Is hospital admission for initiation of antiarrhythmic therapy with sotalol for atrial arrhythmias required? Yield of in-hospital monitoring and prediction of risk for significant arrhythmia complications.

OBJECTIVES: We sought to determine the yield of in-hospital monitoring for detection of significant arrhythmia complications in patients starting sotalol therapy for atrial arrhythmias and to identify factors that might predict safe outpatient initiation. BACKGROUND: The need for hospital admission during initiation of antiarrhythmic therapy has been questioned, particularly for sotalol, with which proarrhythmia may be dose related. METHODS: The records of 120 patients admitted to the hospital for initiation of sotalol therapy were retrospectively reviewed to determine the incidence of significant arrhythmia complications, defined as new or increased ventricular arrhythmias, significant bradycardia or excessive corrected QT (QTc) interval prolongation. RESULTS: Twenty-five patients (20.8%) experienced 35 complications, triggering therapy changes during the hospital period in 21 (17.5%). New or increased ventricular arrhythmias developed in 7 patients (5.8%) (torsade de pointes in 2), significant bradycardia in 20 (16.7%) (rate <40 beats/min in 13, pause >3.0 s in 4, third-degree atrioventricular block in 1, permanent pacemaker implantation in 3) and excessively prolonged QTc intervals in 8 (6.7%) (dosage reduced or discontinued in 6). Time to the earliest detection of complications was 2.1 +/- 2.5 (mean +/- SD) days after initiation of sotalol, with 22 of 25 patients meeting criteria for complications within 3 days of monitoring. Baseline electrocardiographic intervals or absence of heart disease failed to distinguish a low risk group. Multivariate analysis identified absence of a pacemaker as the only significant predictor of arrhythmia complications (p = 0.022). CONCLUSIONS: Because clinically significant complications can be detected with in-hospital monitoring in one of five patients starting sotalol therapy, hospital admission is warranted for initiation of sotalol. Patients without pacemakers are at higher risk for these complications.

Influence of amiodarone on QT dispersion in patients with life-threatening ventricular arrhythmias and clinical outcome.

UNLABELLED: Increased QT dispersion, defined as the difference between the maximum and minimum QT interval on the standard 12-lead electrocardiogram is assumed to reflect regional inhomogeneity of ventricular repolarization and has been shown to be associated with an increased risk of arrhythmic events. The purpose of the present study is to examine the influence of amiodarone on QT dispersion in patients with life-threatening ventricular arrhythmias and to evaluate the predictive value of QT dispersion after amiodarone therapy for further arrhythmic events. ECG's were obtained in 47 patients 1-2 days before and 6-8 weeks after amiodarone was started. All patients had coronary artery disease with a mean EF of 34 +/- 14%. The QT interval was measured in each lead of a digitized ECG displayed on a high resolution monitor (250 mm s-1). Amiodarone therapy resulted in a significant increase in the maximal QTc interval (476 +/- 44 to 505 +/- 44 ms, p < 0.001). However, measurement of QT dispersion (70 +/- 34 vs 73 +/- 29 ms) and Qtc dispersion (78 +/- 37 vs 77 +/- 31 ms) revealed no significant difference before and after amiodarone. During a one year follow-up period 26 patients were free of arrhythmic events and 7 patients developed further arrhythmic events. The remaining 14 patients were excluded from the one year follow-up analysis because of drug discontinuation (n = 8), death due to heart failure (n = 1), medical intervention (n = 3) and incomplete follow-up (n = 2). No measure of QT dispersion was predictive of recurrent arrhythmic events during treatment with amiodarone. CONCLUSION: Treatment with amiodarone results in significant QT prolongation without altering QT dispersion. Measurements of QT dispersion were not predictive of amiodarone efficacy in this patient population.

The effects of antiarrhythmic drugs on the signal-averaged electrocardiogram in patients with malignant ventricular arrhythmias.

Late potentials arise from areas of slowly depolarizing myocardium and may represent the substrate for sustained VTs. Because they may be recorded from the body surface using signal-averaging techniques, they represent a noninvasive marker for potential malignant ventricular arrhythmias. The effects of antiarrhythmic drugs on the SAECG and late potentials are reviewed in this article. Unfortunately, there is no SAECG parameter (either total QRS, late potential, or frequency content) that appears to be useful in predicting drug efficacy. However, there are type-specific changes in global ventricular activation that can be quantified by the SAECG. These changes may be useful in categorizing the effects of new type I antiarrhythmic drugs. The effects of antiarrhythmic drugs on tachycardia cycle length are complex and probably represent combined effects of the drug on conduction and refractoriness. Such changes cannot be reliably categorized by the SAECG. Medical therapy of sustained VTs cannot be guided by the SAECG.

Effects of flecainide and D-sotalol on myocardial conduction and refractoriness: relation to antiarrhythmic and proarrhythmic drug effects.

Programmed electrical stimulation (PES) was used to compare the effects of flecainide and D-sotalol in a canine occlusion-reperfusion infarction model. The increase in the effective refractory period (ERP) was greater with D-sotalol than with flecainide (26.4 +/- 5.2 vs. 10.3 +/- 2.7 ms). In contrast, ventricular activation time was significantly increased by flecainide (from 72 +/- 2 to 87 +/- 3 ms) but was unchanged after D-sotalol administration (from 73 +/- 2 to 75 +/- 2 ms). Thirteen dogs with inducible sustained ventricular arrhythmias at control became noninducible after drug administration. All but one of these favorable drug responses were associated with D-sotalol. In contrast, 10 noninducible dogs at control had sustained ventricular arrhythmias induced after drug administration. All of these adverse responses were associated with flecainide (p < 0.0001). An increase in the ratio of conduction to refractoriness was observed in 100% of adverse drug trials but in only 25% of favorable drug trials (p = 0.003). These data suggest that flecainide enhances induction of sustained ventricular arrhythmias in this postinfarction canine model. This proarrhythmic drug effect may be related to the selective effect of flecainide on myocardial conduction.

Stereospecific effects of disopyramide enantiomers following pretreatment of canine cardiac Purkinje fibers with verapamil and nisoldipine.

The effect of racemic disopyramide and its enantiomers on the action potential was studied in Tyrodes (4.0 mM KCL)-superfused canine cardiac Purkinje fibers. Nonstereodependent depression of action potential amplitude and phase 0 Vmax was observed in control fibers and following pretreatment with either nisoldipine or verapamil. Stereospecific effects of the enantiomers were prominent during repolarization phases of the action potential and could be modified by pretreatment with the calcium channel blocking agents. R(-) disopyramide decreased action potential duration at 90% repolarization and shortened the effective refractory period. S(+) disopyramide increased action potential duration at 90% repolarization and prolonged refractoriness. This disparate effect of the enantiomers was eliminated following pretreatment with verapamil. Stereospecific effects on repolarization persisted when fibers were pretreated with nisoldipine, a more selective calcium channel blocking agent that lacks effects on outward plateau current. The data suggest that the increase in action potential duration and refractoriness produced by disopyramide is mediated by a stereospecific inhibition of outward repolarizing current by the S(+) enantiomer.

Linking in accessory pathways. Functional loss of antegrade preexcitation.

BACKGROUND: Concealed retrograde activation has been proposed as a mechanism for antegrade conduction block in the bundle branches and atrioventricular accessory pathways. We studied this hypothesis (linking) in 10 patients with the Wolff-Parkinson-White syndrome in whom antegrade preexcitation could be persistently blocked by overdrive atrial pacing. METHODS AND RESULTS: An atrial pacing protocol, with a decremental ramp followed by an incremental ramp, defined a range of atrial paced cycle lengths (linking window) associated with both persistent conduction and block in the accessory pathway. Within the limits of the linking window, the ability of an atrial impulse to conduct over the accessory pathway was dependent on the preceding state (i.e., conduction or block). The observed linking window ranged from 70 to 290 msec (mean, 185 +/- 68 msec) and closely approximated the measured delay in retrograde activation of the accessory pathway during persistent antegrade block. The mean antegrade effective refractory period of the accessory pathways was long (486 +/- 156 msec), and in each case, it exceeded the antegrade refractory period of the normal atrioventricular pathway. Critically timed premature ventricular extrastimuli, delivered while linking was maintained in the accessory pathway, were able to interrupt the linking and restore antegrade accessory pathway conduction. CONCLUSIONS: These observations suggest that accessory pathway linking is associated with bidirectional block in the accessory pathway. The ability to initiate linking (and the stability of the phenomenon) depends on a critical relation between antegrade accessory pathway refractoriness and the magnitude of retrograde accessory pathway activation delay.

A technique for rapid transfemoral catheterization of the coronary sinus with multielectrode catheters.

To minimize procedural and fluoroscopic times and avoid the risks of vascular injury and pneumothorax, some investigators have advocated elimination of routine placement of a coronary sinus (CS) catheter during electrophysiological procedures. We hypothesized that expedient and reproducible CS catheterization could be performed with minimal patient risk by utilizing a femoral vein approach. Fifty consecutive patients referred for radiofrequency ablative procedures underwent attempted CS catheterization using a 6-French steerable, quadripolar catheter via a femoral vein. Procedures were performed utilizing single-plane fluoroscopy without contrast angiographic aid by operators experienced in the technique. Successful catheterization was defined by the attainment, in < 15 minutes, of a stable catheter position with the distal electrode at or beyond the lateral margin of the heart. Successful catheterization of the CS was achieved in 47 (94%) patients. Selective pacing of the left atrium without patient discomfort was possible in all, eliminating the need for a right atrial pacing catheter. The median time to successful catheterization was 1.4 minutes (range 0.3-14.7). Only six patients required > 5 minutes. The median fluoroscopic time required was 1.2 minutes (range 0.3-12.7). No clinical variable was predictive of catheterization failure or time to successful catheterization. No complications were observed as a result of this technique. This prospective evaluation demonstrates that catheterization of the CS via a femoral vein approach is highly successful, expedient, and safe. The ability to selectively pace the left atrium may eliminate the requirement for a right atrial catheter.

Amiodarone-related postoperative adult respiratory distress syndrome.

Directed surgical intervention in patients with ventricular tachyarrhythmias who have experienced failure of amiodarone therapy is a common clinical scenario. Sixty-seven patients with malignant ventricular tachyarrhythmias received either an automatic implantable cardioverter-defibrillator (n = 43) or subendocardial resection (n = 24). Nineteen cardiothoracic procedures (automatic implantable cardioverter-defibrillator in six, endocardial resection in 13) were performed in 17 patients who received amiodarone before surgery. Eight received the drug acutely as a loading dose of 1,200 mg/day for 7-14 days; 11 patients were on chronic oral amiodarone at a mean dose of 362 +/- 74 mg/day. Eight patients were removed from amiodarone therapy a mean of 6.6 days before surgery. Adult respiratory distress syndrome (ARDS) developed after surgery in nine (50%) of 18 surgical survivors. ARDS was manifested by hypoxemia, pulmonary infiltrates, and prolonged intubation. Pulmonary capillary wedge pressure and cardiac output were measured before and after surgery and during ARDS. Pulmonary capillary wedge pressure and cardiac output remained constant after surgery at a time that the PaO2/FIO2 ratio fell significantly. By contrast, none of the remaining 44 patients who did not receive amiodarone developed ARDS despite similar preoperative and intraoperative clinical parameters. Patients with ventricular tachyarrhythmias who receive even a short course of amiodarone are at risk for postoperative ARDS.

Use-dependent prolongation of ventricular tachycardia cycle length by type I antiarrhythmic drugs in humans.

BACKGROUND: Type I antiarrhythmic drugs block the cardiac sodium channel in a use-dependent fashion. This use-dependent behavior causes increased drug binding and consequently increased sodium channel blockade at faster stimulation rates. Importantly, the kinetics of drug association and dissociation from the sodium channel differ for each type I antiarrhythmic drug. METHODS AND RESULTS: Thirty-five patients receiving type I antiarrhythmic drugs for the treatment of sustained monomorphic ventricular tachycardia (VT) were studied before and after drug therapy. A total of 41 drug studies were performed (lidocaine, n = 10; procainamide, n = 16; flecainide, n = 15). Sustained monomorphic VT of an identical electrocardiographic morphology was induced during the control and follow-up drug studies. During the control study, there was no significant change in the VT cycle length over time. Compared with control, significant prolongation of the onset VT cycle length was observed after treatment with procainamide and flecainide (increase of 52 +/- 24 and 80 +/- 49 msec, respectively) but not after treatment with lidocaine (increase of 8 +/- 37 msec). Additional drug-induced prolongation of the VT cycle length occurred during a 40-second observation period. This secondary "use-dependent" cycle length prolongation contributed significantly to the steady-state VT cycle length during treatment with flecainide (increase of 82 +/- 34 msec; p < 0.0001). Although a use-dependent increase in VT cycle length was observed with procainamide and lidocaine, the increase was not statistically significant (increase of 12 +/- 15 and 8 +/- 8 msec, respectively). The estimated time constants for the onset of use-dependent VT cycle length prolongation were distinctly different for the three drugs. Flecainide's prolongation of the VT cycle length occurred slowly, with an estimated time constant of 12.5 +/- 5.0 seconds. In contrast, the time course of VT cycle length prolongation was rapid during treatment with lidocaine and intermediate during treatment with procainamide (time constants of 0.52 +/- 0.51 and 4.0 +/- 1.3 seconds, respectively). CONCLUSIONS: Use-dependent prolongation of VT cycle length during treatment with type I antiarrhythmic drugs was observed in humans. This effect was clinically significant during treatment with flecainide (i.e., the use-dependent slowing of the heart rate improved the hemodynamic tolerance of the arrhythmia). Finally, the estimated time constants for the use-dependent prolongation of VT cycle length by the three test drugs are similar to their reported in vitro time constants for use-dependent sodium channel blockade.

Hereditary long QT syndrome associated with cardiac conduction system disease.

This report describes the cardiac conduction abnormalities, detected by invasive electrophysiological study, in two identical siblings with symptomatic congenital long QT syndrome. Both patients had evidence of intra-Hisian conduction delay in response to programmed atrial stimulation and pacing induced infranodal block was seen in one of the two patients. The response of the observed conduction delay to autonomic interventions is described. The observed electrophysiologic abnormalities are consistent with previously reported pathological findings and document the association of functional conduction system disease with congenital QT prolongation.

Hemodynamic and electrophysiologic effects of disopyramide enantiomers in a canine blood superfusion model.

The use of disopyramide is often limited because of adverse hemodynamic or electrophysiologic side effects. We compared the S(+) and R(-) enantiomers of disopyramide to the clinically used racemic mixture in a canine blood superfusion model. Eighteen support animals (group I) provided extracorporeal blood superfusion of isolated canine cardiac Purkinje fibers. Following administration of 2 mg/kg disopyramide intravenously (i.v.) [S(+), R(-), or racemic] hemodynamic and electrocardiographic parameters were temporally assessed in the support animals while simultaneous cellular electrophysiologic effects were recorded from the blood-superfused Purkinje fibers. An additional 13 animals (group II) underwent extended hemodynamic and pharmacokinetic analysis without the external atrioventricular (AV) shunt required for blood superfusion. Mean peak serum concentrations of racemic disopyramide and its enantiomers were similar (2.7 to 3.1 mg/L), but clearance was stereo-specific [half-life (t1/2) of 1.99 h for S(+) vs. 2.79 h for R(-) disopyramide]. Left ventricular (LV) function was impaired following drug administration, irrespective of optical rotation (cardiac output decreased by 20.8%, LV dP/dtmax decreased by 22.4%). Depression of phase 0 Vmax of the Purkinje fiber action potential was also nonstereo-dependent. S(+) disopyramide prolonged the QTC interval by 11.5% and increased terminal action potential duration (APD75) and effective refractory period (ERP) by 21.2 and 19.0%, respectively. R(-) disopyramide slightly increased the QTC interval (+2.3%) but decreased APD75 and ERP by 8.9 and 6.8%, respectively. The effect of racemic disopyramide on repolarization indexes was intermediate to that of its enantiomers. These data support nonstereodependent depression of both myocardial contractility and sodium channel conductance by disopyramide. Changes in APD and refractoriness were dependent on stereochemical configuration.

The effects of type I antiarrhythmic drugs on the signal-averaged electrocardiogram in patients with malignant ventricular arrhythmias.

The effects of type I antiarrhythmic drugs on the signal-averaged electrocardiogram (SAECG) were analyzed in 58 patients with inducible sustained monomorphic ventricular tachycardia. SAECGs were acquired before and after drug therapy. A total of 99 drug trials were analyzed (mean 1.7 per patient). Analysis of temporal domain parameters included the duration of the QRS complex (QRSD), the high frequency total duration of the filtered QRS complex (HFTD), the duration of the signal under 40 microV (D40), initial QRS (HFTD minus D40), and the root mean square amplitude (RMSA) of the terminal 40 msec of the QRS signal. Changes in temporal parameters failed to predict drug efficacy. There were, however, type-specific drug effects on the SAECG. With the exception of type IB drugs, all drugs increased the QRSD, HFTD, and D40. Type IC drugs caused more prolongation of the QRSD and HFTD than type IA, IB, and the combination of IA+IB drugs. Prolongation of the HFTD was related to prolongation of the late potential and the initial portion of the QRS complex. A preferential effect of these drugs on the late potential was not observed. Type IC drugs also caused more prolongation of ventricular tachycardia cycle length than type IA or IB drugs. However, the increase in ventricular tachycardia cycle length did not correlate with a change in the SAECG. In summary, type I antiarrhythmic drugs cause a global slowing of ventricular activation. Although analysis of the SAECG following drug therapy was not useful for predicting drug efficacy, drug induced changes in the SAECG may be helpful for categorizing antiarrhythmic agents.

Retrograde migration of the site of functional block: a mechanism underlying resolution of functional retrograde bundle branch block during AV reentrant tachycardia.

INTRODUCTION: Functional bundle branch blocks during supraventricular tachycardia have been described, and their sustainment has been attributed to concealed conduction. Such blocks frequently resolve spontaneously, but the electrophysiologic mechanism of resolution has not been well described. This report describes the resolution of functional bundle branch block through proximal migration of the site of block. METHODS AND RESULTS: During electrophysiologic study of a patient with reentrant antidromic tachycardia via an atriofascicular accessory pathway, functional retrograde right bundle branch block could be readily induced following tachycardia initiation with right ventricular apical pacing. Resolution of this block was associated with shortening of the tachycardia cycle length. Electrogram recordings along the right bundle branch during tachycardia determined that resolution of the functional retrograde right bundle branch block was associated with migration of the site of block from the distal to the proximal right bundle. When the site of block was directly at the recording site, both anterograde and retrograde activation of the right bundle was demonstrated. CONCLUSION: Migration of the site of block is a mechanism of resolution for functional conduction blocks maintained by concealed conduction.

Diazepam infusion in tetanus: correlation of drug levels with effect.

A patient with muscle spasms and rigidity associated with tetanus was successfully treated with a continuous infusion of diazepam. This beneficial response was associated with a minimal serum diazepam concentration of 500 ng/ml. The major metabolite of diazepam, DMD, did not appear to exert substantial activity. Guidelines for dosing diazepam are provided.

Efficacy, safety, and tolerance of d-sotalol in patients with refractory supraventricular tachyarrhythmias.

The efficacy, safety, and electrophysiologic effects of intravenous and oral d-sotalol, an investigational class III antiarrhythmic agent, are not yet well characterized. We evaluated the electrophysiologic, antiarrhythmic, and hemodynamic effects of d-sotalol infusion (1.5 to 2.75 mg/kg) and of chronic oral therapy (200 to 400 mg bid) in 10 patients with chronic, paroxysmal supraventricular tachyarrhythmias refractory to 5 +/- 2 standard agents. Four patients had paroxysmal supraventricular tachycardia (PSVT), four had paroxysmal atrial fibrillation, two had atrial flutter, and one had nonparoxysmal reciprocating junctional tachycardia (NPRJT). PSVT was inducible or spontaneously present in 4 of 4 before d-sotalol. After intravenous d-sotalol PSVT was noninducible in three patients and slowed by 40% in one. Atrial fibrillation was inducible or spontaneously present in 4 of 4 before therapy. After intravenous d-sotalol, one became noninducible, and three achieved rate-slowing (the mean falling from 69 to 61 bpm). In one patient, atrial flutter became noninducible; in another, d-sotalol slowed the rate of atrial flutter by 28%. D-sotalol restored sinus rhythm in the patient with NPRJT. Intravenous d-sotalol increased the sinus cycle length; the QTc, PR, and AH intervals; and the AV nodal functional refractory period, the AV nodal effective refractory period; and the right ventricular effective refractory period significantly. The atrial effective refractory period, sinoatrial conduction time, and corrected sinus recovery time tended to increase, but did not reach statistical significance. The QRS, PA, and HV intervals did not change. Mean BP fell 13.4 +/- 9.2% after intravenous d-sotalol, but no adverse symptoms developed.(ABSTRACT TRUNCATED AT 250 WORDS)

Evolving concepts in radiofrequency catheter ablation of atrioventricular nodal reentry tachycardia.

Our results and those of others (Table I) suggest that both anatomic and electrogram (potential) approaches are highly successful in eliminating AVNRT. The use of slow-pathway potentials appears to minimize lesion delivery and to be associated with a very small likelihood of complete AV block. Approaches aimed directly at the midseptum also appear to reduce lesion delivery. It is important, however, to understand that the fast and slow AV-nodal pathways are not always confined to anterosuperior (fast) and posteroinferior (slow) locations (at least as they are determined fluoroscopically). On occasion, the slow pathway may be ablated anteriorly and the fast pathway posteriorly. Our three inadvertent successful fast-pathway ablations support these findings. We prefer to conceptualize the AV node as having three ablation zones. Ablation in the anterosuperior zone most often affects fast-pathway conduction; ablation in the posteroinferior zone most often affects slow pathway conduction; and ablation in the midseptal region predominantly affects slow-pathway conduction. Lesions applied to the midseptum do, however, appear more likely to affect inadvertently the fast (or both) pathway(s), probably because of the anatomic convergence of the posteroinferior and anterosuperior AV-nodal approaches in this region. A preliminary report by Wu et al. supports this three-zone concept. The subsequent larger series reported by this group has raised concern that midseptal approaches may be associated with too great a risk of complete AV block. On the other hand, approaches guided exclusively by potentials may be associated with much longer procedure times. Controversy exists over the acceptable end point for ablation procedures. We have not found it necessary routinely to eliminate dual-nodal conduction to maintain a low (3.2%) overall recurrence rate. Aggressive attempts to eliminate all evidence of slow-pathway conduction must be balanced against the risk of inadvertent complete AV block. In conclusion, cumulative data and our clinical experience with ablation of AVNRT suggest that it is possible to be both pragmatic and highly successful. The key components of our approach are (1) an anatomically based, systematic, time-limited search for potentials; (2) elimination of unnecessary lesions that are too atrial or too ventricular to involve the reentrant circuit; (3) a caudocephalad approach that avoids excessively anterior initial lesions, which may result in inadvertent complete AV block; and (4) avoidance of unnecessary lesions in the most inferoposterior sector, which results in patient discomfort and low clinical efficacy. This approach is safe (with minimal risk of AV block), reproducible, and efficacious.

Mechanism of atrioventricular nodal facilitation in the rabbit heart: role of the distal AV node.

We investigated whether atrioventricular (AV) nodal facilitation is the result of distal AV nodal action potential shortening. Atrial and bundle of His (H) electrograms and microelectrode recordings from proximal and distal AV nodal cells were analyzed in eight superfused rabbit AV node preparations in response to two pacing protocols. In the facilitation protocol, an atrial extrastimulus (A3) was preceded by an atrial impulse (A2) introduced 300, 200, 150, or 125 ms after 30 basic beats (A1). The preexcitation protocol differed from the facilitation protocol by the addition of a premature His depolarization (h2) such that the H1-h2 interval was shorter than the H1-H2 interval. Conduction curves (A3-H3 vs. H2-A3, h2-A3, and A2-A3 intervals) were constructed. Facilitation was demonstrated in all preparations when H2-A3 was used (P = 0.02) but not in the A2-A3 format. Compared with facilitation at the same A1-A2 intervals, preexcitation, despite shortening the distal cellular action potential duration, resulted in longer A3-H3 delays (P = 0.002), shorter A2-A3 intervals, and depression of the proximal nodal cellular response. Thus facilitation does not result from altered distal AV nodal characteristics and instead is a manifestation of an uncontrolled pacing protocol-dependent modulation of proximal AV nodal function.

Programmable external automatic antitachycardia pacing as a bridge to definitive therapy in patients with recurrent sustained ventricular tachycardia.

The efficacy and safety of external programmable automatic antitachycardia pacemakers (ATPs) used in the critical care setting for recurrent sustained monomorphic ventricular tachycardia (VT) was evaluated. Ten patients who had failed a mean of 4.0 +/- 1.4 antiarrhythmic medications (range 2-7) and who had previously required electrical cardioversion for VT were enrolled. Prior to ATP use, successful overdrive pacing termination of VT was demonstrated in all patients. Intertach (Intermedics, Inc.; n = 9) and Orthocor II (Cordis, Inc.; n = 1) ATPs were attached to temporary bipolar transvenous or epicardial pacing leads. Mean patient age was 66.4 +/- 11.5 years, and mean left ventricular ejection fraction was 22 +/- 7.5%. At the time of initial ATP use, mean VT cycle length was 347 +/- 88 msec (range 280-550 msec). A burst scanning antitachycardia pacing algorithm was used in each patient; one patient was also treated with a fixed rate burst adapted to VT cycle length. The duration of ATP use ranged from 2-25 days (median 5), successfully terminating greater than 3,369 VT episodes (median 3, range 0 to greater than 3,103 episodes per-patient). Two episodes of ATP induced rate acceleration occurred, each successfully terminated by the ATP. Only two patients required external cardioversion during ATP use, one for primary ventricular fibrillation and one for rapid polymorphic VT associated with antiarrhythmic drug withdrawal. ATPs also provided antibradycardia pacing and allowed for serial programmed ventricular stimulation. No complications were associated with transvenous catheter or ATP use.(ABSTRACT TRUNCATED AT 250 WORDS)

The electrophysiologic effects of upright posture.

In order to determine the effects of upright posture on the electrophysiologic properties of the human heart, 12 patients underwent electrophysiologic studies in the supine and upright positions. Compared to supine, the upright position significantly reduced basic cycle length from 818 +/- 111 to 680 +/- 141 msec, sinoatrial conduction time from 186 +/- 94 to 135 +/- 56 msec, corrected sinoatrial recovery time from 206 +/- 104 to 108 +/- 55 msec, interatrial conduction time from 76 +/- 17 to 70 +/- 16 msec, and the AV nodal conduction time (AH interval) from 88 +/- 19 to 78 +/- 14 msec (all p less than 0.05). Right intra-atrial and His-Purkinje (HV interval) conduction times were not altered. When the subjects assumed the upright position, the effective refractory periods of the right atrium, atrioventricular node, and right ventricle decreased significantly at basic and paced cycle lengths. For the group as a whole, the upright posture did not significantly augment repetitive responses to atrial and ventricular extrastimuli.

Characterization of left atrial appendage Doppler flow in atrial fibrillation and flutter by Fourier analysis.

The aim of this study was to characterize left atrial appendage mechanical function in atrial fibrillation and flutter by Fourier analysis to analyze frequency and regularity of flow. Left atrial appendage function is central to a patient's risk for thromboembolism. Although the function of the appendage can be analyzed by Doppler echocardiography in sinus rhythm, its mechanical function in atrial fibrillation and flutter has not been well characterized. This lack of adequate definition is caused by the complexity and temporal variability of the Doppler flow profiles. We assessed left atrial appendage function in 21 cases of atrial fibrillation (n - 11) and flutter (n = 10) and five in sinus rhythm with transesophageal Doppler echocardiography. Doppler profiles were examined by Fourier analysis, and the power spectra compared and analyzed between patients with atrial fibrillation and flutter. Left atrial appendage Doppler flow in atrial fibrillation produced Fourier spectra over a narrow band of frequencies with a peak frequency of 6.2 +/- 1.0 Hz, significantly higher than in atrial flutter (3.9 +/- 0.6 Hz, p < 0.00001). Additionally, a significant difference in subharmonic modulation (spectral power below the peak frequency) was observed between atrial appendage flow in atrial fibrillation and flutter, because 37% +/- 16% of the total spectral power was achieved before the dominant frequency in atrial fibrillation compared with 20% +/- 14% in atrial flutter (p = 0.02). Conversely, patients in sinus rhythm exhibited broad-banded Fourier spectra with most of the power in discrete frequency spikes at harmonics above the fundamental frequency with very little subharmonic modulation (1% +/- 0.05%). Left atrial appendage function in atrial fibrillation and flutter can be well characterized by Fourier analysis of Doppler flow. Atrial fibrillation has higher dominant frequencies and greater subharmonic modulation compared with flutter. Moreover, atrial fibrillation demonstrated quasiperiodic contraction patterns typically found in chaotic systems. Fourier analysis of left atrial appendage contraction patterns may therefore have significant promise in providing insights into mechanisms of atrial fibrillation and thromboembolism.