Search

Prior studies have demonstrated that sympathetic tone may influence the effects of adenosine on His-Purkinje automaticity, and that enhanced vagal tone may influence its effects on the sinus node. However, the interaction between autonomic tone and the effects of adenosine on the sinus node in humans remains unknown. Therefore, this study was designed to investigate the interaction between different states of autonomic tone and the bradycardiac response of the sinus node to adenosine. In 11 patients without structural heart disease who underwent a clinically indicated electrophysiology procedure, the sinus cycle length was measured before and after a 12-mg bolus of adenosine in the baseline state, during an infusion of 2 mcg/min of isoproterenol, after the administration of 0.2 mg/kg of propranolol, and again after the administration of 0.04 mg/kg of atropine. Adenosine significantly lengthened the sinus cycle length in the baseline state (760 +/- 165 vs 909 +/- 188 ms, P < 0.05), during isoproterenol infusion (516 +/- 67 vs 766 +/- 146 ms, P < 0.05), after propranolol (850 +/- 153 vs 914 +/- 143 ms, P < 0.05) and after the combination of propranolol and atropine (662 +/- 76 vs 801 +/- 121 ms, P < 0.05). The degree of lengthening in sinus cycle length was significantly greater (P < 0.05) during isoproterenol infusion (253 +/- 157 ms, or 51% +/- 40%) than in the baseline state (149 +/- 85 ms, or 20% +/- 12%), after propranolol (68 +/- 53 ms, or 8% +/- 8%), and after propranolol and atropine (140 +/- 110 ms, or 21% +/- 18%). The negative chronotropic effect of adenosine is influenced by autonomic tone. The effect of adenosine on the sinus node is accentuated by beta-adrenergic stimulation and unaffected by beta-adrenergic blockade or combined beta-adrenergic and cholinergic blockade.

Background —Conversion of chronic atrial fibrillation (AF) is associated with atrial stunning, but the short-term effect of a brief episode of AF on left atrial appendage (LAA) emptying velocity is unknown. The purpose of this study was to determine whether a short episode of AF affects left atrial function and whether verapamil modifies this effect. Methods and Results —The subjects of this study were 19 patients without structural heart disease undergoing an electrophysiology procedure. In 13 patients, LAA emptying velocity was measured by transesophageal echocardiography in the setting of pharmacological autonomic blockade before, during, and after a short episode of AF. During sinus rhythm, the baseline LAA emptying velocity was measured 5 times and averaged. AF was then induced by rapid right atrial pacing. After either spontaneous or electrical conversion, LAA emptying velocity was measured immediately on resumption of sinus rhythm and every minute thereafter. The mean duration of AF was 15.3±3.8 minutes. The mean baseline emptying velocity was 70±20 cm/s. The first post-AF emptying velocity was 63±20 cm/s ( P =0.02 versus baseline emptying velocity). The post-AF emptying velocity returned to the baseline emptying velocity value after 3.0 minutes. The mean percent reduction in post-AF emptying velocity was 9.7±21% (range, 15% increase to 56% decrease). A second group of 6 patients were pretreated with verapamil (0.1-mg/kg IV bolus followed by an infusion of 0.005 mg · kg −1 · min −1 ). In these patients, the first post-AF emptying velocity, 58±14 cm/s, was not significantly different from the pre-AF emptying velocity, 60±13 cm/s ( P =0.08). Conclusions —In humans, several minutes of AF may be sufficient to induce atrial contractile dysfunction after cardioversion. When atrial contractile dysfunction occurs, there is recovery of AF within several minutes. AF-induced contractile dysfunction is attenuated by verapamil and may be at least partially mediated by cellular calcium overload.

OBJECTIVE The purpose of this study was to determine if the atrial response upon cessation of ventricular pacing associated with 1:1 ventriculoatrial conduction during paroxysmal supraventricular tachycardia is a useful diagnostic maneuver in the electrophysiology laboratory. BACKGROUND Despite various maneuvers, it can be difficult to differentiate atrial tachycardia from other forms of paroxysmal supraventricular tachycardia. METHODS The response upon cessation of ventricular pacing associated with 1:1 ventriculoatrial conduction was studied during four types of tachycardia: 1) atrioventricular nodal reentry (n = 102), 2) orthodromic reciprocating tachycardia (n = 43), 3) atrial tachycardia (n = 19) and 4) atrial tachycardia simulated by demand atrial pacing in patients with inducible atrioventricular nodal reentry or orthodromic reciprocating tachycardia (n = 32). The electrogram sequence upon cessation of ventricular pacing was categorized as “atrial-ventricular” (A-V) or “atrial-atrial-ventricular” (A-A-V). RESULTS The A-V response was observed in all cases of atrioventricular nodal reentrant and orthodromic reciprocating tachycardia. In contrast, the A-A-V response was observed in all cases of atrial tachycardia and simulated atrial tachycardia, even in the presence of dual atrioventricular nodal pathways or a concealed accessory atrioventricular pathway. CONCLUSIONS In conclusion, an A-A-V response upon cessation of ventricular pacing associated with 1:1 ventriculoatrial conduction is highly sensitive and specific for the identification of atrial tachycardia in the electrophysiology laboratory.

With use of transesophageal echocardiography, the short-term effects of transthoracic electrical cardioversion of atrial flutter (AFI) on atrial mechanical function and spontaneous echo contrast were determined. Thirty patients who had AFI for a mean of 6.4 +/- 12.2 months underwent transthoracic cardioversion. A transesophageal echocardiogram was recorded immediately before cardioversion, and left atrial appendage emptying velocity and spontaneous contrast were assessed serially at 1, 3, and 5 minutes after cardioversion in 28 patients, and also at 8, 10, and 15 minutes after cardioversion in a subgroup of 13 patients. Cardioversion was deferred in 2 patients (7%) because a thrombus was found in the left atrial appendage. Before cardioversion, spontaneous contrast was present in the left atrium in 7 of 28 patients (25%) who underwent cardioversion. The mean left atrial appendage emptying velocity of 54 +/- 22 cm/s before cardioversion fell by 26% to 40 +/- 25 cm/s at 1 minute after restoration of sinus rhythm (p

Purpose: Adenosine is a useful agent for the diagnosis and termination of tachycardias. The purpose of this study was to identify the rhythms for which adenosine is prescribed in hospitalized adults and to identify the reasons for its misuse. Patients and Methods: Data were collected from the medical records of 100 patients who received intravenous adenosine while hospitalized at a university medical center. The characteristics of the patients, rhythms treated with adenosine, and dosages of adenosine were analyzed. In addition, internal medicine house officers were administered a questionnaire referring to an electrocardiogram of atrial fibrillation with a rapid ventricular response. Results: The arrhythmias for which adenosine was administered consisted of regular, narrow-QRS complex tachycardias in 33% of patients; atrial fibrillation in 32% of patients; regular, wide-QRS complex tachycardias in 23% of patients; atrial flutter in 10% of patients, and multifocal atrial tachycardia in 2% of patients. The mean (± SD) number of doses of adenosine given to each patient was 1.6 ± 0.8, and the mean dose of adenosine was 7.8 ± 2.8 mg. Internal medicine house officers prescribed 70% of the doses of adenosine and were as likely to use it for patients with atrial fibrillation as were surgical house officers. There was a 2% incidence of proarrhythmia, including asystole and polymorphic ventricular tachycardia. Thirty-one percent of the 100 house officers in our survey misdiagnosed a 12-lead electrocardiogram of rapid atrial fibrillation as paroxysmal supraventricular tachycardia, suggesting that adenosine may have been misused for atrial fibrillation because of errors in rhythm diagnosis. Only 5% of those who correctly diagnosed atrial fibrillation also answered that adenosine would be likely to terminate the arrhythmia, suggesting that a misunderstanding that adenosine terminates atrial fibrillation is not a common reason for its misuse. Conclusions: Approximately 40% of hospitalized adults who are treated with adenosine receive the medication unnecessarily for atrial fibrillation or atrial flutter, and this misuse results in unnecessary expenses and risks of adverse effects. The primary reason that adenosine is misused for atrial fibrillation is the inability to recognize that rhythm on an electrocardiogram. House officers need additional education on the electrocardiographic recognition of atrial fibrillation.

Background Atrial fibrillation (AF) shortens the atrial effective refractory period (ERP) and predisposes to further episodes of AF. The purpose of this study was to determine the effect of verapamil and procainamide on these manifestations of AF-induced electrical remodeling. Methods and Results In adult patients without structural heart disease, the atrial ERP was measured before and after AF after pharmacological autonomic blockade and administration of verapamil (17 patients), procainamide (10 patients), or saline (20 patients). AF was then induced by rapid pacing. Immediately on AF conversion, the post-AF ERP was measured at alternating drive cycle lengths of 350 and 500 ms. In the saline group, the pre-AF and first post-AF ERPs at the 350-ms drive cycle length were 206±19 and 179±27 ms ( P P P =.8) or 500-ms (230±17 versus 232±20 ms, P =.6) drive cycle length. During determinations of the post-AF ERP, 105 secondary episodes of AF were unintentionally induced in 12% of verapamil patients compared with 90% and 80% of saline and procainamide patients ( P Conclusions Pretreatment with the calcium channel antagonist verapamil, but not the sodium channel antagonist procainamide, markedly attenuates acute, AF-induced changes in atrial electrophysiological properties. These data suggest that calcium loading during AF may be at least partially responsible for AF-induced electrical remodeling.

Unipolar Electrogram. introduction: The purpose (if this study was to determine the accuruey of the unipolar electrogram tor identifying the earliest site of ventricular activation. The earliest site of ventricular activation may he identified with the unipolar electrogram hy the absence of an R wave. However, the accuracy of this technique is unknown. Methods and Results: A sJn^^Ie ventricular premature complex was induced mechanically at the tip of an electrode catheter to simulate a ventricular premature depolarization site of origin. Unipolar electrograms were recorded from the right ventricular septum at the tip electrode and at 2, 5, 8, and 11 nmi from the electrode tip in 20 patients. No R waves were detected at the ventricular premature depolarization site of origin. R waves were detected in 4 of 20 patients (20%) at 2 mm from the tip electrode and 7 of 20 patients (35%) at 5. 8. and 11 mm from the tip electrode. An R wave was not ohserved at distances < 11 mm from the site of tachycardia origin in 13 of 20 patients (65%), Conclusions: While an R wave in the unipolar electrogram can he seen as close as 2 mm fnmi the site of impulse origin, the ahsence of an R wave as an indicator of the site of impulse origin in the right ventricle is highly inaccurate. Therefore, the ahsence of an R wave in the unipolar electrogram is unlikely to he an adequate guide for identiHcation of an effective target site for ahlation of right ventricular tachycardia. (./ Cardiovusc Electrophysiol. Vol. H. pp. 974-979, Scptemlwr

Background The probability of successful defibrillation has been determined in normal animals but not in patients undergoing defibrillator implantation. Therefore, the purpose of this prospective study was to determine the probability of successful defibrillation in humans on the basis of a step-down defibrillation energy requirement. Methods and Results Fifty-three consecutive patients underwent five separate inductions of ventricular fibrillation after the defibrillation energy requirement was determined with the use of small decrements and a step-down protocol (20, 15, 12, 10, 8, 6, 5, 4, 3, 2, 1, and 0.8 J). The first shock energy for defibrillation was either 1.0, 1.3, 1.5, 1.7, or 2.0 times the defibrillation energy requirement, and the likelihoods of successful defibrillation were 70±27%, 84±12%, 86±25%, 80±29%, and 88±32%, respectively ( P =.03). The frequencies of uniformly successful defibrillation (5 of 5 defibrillation attempts) were 30%, 27%, 60%, 64%, and 73%, respectively ( P =.01). Seven patients in whom the defibrillation energy requirement was P =.002). The likelihood of successful defibrillation at twice the defibrillation energy requirement was 98% in the 46 patients with a defibrillation energy requirement of >4 J and 67% in the 7 patients with a defibrillation energy requirement of P =.17). An absolute safety margin of 7 J was associated with a 96% probability of successful defibrillation. Conclusions The probability of successful defibrillation is 70% at the defibrillation energy requirement. The probability plateaus at 88%, at twice the defibrillation energy requirement. A 96% probability of successful defibrillation is achieved at an absolute safety margin of 7 J, and a 98% success rate is achieved at energies that are twice the defibrillation energy requirement if the defibrillation energy requirement is >4 J. If the defibrillation energy requirement is

Objectives. The goal of this study was to determine whether isolated diastolic potentials (IDPs) recorded during ventricular tachycardia (VT) are generated in zones of slow conduction and whether the arcs of block that bound these zones of slow conduction are functional or anatomic in nature. Background. No previous studies have systematically investigated the response to pacing during VT and sinus rhythm at sites where IDPs are recorded. Methods. The study included 11 patients with a previous infarction who underwent radiofrequency catheter ablation of 15 hemodynamically stable, sustained VTs and in whom an IDP that could not be dissociated from the VT was detected during mapping. Results. Pacing during VT at the site where the IDP was recorded resulted in concealed entrainment in each of the 15 VTs. In 10 of the 15 VTs, an IDP was present during sinus rhythm at the same site at which a diastolic potential was recorded during VT. In nine VTs, the isolated potential occurred early in diastole; in these cases, the QRS configuration during pacing in the setting of sinus rhythm was different from that during VT. In six VTs, the isolated potential occurred later in diastole, and in these cases, the QRS configuration during pacing in the setting of sinus rhythm was the same as that during VT. Conclusions. Isolated diastolic potentials may often be generated in an area of slow conduction bounded by arcs of block that are anatomically determined and present during sinus rhythm.

Fascicular Tachycardia. Introduction: Idiopathic left ventricular tachycardia typically has a right bundle branch block configuration. The purpose of this case report is to demonstrate that idiopathic ventricular tachycardia arising in or near the left posterior fascicle also may have a left bundle branch block configuration. Methods and Results: A 27-year-old woman underwent an electrophysiologic procedure because of recurrent, verapamil-responsive, wide QRS complex tachycardia. Two types of ventricular tachycardia (cycle lengths 330 to 340 msec) were reproducibly inducible, one with a right bundle branch block configuration and left-axis deviation that had been documented clinically, and the other with a left bundle branch block configuration and axis of zero. A Purkinje potential recorded at the junction of the left ventricular mid-septum and inferior wall preceded the ventricular complex by 40 msec in both tachycardias. A single application of ra-diofrequency energy at this site successfully ablated both ventricular tachycardias. Conclusion: The findings of this case report demonstrate that idiopathic ventricular tachycardia arising in or near the left posterior fascicle may have a left bundle branch block configuration

The chronic defibrillation energy requirement (DER) is believed to remain clinically stable in patients with defibrillators. Six patients (two with an epicardial and four with a nonthoracotomy system) were identified with a rise in their chronic DER, which eliminated a 10-J safety margin, thus necessitating a defibrillator lead system revision. The mean increase in DER was 14.7 +/- 4 J and was discovered at a mean of 16.0 +/- 18 months (range 2-41) following implantation. Management included placement of a defibrillator with a biphasic waveform, placement of an additional defibrillation electrode, or both. At 2 months following revision of the defibrillation system, a 10-J DER safety margin was present in each patient. In some patients, there is a progressive increase in the chronic DER with elimination of a 10-J safety margin necessitating revision of the defibrillation system. Routine reevaluation of the chronic DER, therefore, is necessary to identify these patients.

Background Concealed entrainment has been useful in guiding catheter ablation of monomorphic ventricular tachycardia in patients with coronary artery disease. However, not all sites with concealed entrainment result in successful ablation of the targeted ventricular tachycardia. The purpose of this prospective study was to identify factors at sites that demonstrate concealed entrainment that differentiate effective from ineffective target sites. Methods and Results In 14 consecutive patients with hemodynamically stable monomorphic ventricular tachycardia and coronary artery disease, radiofrequency ablation of 26 ventricular tachycardias was performed. Ablation was attempted at 46 sites that demonstrated concealed entrainment. Twenty-five of the targeted ventricular tachycardias (96%) were successfully ablated. The positive predictive value of concealed entrainment for successful ablation was 54%; it increased to 72% in the presence of a stimulus-QRS interval/ventricular tachycardia cycle length ratio of ≤70%, to 82% in the presence of a match of the stimulus-QRS and electrogram-QRS interval, and to 89% in the presence of isolated middiastolic potentials that could not be dissociated from ventricular tachycardia during entrainment. Conclusions The positive predictive value of concealed entrainment for identification of successful ablation sites in patients with sustained ventricular tachycardia and coronary artery disease can be significantly enhanced by the presence of associated mapping criteria, particularly an isolated mid diastolic potential that cannot be dissociated from the tachycardia.

Objectives. The purpose of this study was to describe the long-term follow-up results in 62 patients with atrial fibrillation and an uncontrolled ventricular rate, who underwent radiofrequency modification of the atrioventricular (AV) node.Background. Previous studies in small numbers of patients have suggested that radiofrequency modification may be effective in controlling the ventricular rate in patients with atrial fibrillation, but long-term follow-up data have been lacking.Methods. The subjects of this study were 62 consecutive patients (mean age ± SD 65 ± 14 years; 43 with structural heart disease) who underwent an attempt at radiofrequency modification of the AV node because of symptomatic, drug-refractory atrial fibrillation with an uncontrolled ventricular rate. The atrial fibrillation was chronic in 46 patients and paroxysmal in 16. Radiofrequency energy was applied to the posteroseptal or midseptal right atrium to lower the ventricular rate in atrial fibrillation to 120 to 130 beats/min during an infusion of 4 μg/min of isoproterenol.Results. Short-term control of the ventricular rate was successfully achieved without the induction of pathologic AV block in 50 (81%) of 62 patients. Inadvertent high degree AV block occurred in 10 (16%) of 62 patients, with the AV block occurring at the time of the procedure in 6 patients and 36 to 72 h after the procedure in 4. During 19 ± 8 months of follow-up (range 4 to 33), 5 (10%) of 50 patients had a symptomatic recurrence of an uncontrolled rate during atrial fibrillation. Overall, adequate rate control at rest and during exertion, without pathologic AV block, was achieved long term in 45 (73%) of 62 patients. Among 37 patients with a successful outcome, left ventricular ejection fraction increased from (mean ± SD) 0.44 ± 0.14 to 0.51 ± 0.10 one year later (p < 0.001). Complications other than AV block included polymorphic ventricular tachycardia 10 to 24 h after the procedure in two patients who had a predisposing factor for ventricular tachycardia and sudden death 1 to 5 months after the procedure in two patients with idiopathic dilated cardiomyopathy, one of whom had a pacemaker for AV block.Conclusions. In ∼70% of properly selected patients with atrial fibrillation and an uncontrolled ventricular rate, radiofrequency modification of the AV node results in excellent long-term control of the ventricular rate at rest and during exertion.(J Am Coll Cardiol 1997;27:113–21)>

The main finding of this prospective, controlled study is that amiodarone and desethylamiodarone plasma concentrations < 1 mg/L are associated with a 23% increase in the acute defibrillation energy requirement and with a 31% increase in the requirement for a subcutaneous patch or array. The defibrillation energy requirement does not correlate with the plasma concentrations of amiodarone, desethylamiodarone, amiodarone plus desethylamiodarone, or with the duration or daily dosage of amiodarone therapy.

Introduction: A variety of factors, including the number of defibrillation electrodes and shocking capacitance, may influence the defibrillation efficacy of an implantable defibrillator system. Therefore, the purpose of this study was to compare the defibrillation energy requirement using a 125 uF two-electrode defibrillation system and a 90 uF three-electrode defibrillation system. Methods and Results: The defibrillation energy requirements measured with both systems were compared in 26 consecutive patients. The two-electrode system used a single transvenous lead with two defibrillation coils in conjunction with a biphasic waveform from a 125 uF capacitor. The three-electrode system used the same transvenous lead, utilized a pectoral implantable defibrillator generator shell as a third electrode, and delivered the identical biphasic waveform from a 90 uF capacitor. The two-electrode system was associated with a higher defibrillation energy requirement (10.8±5.5 J) than was the three-electrode system (8.9±6.7 J, p < 0.05), however, the leading edge voltage was not significantly different between systems (361±103 V vs. 397±123 V, P e 0.07). The two-electrode system also had a higher shocking resistance (49.0±9.0 ohms vs. 41.4±7.3 ohms, p < 0.001) and a lower peak current (7.7±2.6 A vs. 10.1±3.7 A, p < 0.001) than the three-electrode system. Conclusions: A three-electrode defibrillation system that utilizes a dual coil transvenous lead and a subcutaneous pectoral electrode with lower capacitance is associated with a lower defibrillation energy requirement than is a dual coil defibrillation system with higher capacitance. This finding suggests that the utilization of a pectoral generator as a defibrillation electrode in conjunction with smaller capacitors is a more effective defibrillation system and may allow for additional miniaturization of implantable defibrillators.

Temperature monitoring may be helpful for ablation of accessory pathways, however its role in ablation of atrioventricular nodal reentrant tachycardia (AVNRT) using the slow pathway approach is unclear. Therefore, the purpose of this study was to prospectively compare slow pathway ablation for AVNRT using fixed power or temperature monitoring. The study included 120 patients undergoing ablation for AVNRT. Patients were randomly assigned to receive either fixed power at 32 watts, or to temperature monitoring with a target temperature of 60°C. The primary success rate was 72% in the fixed power group and 95% in the temperature monitoring group (p=0.001). The ablation procedure duration (35±29 min vs 35±30 min; p=0.9), fluoroscopic time (32±17 vs 35±19 min; p=0.4), mean number of applications (10.2±8.1 vs 8.4±7.9; p=0.2), and coagulum formation per application (0.2% vs 0.5%; p=0.6) were statistically similar in the fixed power and temperature monitoring groups, respectively. The mean temperature (47.3±4.8°C vs 48.6±3.8°C; p

The purpose of this study was to compare the atrial-His intervals generated during programmed atrial stimulation in patients with and without dual atrioventricular nodal physiology and with and without inducible atrioventricular nodal reentrant tachycardia. Programmed atrial stimulation at a basic-drive cycle length of 500 to 600 msec was performed in 180 patients. The minimum atrial-His interval was defined as the atrial-His interval of the basic-drive beats. The maximum atrial-His interval was defined as the longest A2H2 interval. The criterion for dual atrioventricular nodal physiology was an increment of 50 msec in the A2H2 interval in association with a 10 msec decrement in the A1A2 interval. The minimum atrial-His interval was significantly shorter (106 +/- 34 msec vs 116 +/- 29 msec; p0.05) and the maximum atrial-His interval significantly longer (304 +/- 101 msec vs 222 +/- 56 msec; p0.001) in the 87 patients who had atrioventricular nodal reentry than in the 93 patients who did not. Among the 87 patients who had atrioventricular nodal reentry, the maximum atrial-His interval was significantly longer in 53 patients who had dual atrioventricular nodal physiology than in 34 patients who did not (340 +/- 105 msec vs 249 +/- 62 msec; p0.001). Among the 66 patients who had dual atrioventricular nodal physiology, the maximum atrial-His interval was significantly longer in 53 patients who had atrioventricular nodal reentry than in 13 patients who did not (340 +/- 105 msec vs 268 +/- 61 msec; p0.01). The insensitivity of the conventional dual atrioventricular nodal physiology criterion for the detection of dual atrioventricular nodal pathways is in part attributable to a lesser degree of slowing of conduction in the slow pathway relative to the fast pathway in some patients who have atrioventricular nodal reentry. The inability to demonstrate atrioventricular nodal reentry despite the presence of dual atrioventricular nodal physiology in some persons may be attributable in part to an inadequate degree of conduction delay in the slow pathway.

Objectives. The purpose of this study was to assess the clinical efficacy of radiofrequency ablation of the slow pathway in patients with documented but noninducible paroxysmal supraventricular tachycardia (PSVT) who have evidence of dual atrioventricular (AV) node pathways.Background. Patients with a documented history of PSVT at times do not have inducible PSVT in the electrophysiology laboratory. Because dual AV node pathways serve as the substrate for AV node reentrant tachycardia (AVNRT), ablation of the slow pathway potentially may be useful in these patients.Methods. The subjects in this prospective study were seven consecutive patients who underwent an electrophysiologic procedure because of documented PSVT and were found to have dual AV node physiology or inducible single AV node echo beats, but no inducible PSVT despite the administration of isoproterenol and atropine. Their mean (±SD) age was 33 ± 13 years, and they had been symptomatic for 12 ± 12 years. The frequency of the episodes of PSVT ranged from ≥1/day to 1/month. The rate of the documented episodes ranged from 170 to 260 beats/min, and discrete P waves were not apparent. Slow pathway ablation was performed with 9 ± 4 applications of radiofrequency energy using a combined anatomic and electrogram mapping approach.Results. All evidence of dual AV node pathways was eliminated in six patients, and dual AV node physiology remained present in one patient. During a mean follow-up period of 15 ± 10 months (range 8 to 27), no patient had a recurrence of symptomatic tachycardia (success rate 95% confidence interval 65% to 100%).Conclusions. Slow pathway ablation may be clinically useful in patients with documented but noninducible PSVT who have evidence of dual AV node pathways.

Background The acute effect of atrial fibrillation (AF) on the atrial effective refractory period (ERP) in humans is unknown. Methods and Results In 20 patients without structural heart disease, the atrial ERP was measured before and after pacing-induced AF at drive cycle lengths of 350 and 500 ms. Immediately after spontaneous AF conversion, the post-AF ERP was measured. The pre-AF ERPs at 350 and 500 ms were 206±23 and 216±17 ms, respectively. The time to spontaneous conversion of AF was 7.3±1.9 minutes. The first post-AF ERPs at drive cycle lengths of 350 and 500 ms were 175±30 ms ( P P P r =.5). Conclusions In humans, several minutes of induced AF is sufficient to shorten the ERP for up to ≈8 minutes. The temporal recovery of the ERP is reflected in progressively shorter episodes of reinduced AF. These data imply that AF transiently shortens the atrial wavelength and suggest a mechanism by which AF may perpetuate itself.

Background The purpose of this study was to examine the spatial resolution of unipolar atrial pace mapping by pacing at adjacent sites within the coronary sinus and the right atrium. Methods and Results Unipolar pacing from each pole of a quadripolar catheter was performed in the coronary sinus (n=29) and in the right atrium (n=10). Pacing from the distal electrode was used to simulate the site of origin of an atrial tachycardia. These P waves were compared with the P waves generated by unipolar pacing from each of the three proximal electrodes. The P waves were analyzed for changes in amplitude, duration, and configuration. Pacing within the coronary sinus resulted in significant changes in amplitude and duration at distances of 17 and 21 mm from the distal pole, respectively. Similarly, pacing in the right atrium resulted in significant changes in amplitude and duration at distances of 17 and 32 mm from the distal pole, respectively. No significant changes in configuration were noted in the coronary sinus in any lead at pacing sites ≤32 mm from the distal pole. Configurational changes were noted in the right atrium at pacing sites 17 mm from the distal pole. Conclusions The spatial resolution of unipolar atrial pace mapping is ≈17 mm. These findings indicate that mapping techniques that depend on the accurate discrimination of P-wave morphology, such as pace mapping or concealed entrainment, are likely to be imprecise when used in the atria.

Biphasic shocks are believed to be superior to monophasic shocks. Monophasic anodal shocks, as opposed to cathodal shocks, are associated with improved defibrillation energy requirements (DERs). However, it is unclear how the DER of anodal monophasic shocks compare with conventional biphasic shocks. Therefore the purpose of this study was to prospectively compare the DER of an anodal monophasic shock with that of a cathodal biphasic shock. A transvenous defibrillation lead with distal and proximal shocking electrodes was used. The subjects of this study were 20 consecutive patients with a mean age of 64.2 +/- 10.5 years ( +/- SD) and a mean left ventricular ejection fraction of 0.36 +/- 0.18. Six had had cardiac arrest. The DER, defined as the lowest energy that converted ventricular fibrillation to sinus rhythm, was determined twice with a step-down protocol (25 J, 20 J, 15 J, 10 J, 5 J, 3 J, 1 J). If the DER wasor = 25 J, then a subcutaneous patch was deemed necessary for system implantation. In random order the DER was determined with a monophasic anodal shock (distal electrode positive) and then with a cathodal (first phase, distal electrode negative) biphasic shock. The mean DER with anodal monophasic shocks was 15.1 +/- 8.5 J compared with 13.6 +/- 8.1 J with cathodal biphasic shocks (p = 0.4). A DERor = 25 J was present in three patients with the monophasic waveform and in three patients with the biphasic waveform (p = NS). In conclusion, the DER and frequency of subcutaneous patch use with an anodal monophasic waveform is comparable to that obtained with cathodal biphasic waveform.

A study during the era of surgical ablation suggested that atrioventricular (AV) nodal conduction is faster in patients with accessory pathways than in controls. In the present study, AV nodal characteristics were studied in 30 patients who underwent radiofrequency ablation of an accessory pathway and compared to 23 control patients. Sinus cycle length, AH and HV intervals, AV block cycle length, ventriculoatrial (VA) block cycle length, AV nodal effective refractory period, and VA effective refractory periods were measured in control and postablation accessory pathway patients before and after autonomic blockade with 0.04 mg/kg of atropine and 0.2 mg/kg of propranolol. The mean sinus cycle length in the control and accessory pathway groups did not differ significantly at baseline (798 +/- 211 and 766 +/- 156 msec, respectively) or after autonomic blockade (654 +/- 98 and 649 +/- 108 msec, respectively). The mean AH interval in the accessory pathway group (77 +/- 15 msec) was significantly shorter than in the control group (91 +/- 22 msec; p0.05) at baseline; however, there was no difference after autonomic blockade. No other significant differences were observed between the accessory pathway and control groups. These results demonstrate that AV nodal properties of patients with accessory pathways are not significantly different from controls and suggest that previously reported differences may have been due to selection bias.

The Accufix (Telectronics Pacing Systems, Englewood, Colo.) atrial active fixation pacemaker lead has a preformed J stiff retention wire than can fracture and erode through the atrium. We screened 85 patients with digital fluoroscopy and detected 18 (21%) lead fractures. Fourteen (16%) leads were successfully extracted by percutaneous techniques. The mean time for extraction and placement of a new atrial lead was 109 ± 53 min, and a lead > 1 year old but not in the presence of a fracture was associated with a significantly longer extraction time. There were two extraction complications. One patient had a fever following the extraction, and one patient had a focal sensory deficit 1 week after the extraction probably caused by a paradoxical embolus. Standard percutaneous extraction tools can be used for successful and safe removal of a fractured Accufix lead.

This study examines the relation between QT dispersion and the inducibility of ventricular tachycardia (VT) in 35 consecutive patients with coronary artery disease who underwent electrophysiologic testing for evaluation of nonsustained VT. The mean age of the patients was 66 +/- 9 years (+/- SD) and the mean left ventricular ejection fraction was 0.36 +/- 0.14. In 6 patients in whom sustained, monomorphic VT was inducible by programmed ventricular stimulation, QT dispersion was significantly greater than in the 29 patients in whom VT was not inducible (126 +/- 35 vs 67 +/- 25 ms, p0.001). All patients who had a QT dispersion120 ms had inducible sustained monomorphic VT, and no patient who had a QT dispersion90 ms had inducible VT. The patients who had inducible VT dis not differ significantly from those who did not with regard to age, gender, ejection fraction, RR interval, or mean QT. In conclusion, in patients with coronary artery disease who have nonsustained VT, inducibility of monomorphic VT is associated with an increase in QT dispersion. QT dispersion may be helpful in predicting which patients with nonsustained VT are and are not likely to have inducible VT by programmed stimulation.

Previous studies have reported a significant morbidity and mortality associated with coronary artery bypass graft (CABG) surgery in conjunction with the placement of an implantable cardioverter defibrillator (ICD) with an epicardial lead system. In the absence of a control group, how significantly the component of concomitant placement of the ICD system contributes to these untoward outcomes remains unknown. The purpose of this study was to assess the short- and long-term complications in patients undergoing CABG surgery in conjunction with the placement of an ICD with epicardial leads and to compare these complications with those of patients who had only CABG surgery (control group). The study group (group A) consisted of 56 patients who underwent CABG surgery and placement of an ICD pulse generator with epicardial leads. A control group (group B) consisted of 56 patients who underwent CABG surgery only during the same time period. The two groups were matched for age, sex distribution, left ventricular function, surgical approach, number of bypass grafts per patient, bypass pump time, and length of follow-up period. The early mortality for group A was 7.1% versus 1.8% for group B (p > 0.05). The incidence of early morbidity (congestive heart failure, infection, supraventricular and ventricular arrhythmias) for groups A and B was similar (26.8% vs 25.0%, p > 0.05). The incidence of late mortality and morbidity (progression of congestive heart failure, recurrence of coronary events, chronic atrial fibrillation) for groups A and group B were 7.7% versus 5.5% (p > 0.05) and 23.1% versus 21.8% (p > 0.05), respectively. However, death caused by cardiopulmonary difficulties was more frequent in group A than group B (12.5% vs 1.8%, p < 0.05). With the availability of the nonthoracotomy lead system and the pulse generator capable of delivering biphasic shock waveform, to place such an ICD system at a later time after the CABG surgery appears to be the preferred approach to treat patients who need both surgical coronary revascularization and ICD.

Long RP Tachycardia, introduction: The purpose of this study is to describe a simple and reliuhle diagnostic maneuver that allows for the rapid differentiation of atypical AV nodal reentrant tachycardia (AVNRT) from other causes of long KP tachycardia. Lonf^ KP tachycardias may he caused by atypical AVNRT, orthodrnmic reciprocating tachycardia (ORT) involving a .slowly conducting retrograde accessory pathway, or atrial tachycardia. The dilTerentiation of atypical AVNRT from ORT or atrial tachycardia may be difficult, especially when the differential diagnosis includes a posteroseptal accessory pathway or an atrial tachycardia arising in the posteroseptal right atrium. Methods and Results: Twelve patients with atypical AVNRT, 21 with ORT, and 12 with an atrial tachycardia diagnosed using conventiitnal criteria were enrolled In this study. The atrialHis (AH) interval was measured at the His-hundle position during the tachycardia and during atrial pacing from the high right atrium at the tachycardia cycle length in the setting of sinus rhythm. In patients with atypical AVNRT, the mean AH interval was 69 msec ± 50 msec (± SD) longer during high right atrial pacing than during the tachycardia (P < 0.001). In 10 of 12 patients with atypical AVNRT, the AH interval during atrial pacing was more than 40 msec longer than the .\H interval measured during the tachycardia. In contra.st. In patients with ORT or atrial tachycardia, the difYerences in .AH interval hetween atrial pacing and tachycardia were never more than 20 and 10 msec, respectively. Conclusion: The difference in the AH interval between atrial pacing and the tachycardia allows a simple and rapid means of difierentiating atypical AVNRT from other types of long RP tachycardias. (J Cardiovasc Electrophysiol, Vol. 6, pp. 700-710. September 1995)

Coronary Sinus Ostium. Introdttctlon: Tbe purpose of tbis study was to perform a quantitative fluoroscopic analysis of the coronary sinus ostium and its relationship to the His bundle in patients witb and without AV nodal reentrant tacbycardia. Sites of slow patbway ablation are often near the coronary sinus ostium, which can be located witbin a few millimeters of tbe His bundle. Wbetber such close proximity of the coronary sinus ostium to tbe His bundle is unique to patients with AV nodal reentrant tachycardia is unknown. Methods and Results: Fifty consecutive patients (mean age 39 ± 14 years) with no structural heart disease underwent electropbysiologic testing and radiofrequency ablation. Tbe study group consisted of 28 patients witb inducible AV nodal reentrant tachycardia or dual AV nodal physiology and 22 patients in tbe control group. A coronary sinus venogram was performed in each patient. The coronary sinus ostium was similar in size in tbe study group (II.4 ± 4.5 mm) and in the control group (10.5 ± 3.6 mm, P = 0.2). The coronary sinus ostium was funnel shaped in balf of the study patients and in half of the control patients {P = LO). Tbe mean distance from the upper lip of tbe coronary sinus ostium to tbe tip of tbe His bundle catheter was 9.7 ± 5.5 mm in the study group and 10.4 ± 5.1 mm in the control group (P = 0.7). The mean distance from tbe lower lip of tbe coronary sinus ostium to tbe tip of the His-bundle catheter in tbe study group was 20.1 ± 6.1 mm and 19.5 ± 5.6 mm in tbe control group {P = 0.7). Conclusion: This study demonstrates a wide range of normal coronary sinus ostium diameters, morphology, and anatomic relationships witb surrounding structures, with no demonstrable correlation to the presence or absence of dual AV node pbysiology or AV nodal reentrant

Coronary revascularization has been suggested as sole therapy for secondary prevention of sudden cardiac arrest associated with ischemia. The use of implantable defibrillators (ICD) in combination with coronary revascularization for this patient population is unclear. Among 412 consecutive patients receiving an ICD, 23 (6%) were identified as sudden cardiac arrest survivors who were noninducible with programmed stimulation and had unstable angina or ischemia on a functional study; they underwent successful coronary revascularization. During a follow-up of 34 ± 18 months, 10 (43%) of the 23 patients received ICD shocks (8 ± 8 per patient, range 1 to 22 shocks), and nine of the 10 patients had syncope/presyncope associated with at least one ICD discharge. Patients with ICD discharges were compared with those without ICD discharges, and no clinical characteristics were statistically different between the two groups. In conclusion, revascularization alone may be inadequate therapy for survivors of sudden cardiac arrest associated with ischemia who are noninducible with programmed stimulation, and clinical variables cannot predict which patients are likely to have recurrent malignant ventricular arrhythmias.

Background Multicomponent atrial electrograms and “slow pathway potentials” are helpful in identifying target sites for radiofrequency catheter ablation of the slow pathway in patients with atrioventricular (AV) nodal reentrant tachycardia. The purpose of this study was to compare the atrial electrograms recorded at various locations in the right atrium in patients with and without AV nodal reentrant tachycardia to assess the specificity of multicomponent atrial electrograms and possible slow pathway potentials both for the posteroseptal right atrium and for patients with AV nodal reentrant tachycardia. Methods and Results In 25 patients with AV nodal reentrant tachycardia and 23 control patients without AV nodal reentrant tachycardia or dual AV nodal physiology, atrial electrograms with an AV ratio of ≤1:2 were recorded at the posteroseptal right atrium near the coronary sinus ostium and in the right atrium near the posterior, lateral, and anterior aspects of the tricuspid annulus. Attempts were made to identify broad, multicomponent, and double atrial electrograms. There were no significant differences between the patients with and without AV nodal reentrant tachycardia in the mean number of deflections in the atrial electrograms or in the mean duration of the atrial electrograms recorded at any of the atrial sites. In all patients, the number of atrial electrogram deflections and the atrial electrogram duration were significantly greater at the posteroseptal position than at the other three atrial sites. The prevalence of potentials with the appearance of slow pathway potentials in the posterior septum was similar in patients with and without AV nodal reentrant tachycardia (68% and 70%, respectively). The prevalence of these potentials was 6% to 25% at the other three atrial sites ( P Conclusions The atrial electrogram characteristics that have been found to be useful in identifying effective posteroseptal slow pathway ablation sites in patients with AV nodal reentrant tachycardia are equally prevalent in patients without AV nodal reentrant tachycardia or dual AV nodal physiology. Atrial electrograms in the posteroseptal area are broader and contain more deflections than at other areas in the right atrium, possibly because of conduction properties of the posterior transitional zone that are independent of the presence of AV nodal reentrant tachycardia.

No prospective studies have compared sotalol and amiodarone during electropharmacologic testing. The purpose of this prospective, randomized study was to compare the electrophysiologic effects of sotalol and amiodarone in patients with coronary artery disease and sustained monomorphic ventricular tachycardia (VT). Patients with coronary artery disease and sustained monomorphic VT inducible by programmed stimulation were randomly assigned to receive either sotalol (n = 17) or amiodarone (n = 17). The sotalol dose was titrated to 240 mg twice daily over 7 days. Amiodarone dosing consisted of 600 mg 3 times daily for 10 days. An electrophysiologic test was performed in the baseline state and at the end of the loading regimen. An adequate response was defined as the inability to induce VT or the ability to induce only relatively slow hemodynamically stable VT. During the follow-up electrophysiologic test, 24% of patients taking sotalol and 41% of those taking amiodarone had an adequate response to therapy (p = 0.30). Amiodarone lengthened the mean VT cycle length to a greater degree than sotalol (28% vs 12%, p < 0.01). There were no significant differences in the effects of sotalol and amiodarone on the ventricular effective refractory period. In patients with coronary artery disease, amiodarone and sotalol are similar in efficacy in the treatment of VT as assessed by electropharmacologic testing. The effects of the 2 drugs on ventricular refractoriness are similar, but amiodarone slows VT to a greater extent than sotalol.

The purpose of this study was to compare implant charges and convalescence for transvenous and epicardial defibrillation systems. Hospital stay, intensive care utilization, professional fees, and hospital bills were compared in 44 patients who underwent implantation of a cardiac defibrillator between September 1991 and May 1993. Twenty-five consecutive patients received an epicardial lead system, while 19 consecutive patients underwent implantation of the entire transvenous defibrillation system in the electrophysiology laboratory. There were no significant differences between the two groups in mean age or left ventricular ejection fraction. There was a significant reduction in postoperative hospital convalescence from 7.2 ± 2.0 days with epicardial systems to 3.1 ± 1.5 days with transvenous systems (P < 0.001). Postoperative intensive care unit stay was significantly reduced with transvenous systems compared with epicardial systems (0.1 ± 0.2 vs 1.5 ± 0.9 days; P < 0.001). Hospital charges were also significantly reduced with the transvenous lead system implants. Mean implant charges were lower with transvenous systems; $32,090 ±$2,620 vs $38,307 ±$2,701 (P < 0.001); convalescence charges were lower: $5,861 ±$5,010 vs $12,447 ±$4,969 (P < 0.001); the total hospital bill was also significantly lower with transvenous systems: $53,459 ±$12,588 vs $71,981 ±$16,172 (P < 0.001). Professional fees for implantation ($4,131 ±$1,724 vs $6,100 ± 0, P < 0.001), convalescence care ($1,258 ±$960 vs $2,846 ±$1,770; P < 0.001), and total professional fees ($12,925 ±$4,772 vs $15,731 ±$4,055, P < 0.05) were lower in the transvenous defibrillation group. In conclusion, transvenous defibrillation lead systems are associated with significantly shorter postoperative recovery and significantly lower hospital and professional charges.

Double Atrial Response. This case report describes a patient in whom a single ventricular depolarization resulted in a double atrial response and the initiation of atypical AV nodal reentrant tachycardia after successful radiofrequency ablation of typical AV nodal reentrant tachycardia using the slow pathway approach. (J Cardiovasc Electrophysiol, Vol. 4, pp. 695-701

Ablation of Atypical Atrioventricular Nodal Reentrant Tachycardia. Introduction: Published reports of radiofrequency ablation of atypical atrioventricular nodal reentrant tacbycardia (AVNRT) have been limited. We present our experience in 10 consecutive patients with atypical AVNRT wbo underwent radiofrequency ablation of tbe "slow" AV nodal patbway. Methods and Resttlts: Tbere were 9 females and 1 male; tbeir mean age was 44 ± 19 years (± SD). Tbe mean A\ NRT cycle length and ventriculoatrial (VA) interval at tbe His position durin}^ AVNRT were 340 ± 50 msec and 200 ± 70 msec, respectively. Tbe slow putbway was successfully ablated in all patients with a mean of 10 ± 7 radiofrequency energy applications in the postLTO.septal rigbt atritim near the coronary sinus os. Tbe mean procedure duration was 100 ± 35 minutes. Tbere were no complications. In 4 patients, target sites were identified during sinus rbytbm by mapping for possible slow patbway potentials. In tbe other 6 patients, target sites were identified by mapping retrograde atrial activation during AVNRT or ventricular pacing. Tbe VA times at successful target sites were a mean of 45 ± 30 msec less tban tbe VA time at tbe His catbetcr during AVNRT. There were no differences in success rate, number of radiofrequency energy applications, or procedure duration between patients in wbom mapping was guided by possible slow patbway potentials or by retrograde atrial activation. During 6 ± 3 months of follow-up, I patient bad a recurrence of atypical AVNRT and underwent a second ablation procedure, wbich was successful. Conclusion: Radiofrequency ablation of atypical AVNRT can be safely and effectively accomplisbed when target sites are identified based eitber on possible slow patbway potentials during sinus rbytbm or retrograde atrial activation times during tachycardia, f./ Cardiovasc Electrophysiol, Vol. 4, pp. 526-532, October 1993) ia. (.i

Twenty-three consecutive patients (20 men and 3 women) with coronary artery disease and nonsustained ventricular tachycardia (VT) in whom sustained VT was not inducible in a baseline electrophysiology test underwent repeated testing during isoproterenol infusion to determine the inducibility of sustained monomorphic VT. After the baseline study, each patient received a 2 to 4 microgram/min infusion of isoproterenol (mean 2.5 +/- 0.8 microgram/min). The sinus cycle length shortened by a mean of 29% +/- 9% and programmed stimulation was repeated. Nineteen patients had no inducible sustained, monomorphic VT, two patients had only inducible nonsustained VT, and two patients had ventricular fibrillation. Patients were followed up for 10 to 20 months (mean 14.4 +/- 2.9 months) and had no syncope, sustained monomorphic VT, or sudden death. Isoproterenol infusion during programmed stimulation in patients with coronary heart disease and nonsustained VT does not facilitate the induction of sustained monomorphic VT.

Some centers have suggested complete elimination of slow pathway function to ensure a successful long-term outcome after slow pathway ablation to eliminate AVNRT. 1 The results of the present study demonstrate that this may not be necessary. As long as an isoproterenol infusion is administered and AVNRT is no longer inducible, residual slow pathway function with or without a single AV nodal echo beat is an adequate end point for the ablation procedure. Once the inducibility of AVNRT has been eliminated, attempts to completely ablate the slow pathway may serve only to prolong the procedure and to expose the patient and the operators to unnecessary radiation exposure.

Implantable cardioverter-defibrillators (ICDs) with nonthoracotomy lead systems are widely available, and are implanted either in the electrophysiology laboratory or the operating room. The purpose of this study was to prospectively evaluate the safety and efficacy of nonthoracotomy ICD implantation in an electrophysiology laboratory versus an operating room. During a 7-month period, 62 consecutive ICDs with nonthoracotomy lead systems were implanted in patients in an electrophysiology laboratory. During the next 10 months, 110 consecutive ICDs were implanted in patients in a surgical operating room. All ICD implantations were performed under general anesthesia by electrophysiologists. There were no differences in age (58 ± 14 vs 62 ± 12 years , p = 0.06), gender distribution ( p = 0.3), frequency of structural heart disease (97% vs 97%, p = 0.9), ejection fraction (0.31 ± 0.15 vs 0.29 ± 0.13, p = 0.3), or presentation with cardiac arrest (65% vs 53%, p = 0.2) between patients undergoing ICD implantation in the electrophysiology laboratory and operating room, respectively. The rate of successful implantation and of complications for systems implanted in the electrophysiology laboratory (95% and 13%, respectively) and in the operating room (98% and 14%, respectively) were similar ( p = 0.4 and p = 0.8, respectively). Specifically, the rate of infection (0% vs 4%, p = 0.3) and hematoma formation (2% vs 4%, p = 0.8) were not statistically significantly different. Three patients who had undergone ICD implantation in an operating room died within 30 days. ICDs with nonthoracotomy lead systems can be implanted with a similarly high rate of success and acceptable complication rate in the electrophysiology laboratory and in the operating room.

A 46-year-old man with a history of sustained monomorphic ventricular tachycardia underwent an implantation of a third generation multiprogrammable implantable cardioverter defibrillator. One year post implant, while manipulating a remote control to a radiofrequency modulated toy car, the patient experienced a defibrillator discharge not preceded by an arrhythmia prodrome. Subsequent interrogation of the defibrillator revealed that a 34-ioule shock had been delivered and had been preceded by RR intervals ranging from 141–406 msec, consistent with sensing lead noise. The remote control utilizes a 12-volt battery and has a carrier frequency of 75.95 MHz and a modulating frequency of 50 Hz. Evaluation of the remote control and de/ibrillator interaction revealed that the remote control was able to trigger tachyarrhythmia sensing and reproduce the clinical episode. Interference was present only when the remote control was within 8 cm of the pulse generator and at specific angles relative to the device and only when the antenna length was > 45 cm. Interference was eliminated when a ground wire was attached to the antenna and when an aluminium shield was placed between the pulse generator and the remote control. This case report suggests that patients with third generation multiprogrammable defibrillators should be cautioned against close contact with potential sources of electromagnetic interference, such as remote control units.

No prior studies have evaluated the relationship between the site of right ventricular stimulation, the site of prior infarction, and the inducibility of ventricular tachycardia (VT). This study was performed to determine if the location of pathologic Q waves influences the inducibility of VT at various right ventricular sites in patients with coronary artery disease (CAD) and a history of myocardial infarction (MI). In 30 patients with a history of sustained, monomorphic VT, CAD, prior MI, and pathologic Q waves, programmed ventricular stimulation was performed at the right ventricular apex, septum, and outflow tract, in random order. There was electrocardiographic evidence of an MI that was inferior in 11 patients, anterior in 10 patients, and both inferior and anterior in 9 patients. Sustained, monomorphic VT was induced in 27 of 30 patients (90%). There were no significant differences among the three sites in the rate of inducibility of VT. The rate of inducible VT at each of the three right ventricular sites was not affected by the location of prior infarction. In conclusion, among patients with sustained, monomorphic VT, CAD, and a history of MI, the incidence of inducible sustained, monomorphic VT is not influenced by the location of prior infarction, regardless of whether programmed ventricular stimulation is performed at the right ventricular apex, septum, or outflow tract.

Defibriiiation Energy Requirements. Introduction: Defibrillation energy requirements in patients with nonthoracotomy defibrillators may increase within several months alter implantation. However, the stability of the defibrillation energy requirement beyond I year has not heen reported. The purpose of this study was to characterize the defihrillation energy requirement during 2 years of clinical follow-up. Methods and Results: Thirty-one consecutive patients with u biphasic nonthoracotomy defihrillation system underwent defibrillation energy requirement testing using a step-down technique (20, 15, 12. 10, 8, 6, 5, 4, 3, 2, and I J) during defibrillator implantation, and then 24 hours, 2 months, 1 year, and 2 years after implantation. The mean defihrillation energy requirement during these evaluations was 10.9 ± 5.5 J, 12.3 ± 7.3 J, 11.7 ± 5.6 J, 10.2 ± 4.0 ,|, and 11.7 ± 7.4 J, respectively (P = 0.4). The defibrillation energy requirement was noted to have increased hy 10 J or more after 2 years of follow-up in five patients. In one of these patients, the defihrillation energy requirement was no longer associated with an adequate safety margin, necessitating revision of the defihrillation system. There were no identifiahle clinical characteristics that distinguished patients who did and did not develop a 10-J or more increase in the defihrillation energy requirement. Conclusion: The mean defibrillation energy requirement does not change significantly after 2 years of hiphasic nonthoracotomy detihrillator system implantation. However, approximately 15% of patients develop a 1((-J or greater elevation in the defihrillation energy requirement, and 3% may require a defihrillation system revision. Therefore, a yearly evaluation of the defibrillation euergy requirement may he appropriate. (J Cardiovasc Electrophysiol, Vol. 9, pp. 916-920. Septemtwr 1998)

The effect of implantable defibrillator shocks on cardiac hemodynamics is poorly understood. The purpose of this study was to test the hypothesis that ventricular defibrillator shocks adversely effect cardiac hemodynamics.The cardiac index was determined by calculating the mitral valve inflow with transesophogeal Doppler during nonthoracotomy defibrillator implantation in 17 patients. The cardiac index was determined before, and immediately, 1 minute, 2 minutes, and 4 minutes after shocks were delivered during defibrillation energy requirement testing with 27- to 34-, 15-, 10-, 5-, 3-, or 1-J shocks. The cardiac index was also measured at the same time points after 27- to 34-, and 1-J shocks delivered during the baseline rhythm. The cardiac index decreased from 2.30 +/- 0.40 L/min per m2 before a 27- to 34-J shock during defibrillation energy requirement testing to 2.14 +/- 0.45 L/min per m2 immediately afterwards (P = 0.001). This effect persisted for4 minutes. An adverse hemodynamic effect of similar magnitude occurred after 15 J (P = 0.003) and 10-J shocks (P = 0.01), but dissipated after 4 minutes and within 2 minutes, respectively. There was a significant correlation between shock strength and the percent change in cardiac index (r = 0.3, P = 0.03). The cardiac index decreased 14% after a 27- to 34-J shock during the baseline rhythm (P0.0001). This effect persisted for4 minutes. A 1-J shock during the baseline rhythm did not effect the cardiac index.Defibrillator shocks9 J delivered during the baseline rhythm or during defibrillation energy requirement testing result in a 10% to 15% reduction in cardiac index, whereas smaller energy shocks do not affect cardiac hemodynamics. The duration and extent of the adverse effect are proportional to the shock strength. Shock strength, and not ventricular fibrillation, appears to be most responsible for this effect. Therefore, the detrimental hemodynamic effects of high-energy shocks may be avoided when low-energy defibrillation is used.

Background: The electrophysiologic effects of norepinephrine (NE) in human beings have not been previously described. Methods: The electrophysiologic effects of NE infused at a rate of 25 ng/kg/min were determined in 21 patients with a mean age of 41 ± 11 years and without structural heart disease who underwent an electrophysiology procedure. In a subgroup of 10 patients electrophysiologic parameters were measured at baseline, after the infusion of NE, and after administration of β-blockade while in continuous NE infusion. Results: The baseline NE plasma concentration of 298 ± 153 pg/ml increased to 708 ± 419 pg/ml after the infusion of NE. NE significantly increased the mean blood pressure, sinus cycle length, corrected sinus node recovery time, ventriculoatrial block cycle length, and the atrial and ventricular effective refractory periods. In a subset of 10 patients 0.2 mg/kg propranolol administered during continued infusion of NE resulted in a further increase in sinus cycle length, atrial-His interval, and ventricular refractoriness. Conclusion: A physiologic elevation in the plasma NE concentration results in a depression of sinus node function and atrioventricular conduction and in prolongation of atrial and ventricular refractoriness. Some of NE's effects are partially offset by β-adrenergic stimulation. (Am Heart J 1998;135:945-51.)

Ventricular pace mapping may be used to identify the site of origin of idiopathic ventricular tachycardia. Isoproterenol is often required to induce this type of ventricular tachycardia, but its effect on QRS morphology during pace mapping is unknown. Therefore, this study was performed to evaluate the effect of isoproterenol on QRS morphology during ventricular pacing. The study population consisted of 20 patients (mean age 38 ± 14 years) undergoing a clinically indicated electrophysiology procedure. Ventricular overdrive pacing was performed in trains of 12 stimuli at cycle lengths of 400, 350, 300, and 250 ms, first in the baseline state during an infusion of isoproterenol, and again after isoproterenol washout. Pacing was performed at the right ventricular apex in 10 patients, in the right ventricular outflow tract in 6 patients, and in the left ventricle in 4 patients. Visual evaluation revealed no apparent effects of isoproterenol on QRS morphology at any of the three pacing sites or at any of the pacing cycle lengths. It was concluded that QRS morphology during ventricular pacing is not affected by isoproterenol infusion. Therefore, in patients with idiopathic ventricular tachycardia, even if the induction of tachycardia requires infusion of isoproterenol, successful pace mapping may be performed in its absence.

Cardiac Memory. Introduction: “Cardiac memory” (primary T wave change) is thought to occur after 15 minutes to several hours of right ventricular (RV) pacing. The two components of the temporal change in repolarization are memory and accumulation. The purpose of this study was to examine quantitatively the effect of short periods of ventricular pacing on the human cardiac action potential, using monophasic action potential (MAP) recordings. Methods and Results: Thirty-one patients (ages 43 ± 14 years) with structurally normal hearts undergoing a clinically indicated electrophysiologic procedure were enrolled. Catheters were placed in the right atrium (RA) and RV, and a MAP catheter was positioned at the RV septum. APD90 was calculated from digitized MAP recordings. MAP morphology comparisons were performed using the root mean square (RMS) of the difference between complexes. All pacing was at 500-msec cycle length. There were four pacing protocols: (1) RA pacing was performed for approximately 15 minutes to evaluate temporal stability of the MAP recordings (5 pts); (2) to evaluate the memory phenomenon, four successive 1-minute episodes of RV pacing were interspersed with 2 minutes of RA pacing (5 pts); (3) the accumulation phenomenon was evaluated by assessing the effects of 1, 5, 10, and 15 minutes of RV pacing on the MAP during RA pacing (16 pts); and (4) 20 minutes of RV pacing was followed by 10 minutes of RA pacing to correlate visually apparent T wave changes with changes in MAP recordings (5 pts). In the control patients, no changes in APD90 or RMS analysis were noted during 14.9 ± 1.4 minutes of RA pacing. In the second protocol, RMS of the difference between the baseline MAP complexes and the signal average of the first 50 beats following each of four 1-minute RV pacing trains demonstrated progressively greater differences in morphology after successive episodes of RV pacing. In protocol 3, RMS analysis identified a progressively greater difference between the baseline MAP recording and the average of the first 50 beats after 1,5, 10, and 15 minutes of RV pacing. In protocol 4, visually apparent changes in T waves occurred in parallel with the RMS of the difference between the baseline MAP recordings and the average of the first 50 beats after 20 minutes of RV pacing. Similar changes also were demonstrated by APD90 analysis. Conclusion: This study is the first to demonstrate that episodes of abnormal ventricular activation as short as 1 minute in duration may exert lingering effects on the repolarization process once normal ventricular activation resumes.

Atrial fibrillation occurs commonly after open-heart surgery and may delay hospital discharge. The purpose of this study was to assess the use of preoperative amiodarone as prophylaxis against atrial fibrillation after cardiac surgery.In this double-blind, randomized study, 124 patients were given either oral amiodarone (64 patients) or placebo (60 patients) for a minimum of seven days before elective cardiac surgery. Therapy consisted of 600 mg of amiodarone per day for seven days, then 200 mg per day until the day of discharge from the hospital. The mean (+/-SD) preoperative total dose of amiodarone was 4.8+/-0.96 g over a period of 13+/-7 days.Postoperative atrial fibrillation occurred in 16 of the 64 patients in the amiodarone group (25 percent) and 32 of the 60 patients in the placebo group (53 percent) (P=0.003). Patients in the amiodarone group were hospitalized for significantly fewer days than were patients in the placebo group (6.5+/-2.6 vs. 7.9+/-4.3 days, P=0.04). Nonfatal postoperative complications occurred in eight amiodarone-treated patients (12 percent) and in six patients receiving placebo (10 percent, P=0.78). Fatal postoperative complications occurred in three patients who received amiodarone (5 percent) and in two who received placebo (3 percent, P= 1.00). Total hospitalization costs were significantly less for the amiodarone group than for the placebo group ($18,375+/-$13,863 vs. $26,491+/-$23,837, P=0.03).Preoperative oral amiodarone in patients undergoing complex cardiac surgery is well tolerated and significantly reduces the incidence of postoperative atrial fibrillation and the duration and cost of hospitalization.

Background Because it is not clear which technique is less expensive, the purpose of this study was to compare the cost of radiofrequency modification and ablation of the atrioventricular (AV) node in drug-refractory patients with atrial fibrillation and an uncontrolled ventricular rate. Methods and Results The initial nominal charges for a successful procedure were compared in 10 patients with chronic atrial fibrillation who underwent modification of the AV node ($13 109±2002) and 14 similar patients who underwent ablation and pacemaker implantation ($28 302±2023, P P Conclusions The initial charges generated by AV node modification are significantly lower than for AV node ablation in patients with chronic atrial fibrillation. Even when adjusted for higher failure and recurrence rates, the modification procedure retains a major cost advantage over ablation during long-term follow-up.

Background Implantable cardioverter-defibrillator (ICD) therapy is integral to current therapy for ventricular tachycardia. Patients with an ICD frequently require concomitant antiarrhythmic drug therapy. Despite this, some patients still receive frequent ICD therapies for ventricular tachycardia. Therefore, the purpose of this prospective study was to determine the utility of ablation of ventricular tachycardia in patients with an ICD who experience frequent ICD therapies. Methods and Results Twenty-one consecutive patients with frequent ICD therapies despite antiarrhythmic drug therapy were the subjects of this study. The mean age was 69±6 years, and 17 were men. The mean ejection fraction was 0.22±0.08, and all patients had coronary artery disease. During the 36±51 days (range, 4 days to 7 months) preceding the ablation procedures, the patients received 34±55 ICD therapies for the clinical ventricular tachycardia, or a mean of 25±88 ICD therapies per month. The patients underwent radiofrequency ablation of the presumed clinical ventricular tachycardia by inducing the tachycardia and mapping according to endocardial activation, continuous electrical activity, pace mapping, concealed entrainment, or mid-diastolic potentials. Ablation of the clinical arrhythmia was successful in 76% of patients during 1.4±0.6 (range, 1 to 3) ablation procedures and required 12.5±9.2 applications of energy. During 11.8±10.0 months of follow-up, the frequency of ICD therapies per month decreased from 60±80 before successful ablation to 0.1±0.3 ICD therapies per month after ablation ( P =.01). A quality-of-life assessment demonstrated a significant improvement after successful ( P =.02) but not unsuccessful ablation ( P =.9). Conclusions Radiofrequency ablation of ventricular tachycardia as adjuvant therapy in patients with coronary artery disease and an ICD has a reasonable success rate, significantly reduces ICD therapies, and appears to be associated with an improved quality of life.

This study demonstrates that shocks

Impairment of cardiac function in atrial fibrillation has been attributed to loss of atrial contraction and to a rapid ventricular rate. The results of this study suggest that irregularity of the ventricular rhythm, independent of the ventricular rate, may also contribute to impairment of cardiac function during atrial fibrillation.

Background Ventricular pace mapping is performed by comparing the QRS morphology of ventricular paced complexes to that of a template arrhythmia, either a premature ventricular depolarization or a QRS complex during ventricular tachycardia. The objective of this study was to evaluate the effect of coupling interval and pacing cycle length on QRS morphology. Methods and Results The study population consisted of 20 patients (mean age, 38±16 years) undergoing a clinically indicated electrophysiology procedure. In the first 10 patients, the effect of coupling interval on the morphology of single paced ventricular complexes was evaluated visually and by signal processing techniques. Visually apparent differences in QRS morphology occurred in a mean of 4/12 electrocardiographic leads with a change in coupling interval of ≥100 ms. In the next 10 patients, the QRS complex morphology during ventricular overdrive pacing at cycle lengths of 600 and 300 ms was found to differ significantly in a mean of 4/12 leads. The QRS morphology during overdrive pacing differed significantly from that of a single paced complex whenever the pacing cycle length differed from the coupling interval of the single paced complex by >80 ms. Conclusions The morphology of single paced QRS complexes may vary, depending on coupling interval, and the QRS morphology during overdrive pacing is affected by the pacing cycle length. During ventricular pace mapping, the coupling interval or cycle length of the template arrhythmia should be matched during pacing. If not, rate-dependent changes in QRS morphology that are independent of the pacing site may confound the results of pace mapping.