Randomized assessment of syncope trial: conventional diagnostic testing versus a prolonged monitoring strategy.

BACKGROUND: Establishing a diagnosis in patients with unexplained syncope is complicated by infrequent and unpredictable events. Prolonged monitoring may be an alternative strategy to conventional testing with short-term monitoring and provocative tilt and electrophysiological testing. METHODS AND RESULTS: Sixty patients (aged 66+/-14 years, 33 male) with unexplained syncope were randomized to "conventional" testing with an external loop recorder and tilt and electrophysiological testing or to prolonged monitoring with an implantable loop recorder with 1 year of monitoring. If patients remained undiagnosed after their assigned strategy, they were offered crossover to the alternate strategy. A diagnosis was obtained in 14 of 27 patients randomized to prolonged monitoring compared with 6 of 30 patients undergoing conventional testing (52% versus 20%, P=0.012). Crossover was associated with a diagnosis in 1 of 6 patients undergoing conventional testing compared with 8 of 13 patients who completed monitoring (17% versus 62%, P=0.069). Overall, prolonged monitoring was more likely to result in a diagnosis than was conventional testing (55% versus 19%, P=0.0014). Bradycardia was detected in 14 patients undergoing monitoring compared with 3 patients undergoing conventional testing (40% versus 8%, P=0.005). CONCLUSIONS: A prolonged monitoring strategy is more likely to provide a diagnosis than conventional testing in patients with unexplained syncope. Consideration should be given to earlier implementation of a monitoring strategy.

Cryothermal ablation of the slow pathway for the elimination of atrioventricular nodal reentrant tachycardia.

BACKGROUND: We report the first successful slow pathway ablation using a novel catheter-based cryothermal technology for the elimination of atrioventricular nodal reentrant tachycardia (AVNRT). METHODS AND RESULTS: Eighteen patients with typical AVNRT underwent cryoablation. Reversible loss of slow pathway (SP) conduction during cryothermy (ice mapping) was demonstrated in 11 of 12 patients. Because of time constraints, only 2 sites were ice mapped in 1 patient. Seventeen of 18 patients had successful cryoablation of the SP. One patient had successful ice mapping of the SP, but inability to cool beyond -38 degrees C prevented successful cryoablation. A single radiofrequency lesion at this site eliminated SP conduction. No patient has had recurrent AVNRT over 4.9+/-1.7 months of follow-up. During cryoablation, accelerated junctional tachycardia was not seen and was therefore not available to guide lesion delivery. Adherence of the catheter tip during cryothermy (cryoadherence) allowed atrial pacing to test for SP conduction. Cryoablation in the anterior septum produced inadvertent transient PR prolongation consistent with loss of fast pathway conduction in 1 patient and transient (6.5 seconds) 2:1 AV block in another. On rewarming, the PR interval returned to normal, and the AV nodal effective refractory period was unchanged in both. Accelerated junctional tachycardia was seen on rewarming in both but not during cryothermy. CONCLUSIONS: Cryothermal ablation of the SP was achieved in patients with this novel technique. Successful ice mapping of both the SP and fast pathway was demonstrated. The ability to test the functionality of specific ablation sites before production of a permanent lesion may eliminate inadvertent AV block.

Canadian implantable defibrillator study (CIDS) : a randomized trial of the implantable cardioverter defibrillator against amiodarone.

BACKGROUND: Patients surviving ventricular fibrillation (VF) or sustained ventricular tachycardia (VT) are at a high risk of death due to a recurrence of arrhythmia. The implantable cardioverter defibrillator (ICD) terminates VT or VF, but it is not known whether this device prolongs life in these patients compared with medical therapy with amiodarone. METHODS AND RESULTS: A total of 659 patients with resuscitated VF or VT or with unmonitored syncope were randomly assigned to treatment with the ICD or with amiodarone. The primary outcome measure was all-cause mortality, and the secondary outcome was arrhythmic death. A total of 328 patients were randomized to receive an ICD. A thoracotomy was done in 33, no ICD was implanted in 18, and the rest had a nonthoracotomy ICD. All 331 patients randomized to amiodarone received it initially. At 5 years, 85.4% of patients assigned to amiodarone were still receiving it at a mean dose of 255 mg/day, 28.1% of ICD patients were also receiving amiodarone, and 21.4% of amiodarone patients had received an ICD. A nonsignificant reduction in the risk of death was observed with the ICD, from 10.2% per year to 8.3% per year (19.7% relative risk reduction; 95% confidence interval, -7.7% to 40%; P=0.142). A nonsignificant reduction in the risk of arrhythmic death was observed, from 4.5% per year to 3.0% per year (32.8% relative risk reduction; 95% confidence interval, -7.2% to 57.8%; P=0.094). CONCLUSIONS: A 20% relative risk reduction occurred in all-cause mortality and a 33% reduction occurred in arrhythmic mortality with ICD therapy compared with amiodarone; this reduction did not reach statistical significance.

Sensitivity and specificity of invasive and noninvasive testing for risk of sudden death in Wolff-Parkinson-White syndrome.

Invasive electrophysiologic testing and noninvasive testing were compared as methods for identifying patients with Wolff-Parkinson-White syndrome at risk for sudden death. Sixty-seven patients were studied, including nine with a history of ventricular fibrillation. Electrophysiologic testing, using the shortest interval between consecutive pre-excited beats (shortest RR interval) less than or equal to 250 ms during induced atrial fibrillation to define risk, identified seven of nine patients with previous ventricular fibrillation. The sensitivity increased to 87.5% if one patient with prior amiodarone therapy was excluded. Electrophysiologic testing had a specificity of 48.3% and a low predictive accuracy (18.9%) when using the shortest RR interval (less than or equal to 250 ms) to identify the risk for sudden death. Continuous pre-excitation after disopyramide (2 mg/kg body weight, intravenously) had a sensitivity of 71.4%, specificity of 26.1% and predictive accuracy of 12.8% for identifying patients with sudden death. Continuous pre-excitation during an exercise test identified these patients with a sensitivity of 80%, a specificity of 28.6% and a predictive accuracy of 11.8%. These noninvasive tests could also be used to predict the shortest RR interval observed during induced atrial fibrillation. Continuous pre-excitation on both tests used in combination had a sensitivity of 91.2%, a specificity of 66.7% and a predictive accuracy of 75.6% for predicting the shortest RR interval less than or equal to 250 ms. Thus, both invasive and noninvasive techniques have a good sensitivity but a low specificity for identifying patients with Wolff-Parkinson-White syndrome and sudden death.(ABSTRACT TRUNCATED AT 250 WORDS)

Sequential pulse defibrillation in humans: orthogonal sequential pulse defibrillation with epicardial electrodes.

A newly described sequential pulse technique, using four mesh electrodes positioned to approximate a true orthogonal system around the heart, was compared with a single pulse system using two of these same electrodes, which were located in positions that would be used for an automatic implantable defibrillator. The influence of electrode size was also assessed. The minimal energy necessary for defibrillation (defibrillation threshold) was determined intraoperatively in 21 volunteer patients undergoing accessory pathway ablation of Wolff-Parkinson-White syndrome. Ventricular fibrillation was induced with alternating current. Ten seconds after fibrillation onset defibrillation shocks were begun using either the single or the sequential pulse technique with stored voltage incremented until defibrillation was accomplished (defibrillation threshold). Selection of the use of a single or sequential pulse technique for the initial attempt was randomized. Defibrillation thresholds were determined in three groups of patients: 1) those with four small mesh electrodes (6 cm2), 2) those with two small and two large (13 cm2) mesh electrodes, and 3) those with four large mesh electrodes. In all cases, the average minimal energy needed for sequential pulse defibrillation was less than that required for single pulse defibrillation in the same patients with the same electrodes (four small, 24.8 +/- 24.7 J single versus 6.7 +/- 8.3 J sequential; two small plus two large, 11.4 +/- 15.0 J single versus 2.7 +/- 1.4 J sequential; four large, 8.1 +/- 5.3 J single versus 3.9 +/- 2.6 J sequential). Using the 6 cm2 electrodes for single pulse defibrillation energies delivered at greater than 45 J in two patients failed to defibrillate the heart.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute effect of disopyramide on atrial fibrillation in the Wolff-Parkinson-White syndrome.

Disopyramide was administered intravenously to 54 patients during atrial fibrillation and predominantly pre-excited QRS configuration at the time of electrophysiologic study. All patients had Wolff-Parkinson-White syndrome and no patient had coexistent heart disease. The drug was given during sustained atrial fibrillation (n = 45) or during sinus rhythm before induction of atrial fibrillation for patients whose atrial fibrillation was self-terminating in the control state (n = 9). Atrial fibrillation converted to sinus rhythm within 15 min after disopyramide in 37 (82%) of the 45 patients. The shortest RR intervals between two pre-excited cycles increased from 208 +/- 42 to 293 +/- 117 ms (p less than 0.0001). The average RR interval of all cycles prolonged from 332 +/- 60 to 396 +/- 117 ms(n = 45, p less than 0.0001). The 9 patients in whom pre-excitation was abolished after the drug had a significantly longer initial shortest RR interval than that of the 36 patients in whom pre-excitation persisted (246 +/- 47 versus 199 +/- 36 ms, p = 0.0022). No patients developed significant hemodynamic or other adverse effects after disopyramide. These data support the intravenous use of disopyramide in patients with normal ventricular function who have atrial fibrillation and a predominant ventricular response over an accessory atrioventricular pathway.

Electrophysiologic substrate associated with pacing-induced heart failure in dogs: potential value of programmed stimulation in predicting sudden death.

To investigate the possible mechanisms of sudden death and the potential role of electrophysiologic testing in congestive heart failure, this study evaluated the electrophysiologic substrate in a model of heart failure induced by rapid pacing. Seventeen mongrel dogs underwent cardiac pacing at 220 to 240 beats/min for 5 weeks (paced group) and 11 other dogs served as a sham-operated control group. Rapid pacing of the right ventricle produced clinical and hemodynamic features of congestive heart failure. Dogs in the paced group had prolonged cardiac conduction time as reflected by longer epicardial activation time (36.1 +/- 2.4 vs. 30.8 +/- 0.8 ms, p less than 0.05). The ventricular effective refractory period was significantly prolonged after the development of heart failure (141 +/- 4 vs. 177 +/- 5 ms, p less than 0.01, at a basic pacing cycle length of 300 ms), whereas no significant change was found in the control group (140 +/- 4 vs. 145 +/- 4 ms, p = NS). The prolongation of the ventricular effective refractory period correlated with an increase in left ventricular end-diastolic pressure (r = 0.55, p less than 0.001) and the ventricular effective refractory period correlated inversely with cardiac index (r = -0.49, p less than 0.025). The rest membrane potential of ventricular muscle was less negative in the paced group compared with the control group (-80.7 +/- 2.2 vs. -85.6 +/- 2.2 mV, p less than 0.05). Intracellularly recorded action potential duration of ventricular muscle was longer in the paced than in the control group (236 +/- 9.8 vs. 198.9 +/- 2.6 ms, p less than 0.01), action potential duration at 90% repolarization).(ABSTRACT TRUNCATED AT 250 WORDS)

A placebo-controlled trial of intravenous and oral disopyramide for prevention of neurally mediated syncope induced by head-up tilt.

OBJECTIVES: A double-blind randomized trial was designed to determine the efficacy of intravenous and oral disopyramide phosphate in preventing neurally mediated syncope induced by a head-up tilt test. BACKGROUND: Neurally mediated syncope is a frequent cause of syncope and may be induced by head-up tilt testing. Recent uncontrolled trials have suggested that disopyramide may be an effective therapy in patients with neurally mediated syncope. METHODS: Twenty-two consecutive patients with recurrent neurally mediated syncope and two or more successive positive head-up tilt test responses were randomly allocated to receive either intravenous disopyramide or placebo. Head-up tilt testing at 60 degrees was performed for 15 min. If presyncope or syncope was not provoked, isoproterenol infusion was started at a rate of 1 microgram/min and the rate gradually increased until a 25% increase in heart rate was achieved. Eleven patients were subsequently randomized in crossover fashion to receive oral disopyramide (800 mg/day) or placebo during 1 week. The primary end point was prevention of syncope or presyncope provoked by head-up tilt testing. RESULTS: Head-up tilt test results were positive for syncope in 12 (75%) of 16 patients receiving intravenous placebo and in 12 (60%) of 20 patients receiving disopyramide (p = 0.55 Fisher exact test, 95% confidence interval [CI] -14% to 40%). In the intravenous phase, complete crossover was achieved in 15 patients. Head-up tilt test results during this phase were positive in 13 patients (87%) receiving placebo and in 12 patients (80%) receiving disopyramide (p = 0.50 Fisher exact test, 95% CI -19% to 32%) and were positive in all patients receiving their initially randomized drug or placebo. In the oral phase, head-up tilt results were positive in only two patients (18%) assigned to placebo and in three patients (27%) receiving disopyramide (p = 0.54 Fisher exact test, 95% CI -42% to 24%). A mean follow-up time of 29 +/- 8 months was obtained in 21 of the 22 patients. Syncope recurred in 3 (27%) of the 11 patients receiving disopyramide and 3 (30%) of the 10 patients not treated pharmacologically (p > 0.05). CONCLUSIONS: Intravenous disopyramide was ineffective for the prevention of neurally mediated syncope provoked by head-up tilt testing. No significant effect was observed after oral therapy with disopyramide. There was a striking decrease in the incidence of positive tilt test results over time regardless of intervention, thus discouraging the use of head-up tilt as the single method of assessing therapeutic efficacy. Recurrence of syncope after the investigative protocol was infrequent over long-term follow-up regardless of treatment group.

Combination biphasic waveform plus sequential pulse defibrillation improves defibrillation efficacy of a nonthoracotomy lead system.

OBJECTIVES: We hypothesized that combining biphasic waveform and sequential pulse defibrillation techniques would lower the defibrillation threshold of a nonthoracotomy lead system in humans below that obtained with biphasic or sequential pulse defibrillation alone. BACKGROUND: Previous studies have shown that sequential pulse monophasic shocks and biphasic waveform shocks are more effective than single monophasic shocks for ventricular defibrillation. METHODS: Thirteen patients aged 48 to 71 years undergoing nonthoracotomy defibrillation lead testing participated in the study. Transvenous electrodes were positioned in the right ventricular apex, superior vena cava and coronary sinus. A cutaneous patch electrode was placed on the left chest wall. All electrodes were connected to an external defibrillator. In random order, defibrillation threshold measurements were made for biphasic defibrillation alone, sequential defibrillation alone and combined biphasic plus sequential defibrillation. RESULTS: The mean defibrillation threshold-delivered energy was 18.0 +/- 11.9 J for biphasic defibrillation and 16.3 +/- 9.0 J for sequential defibrillation. Biphasic plus sequential defibrillation significantly reduced the threshold energy to 10.2 +/- 5.3 J (p < 0.001). Threshold peak voltage and current values showed corresponding reductions. The combined waveform resulted in a greater reduction in defibrillation threshold in patients with threshold energies > 18 J versus those with threshold values < or = 18 J for sequential (p = 0.001) or biphasic (p < 0.01) waveform alone. The nonthoracotomy lead implantation rate was improved from 62% with each of the single techniques (biphasic waveform or sequential pulse defibrillation) to 85% with the combined waveform. CONCLUSIONS: Adding biphasic waveform to sequential pulse defibrillation significantly reduced the defibrillation threshold compared with either technique alone, and nonthoracotomy lead system implantation can be enhanced by this combined technique.

Mode of onset of atrial fibrillation in the Wolff-Parkinson-White syndrome: how important is the accessory pathway?

The mode of onset of 103 episodes of atrial fibrillation lasting greater than or equal to 30 s was studied in 79 patients with the Wolff-Parkinson-White syndrome during electrophysiologic study. No patient had organic heart disease, and 31 had clinical atrial fibrillation before study. These 79 patients were then compared with a control group of 53 patients with Wolff-Parkinson-White syndrome in whom atrial fibrillation could not be induced. Ninety-five of the 103 episodes were technically suitable for analysis. Atrial fibrillation invariably began with rapid atrial tachycardia that became progressively disorganized within 10 to 20 cycles. It was initiated during right atrial stimulation (n = 52), right ventricular stimulation (n = 8), reciprocating tachycardia (n = 33) and spontaneously (n = 2). Most episodes started at a high right atrial site regardless of accessory pathway location, with only 19% of episodes starting at the electrode closest to the accessory pathway. During reciprocating tachycardia (n = 33), either atrial (n = 8) or ventricular (n = 5) extrastimuli initiated atrial fibrillation. Atrial fibrillation started at the accessory pathway site in 6 of 20 episodes occurring spontaneously during reciprocating tachycardia. Patients with atrial fibrillation had a longer PA interval (54 +/- 14 versus 42 +/- 12 ms, p less than 0.0001), shorter atrial functional refractory period (226 +/- 38 versus 240 +/- 30 ms, p = 0.049) and shorter anterograde effective refractory period of the accessory pathway (279 +/- 26 versus 304 +/- 75 ms, p = 0.03). Clinical reciprocating tachycardia was documented with equal frequency in both the atrial fibrillation and control groups (59.5% versus 52.9%, p = 0.58).(ABSTRACT TRUNCATED AT 250 WORDS)

Defibrillation shocks produce different effects on Purkinje fibers and ventricular muscle: implications for successful defibrillation, refibrillation and postshock arrhythmia.

OBJECTIVES: To understand the mechanisms of postdefibrillation arrhythmias and failed defibrillation, we studied the cellular effects of high voltage shocks on different cardiomyocytes in the dog. BACKGROUND: The causes of postdefibrillation arrhythmias and unsuccessful defibrillation are not clear. METHODS: High voltage shocks with voltage differentials of 9.3 to 97.6 V/cm were delivered to isolated canine papillary muscles with attached Purkinje fibers. Transmembrane potentials were recorded simultaneously from the Purkinje fiber and the ventricular muscle using standard microelectrode techniques. RESULTS: After delivery of high voltage shocks, significant depolarization and rapid firing were observed in Purkinje fibers. The maximal rate of the rapid firing in the Purkinje fibers correlated with shock intensity (r = 0.69, p < 0.05). In contrast, in ventricular muscle, only slight depolarization and a transient refractory state were observed after the shock. The incidence of the refractory state was correlated with both the shock intensity and the rate of the rapid firing in the Purkinje fiber (r = 0.89 and 0.74, p < 0.01 and 0.05, respectively). Propranolol at a concentration sufficient for complete beta-blockade (1 mg/liter) did not change the tissue response to shocks but suppressed or abolished the shock-induced rapid firing of Purkinje fibers at a higher concentration (3 mg/liter). Blockade of the slow calcium channel with verapamil (400 micrograms/dl) did not alter the responsiveness of the preparation to shocks. CONCLUSION: These results indicate that high voltage shocks induce different responses in Purkinje fibers and ventricular muscle. The shock-induced rapid firing in the Purkinje fiber may contribute to postshock arrhythmias and possibly refibrillation in some cases. The shock-induced transient refractory state in the ventricular muscle may prevent the ventricle from responding to the rapid firing and thus may decrease the incidence of postshock arrhythmias.

Junctional tachycardia: a useful marker during radiofrequency ablation for atrioventricular node reentrant tachycardia.

OBJECTIVES: The aim of this study was to evaluate junctional tachycardia as a useful marker during radiofrequency ablation for atrioventricular (AV) node reentrant tachycardia. BACKGROUND: Junctional tachycardia appears to be a response of the atrioventricular node to injury and is seen during both radiofrequency AV node ablation and slow and fast pathway ablation for AV node reentrant tachycardia. We hypothesized that junctional tachycardia heralding AV node block and that associated with slow or fast pathway ablation may have different characteristics that could be useful in preventing inadvertent AV block. METHODS: Characteristics of junctional tachycardia were examined after 59 radiofrequency ablation sessions in 53 consecutive patients with a mean age (+/- SD) of 41.6 +/- 16.5 years. Type 1 junctional tachycardia was followed by transient second- or third-degree AV block (n = 5) or permanent third-degree AV block (n = 1). Type 2 junctional tachycardia was followed by normal AV conduction (n = 53). RESULTS: Fifty-one patients had typical AV node reentrant tachycardia, and two patients had atypical tachycardia. Fast pathway ablation was attempted during 6 sessions and slow pathway ablation during 53 sessions. Patients underwent 15.3 +/- 10 radiofrequency applications, with a mean duration of 24 +/- 9.7 s. Junctional tachycardia was observed an average of 2.8 +/- 1.8 times per ablation session. Type 1 junctional tachycardia had a significantly faster rate than that of type 2 (cycle length 363 +/- 44 vs. 558 +/- 116, p < 0.001). In addition, type 1 junctional tachycardia was associated with predominantly ventriculoatrial block whereas type 2 was associated with predominantly 1:1 ventriculoatrial conduction (2 of 6 vs. 47 of 53 episodes, p < 0.05). CONCLUSIONS: We conclude that junctional tachycardia leading to AV block can be recognized by a faster junctional rate and ventriculoatrial block. This is a useful marker of impending AV block during slow and fast pathway ablation.

"Atypical" posteroseptal accessory pathway in Wolff-Parkinson-White syndrome.

The posteroseptal accessory pathway in the Wolff-Parkinson-White syndrome is associated with a delta wave that is negative in the inferior electrocardiographic (ECG) leads and the occurrence of the earliest retrograde atrial activation near the orifice of the coronary sinus during atrioventricular (AV) reentrant tachycardia. Seventy-two patients with a posteroseptal accessory pathway underwent epicardial mapping before operative ablation. The earliest epicardial activation occurred at the posterosuperior process of the left ventricle in all patients. Dissection of the posteroseptal region (right atrial-left ventricular sulcus) resulted in permanent loss of preexcitation in 69 patients and failure to abolish preexcitation permanently in 3. At reoperation in two patients, preexcitation was abolished by discrete cryoablation of the left side of the interatrial septum near the AV node approached through the atrial septum in the normothermic beating heart. At reoperation, one patient had extensive AV node dissection. All patients have had permanent loss of preexcitation. The vast majority of posteroseptal accessory pathways ("typical") are epicardial and ablated by dissection of the posteroseptal region. Rarely, posteroseptal accessory pathways are "atypical" in that they are intraseptally located near the AV node on the left atrial endocardial surface.

Comparison of the ventricular response during atrial fibrillation in patients with enhanced atrioventricular node conduction and Wolff-Parkinson-White syndrome.

Although ventricular fibrillation is a well known sequel to atrial fibrillation in the Wolff-Parkinson-White syndrome, ventricular fibrillation is not generally associated with supraventricular tachycardia in the presence of enhanced atrioventricular (AV) node conduction without pre-excitation. It was hypothesized that the ventricular response during atrial fibrillation may be less in patients with enhanced AV node conduction than in their counterparts with Wolff-Parkinson-White syndrome matched for anterograde effective refractory period. Slower ventricular rates during atrial fibrillation would suggest an increased propensity for concealed conduction in the enhanced AV node conduction group than in the group with an accessory pathway. Three groups of patients aged 16 to 65 years underwent electrophysiologic testing for supraventricular tachycardia or after surgical correction of Wolff-Parkinson-White syndrome. Sixteen patients had enhanced AV node conduction, 16 had Wolff-Parkinson-White syndrome and 16 had normal AV node conduction. Patients with enhanced AV node conduction and Wolff-Parkinson-White syndrome were well matched for anterograde effective refractory period (245 +/- 22 versus 258 +/- 25 ms) and minimal cycle length, maintaining 1:1 anterograde conduction (261 +/- 21 versus 260 +/- 40). There was no difference in intervals during atrial fibrillation (average RR interval = 372 +/- 37 versus 346 +/- 66) or shortest RR interval (266 +/- 27 versus 243 +/- 51). Thus, patients with Wolff-Parkinson-White syndrome and those with enhanced AV node conduction matched for anterograde refractory period exhibit similar ventricular rates during atrial fibrillation.(ABSTRACT TRUNCATED AT 250 WORDS)

Changes in pacing threshold and R wave amplitude after transvenous catheter countershock.

Transvenous electrode catheter countershock in patients with recurrent ventricular tachyarrhythmias may be followed by transient bradycardia and require temporary pacing with a catheter. The serial changes in R wave amplitude and stimulation threshold after catheter countershock in 11 halothane-anesthetized open chest dogs ranging in weight from 11.8 to 24 kg were studied. Ventricular fibrillation was electrically induced and followed by catheter defibrillation using nonsynchronized trapezoidal waveform (65% tilt) current discharge in incremental doses (5 to 50 J). Significant decreases in bipolar R wave amplitude (8.3 +/- 1 versus 2 +/- 0.2 mV, p less than 0.001) and increases in stimulation threshold (1 +/- 0.1 versus 2.3 +/- 0.4 V, p less than 0.001) were observed using the countershock catheter 15 seconds after countershock; these changes persisted for up to 10 minutes. To determine whether these changes were localized to the defibrillating catheter and whether they were species-specific, a second electrode catheter was positioned in the right ventricle distant from the countershock catheter in five pigs. Increases in stimulation threshold were observed only at the countershock catheter, suggesting that changes were secondary to local changes at the catheter-myocardium interface. No significant change in R wave amplitude or stimulation threshold was observed at the countershock catheter in three pigs given transthoracic shocks (60 to 250 J). It is concluded that current discharge through the countershock catheter results in a significant temporary reduction in R wave amplitude and an increase in pacing threshold. This may make pacing through the countershock catheter unreliable after shock delivery.

Surgical correction of the Wolff-Parkinson-White syndrome in the closed heart using cryosurgery: a simplified approach.

The conventional operation for ablation of accessory atrioventricular (AV) pathways in the Wolff-Parkinson-White syndrome requires an endocardial approach to the AV groove and necessitates the use of cardiopulmonary bypass and induced cardiac arrest. The feasibility of creating transmural atrial fibrosis at the level of the AV anulus in the closed heart in dogs without damaging the vascular contents of the AV fat pad was demonstrated. This was done by dissecting the fat pad from the atrium and applying a cryoprobe to the exposed atrial-anular region after retraction of the fat pad. The technique was then applied to successfully ablate 12 left parietal wall accessory pathways in 11 patients with the Wolff-Parkinson-White syndrome. This simplified approach to any parietal wall accessory pathway does not require cardiopulmonary bypass or induced cardiac arrest and may broaden the indications for this operation.

Differential effect of intravenous procainamide on anterograde and retrograde accessory pathway refractoriness.

Although procainamide may markedly impair or abolish anterograde conduction over an accessory atrioventricular (AV) pathway, orthodromic AV reentry may remain inducible. This difference may be related to a systemic differential effect of procainamide on anterograde and retrograde accessory pathway refractoriness. To examine this phenomenon, an infusion of procainamide producing five incremental blood levels over 75 min was administered to 15 patients with the Wolff-Parkinson-White syndrome. At each procainamide level, accessory pathway effective refractory period and accessory pathway block cycle length were determined in the anterograde and retrograde directions. At baseline, there were no significant differences between anterograde and retrograde accessory pathway effective refractory periods (282 +/- 7 vs. 266 +/- 9 ms, p = 0.08) and block cycle lengths (288 +/- 15 vs. 283 +/- 9 ms, p = 0.66). The concentration of procainamide resulting in 50% prolongation of accessory pathway refractoriness was less in the anterograde direction than in the retrograde direction (27.5 [log concentration -4.56 +/- SE 0.13] vs. 64.6 [-4.19 +/- 0.11] mumol/liter, p = 0.02). Similarly, the concentration of procainamide resulting in 50% prolongation of accessory pathway block cycle length in the anterograde direction (25.1 [-4.60 +/- 0.13] mumol/liter) was less than in the retrograde direction (52.5 [-4.28 +/- 0.07] mumol/liter, p = 0.01). The probability of persistence of accessory pathway conduction in the anterograde direction was less than in the retrograde direction by Kaplan-Meier analysis (p = 0.04).(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of adenosine or adenosine triphosphate on antidromic tachycardia.

OBJECTIVES: This study was designed to determine the effect of adenosine or adenosine triphosphate (ATP) on antidromic tachycardia. BACKGROUND: Adenosine and adenosine triphosphate are useful for differential diagnosis of wide QRS tachycardia. It has been believed that tachycardia termination caused by these agents is due to the preferential depressive effect on the atrioventricular (AV) node, whereas their effect on accessory pathways is minimal. METHODS: We studied the effect of adenosine or ATP on the termination pattern of antidromic tachycardia in 17 patients (10 men, 7 women; mean age [+/- SD] 32 +/- 11 years) with one or more accessory pathways. Adenosine (6 to 12 mg [n = 10]) or ATP (8 to 20 mg [n = 7]) was injected rapidly through a central venous line and followed by 10 ml of saline flush after induction of sustained antidromic tachycardia. RESULTS: Tachycardia was terminated in < 2 min in 14 patients (82%) after the injection and remained unchanged in 3 (18%). Tachycardia termination was due to conduction block in the accessory pathway (anterograde limb) in seven patients (50%) and in the AV node (retrograde limb) in another seven. Adenosine or ATP caused accessory pathway block in seven (88%) of the eight patients lacking retrograde accessory pathway conduction and in none of the nine patients having retrograde accessory pathway conduction (p < 0.01). All five patients with an atriofascicular accessory pathway and unidirectional anterograde conduction had tachycardia termination due to anterograde accessory pathway block after injection of adenosine or ATP. CONCLUSIONS: 1) Adenosine or ATP effectively terminates antidromic tachycardia; 2) the termination is related to block in either the accessory pathway or the AV node; 3) accessory pathway block occurs in patients with a unidirectional, anterogradely conducting accessory pathway, especially an atriofascicular accessory pathway.

Right ventricular pressure during ventricular arrhythmias in humans: potential implications for implantable antitachycardia devices.

Implantable defibrillators use algorithms based on ventricular electrographic data to detect the onset and termination of arrhythmias, but these algorithms do not always differentiate hemodynamically stable from unstable arrhythmias. Although, ideally, left ventricular function should be used to assess the hemodynamic state, right ventricular pulse pressure can be assessed in humans on a long-term basis with a transvenous lead. The potential utility of right ventricular pulse pressure to assess hemodynamic stability was studied in 22 patients with induced ventricular arrhythmias. Right ventricular pressure was measured with use of a transvenous right ventricular endocardial pacing lead with a piezoelectric bender pressure sensor 3 cm from its tip. Single ventricular premature paced beats administered in up to a bigeminal frequency did not alter the mean right ventricular pulse pressure (control 33.7 +/- 26, bigeminy 35.7 +/- 26 mm Hg). Twenty-one episodes of induced ventricular tachycardia were studied in the electrophysiology laboratory. Five seconds after tachycardia induction, hemodynamically stable ventricular tachycardia had a longer cycle length (294 +/- 41 ms) and the right ventricular pulse pressure ratio was higher (0.55 +/- 0.26) than that in unstable ventricular tachycardia (cycle length 256 +/- 55 ms, p = 0.06; pulse pressure ratio 0.26 +/- 0.09, p less than 0.05). Twenty episodes of ventricular fibrillation were induced in eight patients. One second after induction, right ventricular pulse pressure decreased from 25 +/- 5 to 6 +/- 3 mm Hg (p less than 0.05). On the first beat after defibrillation, right ventricular pulse pressure increased to 24 +/- 14 mm Hg, a level not significantly different from that before the induction of ventricular fibrillation.(ABSTRACT TRUNCATED AT 250 WORDS)

Predictive accuracy of electrophysiologic localization of accessory pathways.

Operative ablation of accessory pathways depends critically on preoperative localization when technical limitations preclude complete intraoperative mapping. To assess the accuracy of localization, 345 patients undergoing operative ablation were studied; 316 (91.6%) had a single accessory pathway and 29 (8.4%) had multiple accessory pathways. The electrophysiologic study was diagnostically complete and accurate in 294 patients (93%) with a single accessory pathway and 19 (61%) with multiple accessory pathways. A left lateral accessory pathway was most accurately localized with excellent sensitivity (99%) and positive predictive value (98.5%). Diagnostic errors occurred in 33 patients because of 1) incorrect localization (n = 16), 2) failure to detect a second pathway (n = 9), and 3) diagnosis of a second pathway not verified intraoperatively (n = 8). Multiple pathways were more prevalent in the group with errors (33.3% vs. 5.8%, p = 0.0001), as were unidirectional pathways (48.5% vs. 24.3%, p = 0.003). It is concluded that preoperative localization of accessory pathways is sufficiently accurate to allow intraoperative mapping to be brief and focused.