognized that predictions regarding the number of sinus beats interposed between two consecutive parasystolic beats could be made. In a case of perfect, pure parasystole resulting from unintentional fixed rate ventricular pacing, the following was observed: there were consistently three different values (0,2,3) for the number of interposed sinus beats; only one of these values was odd, and the sum of the two smaller values was one less than the larger value. Our findings, which are in keeping with those obtained in an mathematical model, may be of additional help in the diagnosis of this elusive arrhythmia.

Future evaluation of antiarrhythmic therapy.

The expansion of antiarrhythmic therapy beyond pharmacologic agents to include surgery, devices, and ablation procedures, plus the reaffirmation by the Cardiac Arrhythmia Suppression Trial (CAST) of the need for concurrent placebo-controlled trials to establish a mortality benefit, have resulted in the need to consider the requirements for evaluating therapy. Pharmacologic therapy may be used in three ways: (1) primary; (2) alternative; and (3) adjunctive. To accurately identify a mortality benefit from primary therapy, a placebo-controlled study is necessary. In contrast, control of symptoms may be identified without the same rigorous demands. Current data are limited by the absence of true negative controls for most interventions that claim a possible mortality benefit. Alternative therapy provides a choice between equally effective therapies, neither of which has necessarily been documented to have a mortality benefit. Adjunctive therapy is that which is used for control of symptoms, whereas another therapy is used to provide a presumed or proved mortality benefit. For any of these approaches, therapy must be further evaluated in terms of four modifying variables: (1) impact of therapy on the basis of both its efficacy and efficiency; (2) interpretation of outcome data based on analysis of competing risks; (3) measurement of efficacy in terms of extension of life; and (4) analysis of outcome as the equilibrium between antiarrhythmic benefit and proarrhythmic risk. With these approaches a rational analysis of the effect of therapy and its cost-based benefit can be achieved.

Alternating Wenckebach periods and allied arrhythmias.

Alternating Wenckebach periods (AWPs) are episodes of 2:1 block during which the PR, AH, or AV intervals of the conducted beats gradually increase until a greater degree of block ensues. Most episodes occur at the AV node, but some have also been reported in other structures. AWPs are usually attributed to multilevel block due to transverse (horizontal) dissociation. This assumption was initially based on a method in which the solutions to difficult electrocardiographic rhythms were arrived at by analysis and deduction based on the knowledge existing at that particular time. Subsequently, it was reinforced by information extrapolated from intracardiac recordings performed in patients with documented multilevel block in separate anatomical structures (atria, AV node, and His bundle), as well as from microelectrode studies and computer simulations. Although AWPs are frequently observed in clinical tracings, those occurring at the AV node are best categorized during incremental atrial stimulation because then they occupy a specific point in the wide spectrum of tachycardia dependent AV nodal conduction disturbances. In fact, the A:H ratios occurring in the episodes where the degree of block increases can be represented by "universal" mathematical formulas. However, in the clinical setting, drugs affecting the electrophysiology of the node can alter the pacing induced symmetry by producing additional differential effects on the various levels. The latter still requires further elucidation.