Treatment of underlying atrial fibrillation: paced rhythm obscures recognition.

OBJECTIVES: The purpose of this study was to evaluate the rate of recognition of atrial fibrillation (AF), use of warfarin and prevalence of cerebrovascular accident (CVA) in paced versus unpaced patients during admission to a tertiary care teaching hospital. BACKGROUND: The presence of AF underlying a continuously paced rhythm may be under recognized and result in a lower rate of anticoagulation and higher incidence of CVA. METHODS: The identification of AF on 12 lead electrocardiogram (ECG) and telemetry, "optimal use" of anticoagulants that is, warfarin or aspirin, when warfarin is contraindicated and history of prior CVA was studied in three groups: 1) group A with continuously paced rhythm on ECG and telemetry (n = 30), 2) group B with intermittently paced rhythm on ECG and telemetry (n = 59), and 3) group C with persistent AF and no permanent pacemaker (n = 50). RESULTS: The identification and documentation of AF was significantly lower in the continuously paced group A (20%) versus the intermittently paced group B (44%). Both groups A and B were substantially lower than unpaced controls. "Optimal use" of anticoagulants was significantly lower in group A (40%) compared with groups B (78%) and C (72%) but was not different between groups B and C. The prevalence of prior CVA was not significantly different between the three groups. CONCLUSIONS: All ECGs in patients with paced rhythm should be examined closely for underlying AF to prevent under-recognition and under-treatment with anticoagulants.

Radiofrequency catheter ablation of inappropriate sinus tachycardia guided by activation mapping.

OBJECTIVE: The purpose of this study was to evaluate the value of activation mapping for radiofrequency modification of the sinus node and the long-term success rate of the procedure in a series of patients with inappropriate sinus tachycardia. BACKGROUND: The results of radiofrequency ablation of inappropriate sinus tachycardia have been reported in only a small number of patients. METHODS: The subjects of this study were 29 consecutive drug-refractory patients who underwent catheter ablation of inappropriate sinus tachycardia. Target sites were selected by activation mapping during sinus tachycardia. RESULTS: The ablation procedure was successful acutely in reducing the baseline sinus rate to <90/min and the sinus rate during isoproterenol infusion by >20% in 22 of 29 patients (76%). In 13 of 22 patients (59%) with a successful acute outcome, successive applications of radiofrequency energy at the site of earliest endocardial activation resulted in a cranial-caudal migration of earliest endocardial activation from the high lateral right atrium, along with a step-wise reduction in heart rate. In the other nine patients (41%) with a successful acute outcome, the reduction in sinus rate occurred abruptly, unaccompanied by migration of the site of earliest activation. Symptoms due to inappropriate sinus tachycardia recurred at a mean of 4.4+/-; 3 months after the ablation procedure in 6 of 22 patients (27%). After additional procedures in three patients, symptoms of inappropriate sinus tachycardia ultimately were successfully eliminated over the long-term in 19 of 29 patients (66%). CONCLUSIONS: In conclusion, radiofrequency ablation is at best only modestly effective for managing patients with inappropriate sinus tachycardia. The two different responses of heart rate to radiofrequency ablation may reflect differences in the number and/or multicentricity of subsidiary sites of impulse generation within the sinus node and/or atrium in patients with inappropriate sinus tachycardia.

Short-term effect of atrial fibrillation on atrial contractile function in humans.

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.

Interaction between autonomic tone and the negative chronotropic effect of adenosine in humans.

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.

Randomized comparison of a 90 uF capacitor three-electrode defibrillation system with a 125 uF two-electrode defibrillation system.

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 = 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.

Influence of right ventricular site of stimulation and infarct location on the inducibility of ventricular tachycardia in patients with coronary artery disease.

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.

Acute changes in spontaneous echo contrast and atrial function after cardioversion of persistent atrial flutter.

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 <0.01). There were no significant changes in the mean left atrial appendage-emptying velocity between 1 and 15 minutes after cardioversion. Within 5 minutes after conversion to sinus rhythm, left atrial spontaneous echo contrast developed de novo or worsened in 12 of the 28 patients (43%). In conclusion, the results of this study demonstrate that persistent AFI may be associated with left atrial thrombi before cardioversion and that cardioversion of AFI is associated with a significant degree of atrial stunning and formation of spontaneous echo contrast.

Use of adenosine in patients hospitalized in a university medical center.

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.

Long-term evaluation of the ventricular defibrillation energy requirement.

INTRODUCTION: Defibrillation energy requirements in patients with nonthoracotomy defibrillators may increase within several months after implantation. However, the stability of the defibrillation energy requirement beyond 1 year has not been reported. The purpose of this study was to characterize the defibrillation energy requirement during 2 years of clinical follow-up. METHODS AND RESULTS: Thirty-one consecutive patients with a biphasic nonthoracotomy defibrillation system underwent defibrillation energy requirement testing using a step-down technique (20, 15, 12, 10, 8, 6, 5, 4, 3, 2, and 1 J) during defibrillator implantation, and then 24 hours, 2 months, 1 year, and 2 years after implantation. The mean defibrillation 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 J, and 11.7+/-7.4 J, respectively (P = 0.4). The defibrillation energy requirement was noted to have increased by 10 J or more after 2 years of follow-up in five patients. In one of these patients, the defibrillation energy requirement was no longer associated with an adequate safety margin, necessitating revision of the defibrillation system. There were no identifiable clinical characteristics that distinguished patients who did and did not develop a 10-J or more increase in the defibrillation energy requirement. CONCLUSION: The mean defibrillation energy requirement does not change significantly after 2 years of biphasic nonthoracotomy defibrillator system implantation. However, approximately 15% of patients develop a 10-J or greater elevation in the defibrillation energy requirement, and 3% may require a defibrillation system revision. Therefore, a yearly evaluation of the defibrillation energy requirement may be appropriate.

Effect of ventricular shock strength on cardiac hemodynamics.

INTRODUCTION: 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. METHODS AND RESULTS: 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 for > 4 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 (P < 0.0001). This effect persisted for < 4 minutes. A 1-J shock during the baseline rhythm did not effect the cardiac index. CONCLUSION: Defibrillator shocks > 9 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.

Differential effect of adenosine on anterograde and retrograde fast pathway conduction in patients with atrioventricular nodal reentrant tachycardia.

INTRODUCTION: Several studies have shown that the fast pathway is more responsive to adenosine than the slow pathway in patients with AV nodal reentrant tachycardia. Little information is available regarding the effect of adenosine on anterograde and retrograde fast pathway conduction. METHODS AND RESULTS: The effects of adenosine on anterograde and retrograde fast pathway conduction were evaluated in 116 patients (mean age 47 +/- 16 years) with typical AV nodal reentrant tachycardia. Each patient received 12 mg of adenosine during ventricular pacing at a cycle length 20 msec longer than the fast pathway VA block cycle length and during sinus rhythm or atrial pacing at 20 msec longer than the fast pathway AV block cycle length. Anterograde block occurred in 98% of patients compared with retrograde fast pathway block in 62% of patients (P < 0.001). Unresponsiveness of the retrograde fast pathway to adenosine was associated with a shorter AV block cycle length (374 +/- 78 vs 333 +/- 74 msec, P < 0.01), a shorter VA block cycle length (383 +/- 121 vs 307 +/- 49 msec, P < 0.001), and a shorter VA interval during tachycardia (53 +/- 23 vs 41 +/- 17 msec, P < 0.01). CONCLUSION: Although anterograde fast pathway conduction is almost always blocked by 12 mg of adenosine, retrograde fast pathway conduction is not blocked by adenosine in 38% of patients with typical AV nodal reentrant tachycardia. This indicates that the anterograde and retrograde fast pathways may be anatomically and/or functionally distinct. Unresponsiveness of VA conduction to adenosine is not a reliable indicator of an accessory pathway.

Cardiac electrophysiologic effects of norepinephrine in human beings.

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 beta-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 beta-adrenergic stimulation.

Effect of isoproterenol on QRS complex morphology during ventricular pacing: implications for pace mapping.

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.

Changes in cardiac repolarization following short periods of ventricular pacing.

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.

A prospective evaluation of two defibrillation safety margin techniques in patients with low defibrillation energy requirements.

INTRODUCTION: In patients undergoing defibrillator implantation, an appropriate defibrillation safety margin has been considered to be either 10 J or an energy equal to the defibrillation energy requirement. However, a previous clinical report suggested that a larger safety margin may be required in patients with a low defibrillation energy requirement. Therefore, the purpose of this prospective study was to compare the defibrillation efficacy of the two safety margin techniques in patients with a low defibrillation energy requirement. METHODS AND RESULTS: Sixty patients who underwent implantation of a defibrillator and who had a low defibrillation energy requirement (< or = 6 J) underwent six separate inductions of ventricular fibrillation, at least 5 minutes apart. For each of the first three inductions of ventricular fibrillation, the first two shocks were equal to either the defibrillation energy requirement plus 10 J (14.6+/-1.0 J), or to twice the defibrillation energy requirement (9.9+/-2.3 J). The alternate technique was used for the subsequent three inductions of ventricular fibrillation. For each induction of ventricular fibrillation, the first shock success rate was 99.5%+/-4.3% for shocks using the defibrillation energy requirement plus 10 J, compared to 95.0%+/-17.2% for shocks at twice the defibrillation energy requirement (P = 0.02). The charge time (P < 0.0001) and the total duration of ventricular fibrillation (P < 0.0001) were each approximately 1 second longer with the defibrillation energy requirement plus 10 J technique. CONCLUSION: This study is the first to compare prospectively the defibrillation efficacy of two defibrillation safety margins. In patients with a defibrillation energy requirement < or = 6 J, a higher rate of successful defibrillation is achieved with a safety margin of 10 J than with a safety margin equal to the defibrillation energy requirement.

Preoperative amiodarone as prophylaxis against atrial fibrillation after heart surgery.

BACKGROUND: 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. METHODS: 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. RESULTS: 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). CONCLUSIONS: 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.

A prospective evaluation of catheter ablation of ventricular tachycardia as adjuvant therapy in patients with coronary artery disease and an implantable cardioverter-defibrillator.

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.

Cost comparison of radiofrequency modification and ablation of the atrioventricular junction in patients with chronic atrial fibrillation.

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<.001). On the basis of the long-term follow-up of patients who underwent each procedure, it was assumed that 31% of patients selected for the modification procedure would require a permanent pacemaker for inadvertent AV block or because of AV nodal ablation after a failed modification procedure and that the recurrence rate after AV node ablation would be 2%. The annual charges during follow-up were predicted and adjusted for recurrences and the need for additional procedures. The adjusted total charges at 1 year of follow-up were significantly lower for the modification procedure ($19 389+/-2002) than for the ablation procedure ($28 485+/-2023, P<.001). After 10 years of follow-up, the cumulative, adjusted charges for modification were $20 016 (42%) less than for ablation. 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.

Effect of verapamil and procainamide on atrial fibrillation-induced electrical remodeling in humans.

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<.0001), respectively, and at the 500-ms drive cycle length, the values were 217+/-16 and 183+/-23 ms, respectively (P<.0001). There was a similar significant shortening of the first post-AF ERP in the procainamide group. In the verapamil group, however, there was no difference between the pre-AF and the first post-AF ERP at the 350-ms (226+/-15 versus 227+/-22 ms, 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<.01 versus verapamil). 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.

Adenosine-induced atrial arrhythmia: a prospective analysis.

BACKGROUND: Adenosine is considered safe and effective for paroxysmal supraventricular tachycardia (PSVT), but anecdotal experience suggests that adenosine can precipitate atrial arrhythmias. OBJECTIVES: To determine the frequency and mechanisms of adenosine-induced atrial arrhythmias. SETTING: Clinical electrophysiology laboratory at a university medical center. DESIGN: Prospective observational study. PATIENTS: 200 consecutive patients with PSVT undergoing an electrophysiology procedure. INTERVENTION: During PSVT, 12 mg of adenosine was administered centrally through the femoral vein. MEASUREMENTS: Frequency of adenosine-induced atrial fibrillation. RESULTS: Paroxysmal supraventricular tachycardia terminated after adenosine administration in 198 patients (99% [95% CI, 96% to 100%]). Adenosine led to atrial fibrillation (n = 22) or atrial fibrillation and atrial flutter (n = 2) in 24 patients (12% [CI, 7.5% to 16.5%]). An atrial premature complex occurred in all 24 patients who developed atrial fibrillation, atrial flutter, or both and in 102 of the 176 patients (58%) who did not (P < 0.001). The mean (+/-SD) time from the preceding atrial complex to the atrial premature complex was shorter when an atrial arrhythmia occurred, and the mean ratio of this interval to the preceding atrial cycle length was also lower when atrial fibrillation developed (0.37 +/- 0.16 compared with 0.49 +/- 0.16; P = 0.002). CONCLUSIONS: The incidence of atrial fibrillation induced by 12 mg of adenosine administered through the femoral vein was 12%. Fibrillation seems to be associated with a "long-short" atrial sequence. If the mechanism of PSVT is unknown and the Wolff-Parkinson-White syndrome is possible, administration of adenosine should be limited to medical facilities that have emergency resuscitation equipment.