Metabolism-perfusion imaging to predict disease activity in cardiac sarcoidosis.

FDG-PET is a sensitive but not specific test for myocardial sarcoidosis and its ability to define prognosis remains unclear. Combination with perfusion scanning may improve accuracy by differentiating scar from inflammation. We conducted this retrospective chart review to ascertain the utility of a rubidium -FDG PET scan for assessment of disease activity in patients with cardiac sarcoidosis. The presence of any perfusion-metabolism mismatch or a mismatch of > 6% of the myocardium on the scan were compared with the clinical course. Among 18 subjects, mismatched segments were present in 11 scans, whereas 7 demonstrated mismatch > 6%. There was a suggestion of association between PET scan and active disease using the threshold of any mismatch (p=0.09), with sensitivity of 80% and specificity of 62.5%. The threshold of >6% mismatch improved the specificity to 100% with 70% sensitivity, and the association between PET findings and clinically active disease was highly significant (p=0.0002). Eight patients had follow-up Rb-FDG PET scans, all of which were concordant with the clinical course. The positive predictive value of Rb-FDG PET scan showing >6% mismatch for detecting clinically active cardiac sarcoidosis was 100%. However, the finding of any mismatch still portends a high chance of clinical activity. Further studies to define the utility of Rb-FDG PET scan for management of cardiac sarcoidosis are warranted.

Electrophysiologic characteristics of sudden QRS axis deviation during orthodromic tachycardia. Role of functional fascicular block in localization of accessory pathway.

We analyzed the effect of functional fascicular block (FFB) on ventriculoatrial conduction time (VACT) during orthodromic tachycardia (OT) in 32 patients with single accessory pathway (AP) of the Kent bundle type. The location of AP was left free wall (LFW-AP) in 21 patients, left posteroseptal in 6, right free wall in 2, and right anteroseptal in 3. FFB either alone or in combination with functional left or right bundle branch block (LBBB or RBBB) occurred predominantly at the onset of OT and was initiated with ventricular extrastimulus technique more often than with atrial extrastimulation. In patients with LFW-AP, isolated functional left anterior fascicular block (LAFB) produced significant prolongation in VACT (15-35 ms). A similar magnitude of VACT increase (20-35 ms) was also observed when LAFB was associated with RBBB. Although 25-45-ms prolongation in VACT occurred with functional LBBB and normal axis, an additional 20-55-ms VACT increase was seen when LAFB accompanied LBBB. Functional LAFB, alone or in combination with bundle branch block, however, did not prolong VACT in patients with other AP locations. Furthermore, left posterior fascicular block did not produce prolongation of VACT in any of the cases. It is concluded that in patients with the Wolff-Parkinson-White syndrome, evaluation of VACT during functional LAFB provides important information regarding AP localization and a clear separation of LFW-AP from all other locations.

Electrophysiologic mechanisms of functional bundle branch block at onset of induced orthodromic tachycardia in the Wolff-Parkinson-White syndrome. Role of stimulation method.

The mechanisms of aberrant conduction at the onset of induced orthodromic tachycardia in the Wolff-Parkinson-White syndrome were analyzed in 20 consecutive patients in whom this tachycardia was initiated by the atrial (A2) and/or right ventricular (V2) extrastimulus techniques. Of 13 patients in whom orthodromic tachycardia was induced by the A2 method, functional right bundle branch block occurred at tachycardia onset in four (31%) and left bundle aberrancy in two (15%), one of whom also manifested right bundle aberrancy. The occurrence of bundle branch block at the onset of tachycardia was linked to aberrant conduction of the initiating A2 impulse which, in turn, was associated with attainment of relatively short His1His2 intervals within the tachycardia initiation zone. Aberrant conduction of A2 was also more common in patients without manifest preexcitation. In contrast, of 14 patients in whom orthodromic tachycardia was induced by the V2 method, left bundle aberrancy occurred at the onset of tachycardia in 11 (79%), one of whom manifested right bundle branch block as well. Left bundle aberrancy was more likely to occur when the interval from the initiating V2 (or macro-reentrant V3) impulse to the first anterograde His deflection was less than 300 ms. This suggests that left bundle aberrancy at the onset of orthodromic tachycardia induced by the V2 method results from concealed retrograde penetration of the His-Purkinje system, with the left bundle being last to recover. Our findings provide the conceptual basis for a physiologic approach to the deliberate induction of specific types of aberrant conduction at onset of orthodromic tachycardia in patients with Wolff-Parkinson-White syndrome.

Modulation of conduction and refractoriness in atrioventricular junctional reentrant circuit. Effect on reentry initiated by atrial extrastimulus.

The importance of activation sequence of an atrioventricular junctional reentrant (AVJRe) circuit, before delivery of an extrastimulus, has received little attention in studies concerned with clinical tachycardias. In this study a change in activation sequence was accomplished using bidirectional activation (V-A sequential pacing) during the basic drive (V1A1-V1A1). It was noted that, compared with an atrial extrastimulus (A2) after an atrial drive (A1-A1), earlier activation (by V1 impulse of the V1A1-V1A1 drive) consistently improved conduction, or decreased refractoriness, or both, in the anterograde as well as the retrograde pathway of the AVJRe circuit. In all patients, five with AV nodal reentry and six with Wolff-Parkinson-White syndrome, reentrant tachycardia could be prevented during V-A sequential pacing. In four of eleven patients, reentry was prevented despite achieving the so-called critical atrioventricular nodal delays that had previously caused reentry during control study. This finding suggested that conduction delay necessary for reentry was related to the site of block, which in turn was affected by V-A sequential pacing. We concluded that changing the activation sequence during basic drive modulates conduction and refractoriness in AVJRe circuits, and allows the study of a wide range of electrophysical factors that prevent or permit reentry.

Surface potentials from the region of the atrioventricular node and their relation to dual pathway electrophysiology.

BACKGROUND: Clinical applications of the principles of dual atrioventricular nodal (AVN) electrophysiology in the treatment of AVN reentrant tachycardias rely on empirical findings, such as discontinued conduction curves or the presence of specific catheter-recorded signals. However, neither the shape of the conduction curve nor the surface electrograms have been validated as functionally related to the presence of slow or fast wavefronts. METHODS AND RESULTS: We performed in vitro studies using 10 rabbit atrial-AVN preparations. A bipolar roving electrode was used to explore the endocardial surface of the triangle of Koch during programmed electrical stimulation. Microelectrodes were impaled in AVN cells to correlate surface and intracellular responses. In 7 preparations, a specific area near the compact cell region produced surface electrograms that were dissociated in 2 distinct components, with progressive shortening of prematurity. Similar dissociation was demonstrated during Wenckebach periodicity and increased vagal tone. Cellular recordings supported the presence of early ("fast") and late ("slow") wavefronts, with different refractory properties. Although the fast-slow transition was a basis for discontinued propagation, the AVN conduction curves were smooth in the majority of cases. CONCLUSIONS: Exploration of the triangle of Koch during programmed pacing reveals the presence of dual-wavefront surface potentials. Clinical confirmation of these AVN potentials could provide a new, sensitive tool in defining dual AVN electrophysiology.

Atrioventricular nodal conduction during atrial fibrillation: role of atrial input modification.

BACKGROUND: Posteroseptal ablation of the atrioventricular node (AVN) has been proposed as a means to slow the ventricular rate during atrial fibrillation (AF). The suggested mechanism is elimination of the AVN "slow pathway." On the basis of the unpredictable success of the procedure, we hypothesize that, in fact, the slow pathway is preserved. Therefore, the slowing of the ventricular rate results from reduced bombardment of the AVN. METHODS AND RESULTS: In 8 rabbit heart atrial-AVN preparations, cooling of the posterior and/or the anterior AVN approaches revealed nonspecific effects on the slow and fast pathway portions of the AVN conduction curve. In 13 other preparations, simulated AF during posterior cooling (n=6) prolonged the His-His (H-H) intervals but did not reveal specific slow pathway injury. In the remaining 7 preparations, AF was applied before and after posteroseptal surgical cuts. During AF with posterior origin, the cuts resulted in longer mean H-H along with slowing of the AVN bombardment rate. However, there was no change in the minimum observed H-H, suggesting an intact slow pathway. During AF with anterior origin, the mean and the shortest H-H remained unchanged before and after the cuts in all preparations. This was associated with the maintenance of high-rate AVN bombardment. CONCLUSIONS: Posteroseptal ablation does not eliminate the slow pathway. Ventricular rate slowing can be obtained if the ablation procedure results in a posteroanterior intra-atrial block leading to a reduction of the rate of AV nodal bombardment.

His electrogram alternans reveal dual-wavefront inputs into and longitudinal dissociation within the bundle of His.

BACKGROUND: His electrogram (HE) amplitude and morphology changes were observed in our previous studies during transition from "fast" to "slow" atrioventricular nodal (AVN) conduction. This phenomenon and its significance for the dual-AVN electrophysiology are not well recognized and have not been studied. METHODS AND RESULTS: Experiments were performed on 17 healthy rabbit atrial-AVN preparations during standard programmed electrical pacing. HEs were mapped along the His bundle with roving surface electrodes, along with recording of cellular action potentials (APs). HEs recorded from the superior margin of the His bundle were of greater amplitude during basic beats and decreased substantially, by 42+/-19% (P<0.01), when premature A(1)A(2) shortened to 178+/-20 ms. In contrast, the HEs from the inferior margin increased dramatically, 2.9+/-1.7 times (P<0.01), during short A(1)A(2) and remained high until AVN block occurred. In addition, during long A(1)A(2), the superior HEs consistently preceded the inferior by 1.9+/-0.7 ms. In contrast, at short A(1)A(2), the superior HEs occurred 2.7+/-0.8 ms after the inferior. Cellular AP recordings demonstrated clearly the presence of and the transition between early (fast) and late (slow) excitation wavefronts that accompanied HE alternans. CONCLUSIONS: The morphological-electrophysiological evidence from the AV junction suggests that fast and slow wavefronts reach the His bundle differently, producing functional longitudinal dissociation into 2 domains. The characteristic HE alternans recorded from these domains are a new sensitive tool to determine the presence of distinctly different wavefronts and their participation in the conduction during reentrant or other arrhythmias. These findings provide further understanding of the mechanisms of dual-AVN electrophysiology.

Autonomic modification of the atrioventricular node during atrial fibrillation: role in the slowing of ventricular rate.

BACKGROUND: Postganglionic vagal stimulation (PGVS) by short bursts of subthreshold current evokes release of acetylcholine from myocardial nerve terminals. PGVS applied to the atrioventricular node (AVN) slows nodal conduction. However, little is known about the ability of PGVS to control ventricular rate (VR) during atrial fibrillation (AF). METHODS AND RESULTS: To quantify the effects and establish the mechanism of PGVS on the AVN, AF was simulated by random high right atrial pacing in 11 atrial-AVN rabbit heart preparations. Microelectrode recordings of cellular action potentials (APs) were obtained from different AVN regions. Five intensities and 5 modes of PGVS delivery were evaluated. PGVS resulted in cellular hyperpolarization, along with depressed and highly heterogeneous intranodal conduction. Compact nodal AP exhibited decremental amplitude and dV/dt and multiple-hump components, and at high PGVS intensities, a high degree of concealed conduction resulted in a dramatic slowing of the VR. Progressive increase of PGVS intensity and/or rate of delivery showed a significant logarithmic correlation with a decrease in VR (P<0.001). Strong PGVS reduced the mean VR from 234 to 92 bpm (P<0.001). The PGVS effects on the cellular responses and VR during AF were fully reproduced in a model of direct acetylcholine injection into the compact AVN via micropipette. CONCLUSIONS: These studies confirmed that PGVS applied during AF could produce substantial VR slowing because of acetylcholine-induced depression of conduction in the AVN.

Transthoracic cardioversion of atrial fibrillation: comparison of rectilinear biphasic versus damped sine wave monophasic shocks.

BACKGROUND: Clinical studies have shown that biphasic shocks are more effective than monophasic shocks for ventricular defibrillation. The purpose of this study was to compare the efficacy of a rectilinear biphasic waveform with a standard damped sine wave monophasic waveform for the transthoracic cardioversion of atrial fibrillation. METHODS AND RESULTS: In this prospective, randomized, multicenter trial, patients undergoing transthoracic cardioversion of atrial fibrillation were randomized to receive either damped sine wave monophasic or rectilinear biphasic shocks. Patients randomized to the monophasic protocol (n=77) received sequential shocks of 100, 200, 300, and 360 J. Patients randomized to the biphasic protocol (n=88) received sequential shocks of 70, 120, 150, and 170 J. First-shock efficacy with the 70-J biphasic waveform (60 of 88 patients, 68%) was significantly greater than that with the 100-J monophasic waveform (16 of 77 patients, 21%, P<0.0001), and it was achieved with 50% less delivered current (11+/-1 versus 22+/-4 A, P<0.0001). Similarly, the cumulative efficacy with the biphasic waveform (83 of 88 patients, 94%) was significantly greater than that with the monophasic waveform (61 of 77 patients, 79%; P=0.005). The following 3 variables were independently associated with successful cardioversion: use of a biphasic waveform (relative risk, 4.2; 95% confidence intervals, 1.3 to 13.9; P=0.02), transthoracic impedance (relative risk, 0.64 per 10-Omega increase in impedance; 95% confidence intervals, 0.46 to 0.90; P=0.005), and duration of atrial fibrillation (relative risk, 0.97 per 30 days of atrial fibrillation; 95% confidence intervals, 0.96 to 0.99; P=0.02). CONCLUSIONS: For transthoracic cardioversion of atrial fibrillation, rectilinear biphasic shocks have greater efficacy (and require less energy) than damped sine wave monophasic shocks.

Fully discharging phases. A new approach to biphasic waveforms for external defibrillation.

BACKGROUND: Phase-2 voltage and maximum pulse width are dependent on phase-1 pulse characteristics in a single-capacitor biphasic waveform. The use of 2 separate output capacitors avoids these limitations and may allow waveforms with lower defibrillation thresholds. A previous report also suggested that the optimal tilt may be >70%. This study was designed to determine an optimal biphasic waveform by use of a combination of 2 separate and fully (95% tilt) discharging capacitors. METHODS AND RESULTS: We performed 2 external defibrillation studies in a pig ventricular fibrillation model. In group 1, 9 waveforms from a combination of 3 phase-1 capacitor values (30, 60, and 120 microF) and 3 phase-2 capacitor values (0=monophasic, 1/3, and 1.0 times the phase-1 capacitor) were tested. Biphasic waveforms with phase-2 capacitors of 1/3 times that of phase 1 provided the highest defibrillation efficacy (stored energy and voltage) compared with corresponding monophasic and biphasic waveforms with the same capacitors in both phases except for waveforms with a 30-microF phase-1 capacitor. In group 2, 10 biphasic waveforms from a combination of 2 phase-1 capacitor values (30 and 60 microF) and 5 phase-2 capacitor values (10, 20, 30, 40, and 50 microF) were tested. In this range, phase-2 capacitor size was more critical for the 30-microF phase-1 than for the 60-microF phase-1 capacitor. The optimal combinations of fully discharging capacitors for defibrillation were 60/20 and 60/30 microF. Conclusions-Phase-2 capacitor size plays an important role in reducing defibrillation energy in biphasic waveforms when 2 separate and fully discharging capacitors are used.

First human experience with pulmonary vein isolation using a through-the-balloon circumferential ultrasound ablation system for recurrent atrial fibrillation.

BACKGROUND: Standard mapping and ablation of focal sources of atrial fibrillation are associated with very long procedure times and low efficacy. An anatomic approach to complete pulmonary vein isolation could overcome these limitations. METHODS AND RESULTS: Fifteen patients with atrial fibrillation refractory to medication underwent circumferential isolation of the pulmonary veins by using a novel catheter, with an ultrasound transducer (8-MHz) mounted near the tip, in a saline-filled balloon. Twelve atrial foci and/or atrial fibrillation triggers were identified in 9 patients (pulmonary vein locations: left upper, 3; right upper, 6; right middle, 1; right lower, 1; and left inferior, 1). In 5 patients, lesions were placed in the absence of any mapped triggers. Irrespective of trigger mapping, circumferential isolation of both upper pulmonary veins was attempted in all patients. The lower pulmonary veins were ablated when sinus rhythm activation mapping revealed evidence of a sleeve of atrial muscle in the vein. The median number of lesions per patient required to isolate 1 pulmonary vein was 4 (range, 1 to 29). After ablation, no evidence of narrowing was seen with repeat venography or follow-up computed tomography scan. After a mean follow-up of 35+/-6 weeks, 5 patients had recurrence of atrial fibrillation. Three responded to drugs that were previously ineffective, and 2 remained in atrial fibrillation. CONCLUSIONS: This novel ultrasound ablation system can successfully isolate multiple pulmonary veins. At early follow-up, this approach seems to be effective in preventing recurrent atrial fibrillation in a significant number of patients.

C-reactive protein elevation in patients with atrial arrhythmias: inflammatory mechanisms and persistence of atrial fibrillation.

BACKGROUND: Atrial fibrillation (AF) may persist due to structural changes in the atria that are promoted by inflammation. C-reactive protein (CRP), a marker of systemic inflammation, predicts cardiovascular events and stroke, a common sequela of AF. We hypothesized that CRP is elevated in patients with atrial arrhythmias. METHODS AND RESULTS: Using a case-control study design, CRP in 131 patients with atrial arrhythmias was compared with CRP in 71 control patients. Among arrhythmia patients, 6 had frequent atrial ectopy or tachycardia, 86 had paroxysmal AF, 39 had persistent AF lasting >30 days, and 70 had lone arrhythmias. CRP was higher in arrhythmia than in control patients (median, 0.21 versus 0.096 mg/dL; P<0.001). Arrhythmia patients in AF within 24 hours before sampling had higher CRP than those in sinus rhythm (0.30 versus 0.15 mg/dL; P<0.001). CRP in controls was not different than in patients with atrial ectopy or tachycardia. Lone arrhythmia patients had a CRP of 0.21 mg/dL, which was not significantly lower than arrhythmia patients with structural heart disease (CRP, 0.23 mg/dL) but higher than controls (P=0.002). Persistent AF patients had a higher CRP (0.34 mg/dL) than paroxysmal AF patients (0.18 mg/dL; P=0.008); both groups had higher CRP levels than controls (P

Asymmetry of retrograde conduction and reentry within the His-Purkinje system: a comparative analysis of left and right ventricular stimulation.

OBJECTIVES: The purpose of this study was to delineate retrograde His-Purkinje system conduction and reentry (V3 phenomenon) during left ventricular extrastimulation and compare them with right ventricular extrastimulation. BACKGROUND: The V3 phenomenon has been well described in the past during right ventricular extrastimulation; however, it has not been studied systematically during left ventricular extrastimulation. METHODS: Left and right ventricular pacing were performed in 13 patients. Retrograde and anterograde routes of impulse propagation were determined on the basis of the sequence of His (H) and right bundle (RB) potentials, H-RB intervals, as well as the QRS configuration and axis of V3 beats. RESULTS: During right ventricular pacing, retrograde conduction of V2, when discernible, occurred exclusively through the left bundle at all coupling intervals equal to or shorter than the His-Purkinje relative refractory period, with the exception of two isolated beats. During left ventricular extrastimulation, His bundle activation was through the left bundle in nine patients and through the right or left bundle in three other patients. In one patient, the route could not be determined. The V3 phenomena occurred in eight patients during right ventricular pacing. Seven patients had a left bundle branch block pattern QRS configuration, and one had a right bundle branch block pattern configuration. V3 beats occurred in five patients during left ventricular apex pacing: left bundle branch block pattern configuration in one patient and right bundle branch block pattern configuration in four. In three of these four patients, the reentry was interfascicular and limited to the left bundle branch system. CONCLUSIONS: The left-sided His-Purkinje system is the preferred retrograde route of impulse propagation during both left and right ventricular extrastimulation. Reentry within the His-Purkinje system elicited by right ventricular extrastimulation involves both bundle branches, whereas this reentry tends to occur within the left-sided His-Purkinje system during left ventricular pacing.

Treatment of atrioventricular node reentrant tachycardia with encainide: reversal of drug effect with isoproterenol.

To determine the efficacy of encainide in the treatment of atrioventricular (AV) node reentrant tachycardia, Holter electrocardiographic (ECG) monitoring, exercise treadmill testing and programmed electrical stimulation were performed in 16 patients while they were taking no medication and after steady state levels were reached during treatment with encainide (75 to 200 mg/day; mean 117 +/- 47). In addition, to study the possible reversal of drug effects by sympathetic stimulation, AV node conduction and tachycardia induction were reassessed during isoproterenol infusion (1 to 3 micrograms/min), a dose calculated to increase the rest heart rate by 25 +/- 10%. Sustained AV node reentrant tachycardia could be initiated in all 16 patients in the control state, in 2 patients after encainide and in 10 patients during isoproterenol infusion. The shortest mean atrial paced cycle length sustaining 1:1 AV conduction was 358 +/- 57 ms during the control study, which increased to 409 +/- 59 ms with encainide (p less than 0.01 versus control) and decreased to 313 +/- 31 ms during isoproterenol infusion (p less than 0.01 versus control and encainide). The shortest mean ventricular paced cycle length with 1:1 ventriculoatrial conduction was 337 +/- 56 ms in the control study, 551 + 124 ms with encainide infusion (p less than 0.01 versus control) and 354 +/- 72 ms during isoproterenol infusion in the encainide-loaded state (p less than 0.01 versus both control and encainide). During a mean follow-up period of 19 +/- 10 months, significant clinical recurrences occurred in 4 of the 10 patients in whom tachycardia could still be initiated with encainide (with or without isoproterenol).(ABSTRACT TRUNCATED AT 250 WORDS)

Efficacy of cryosurgery alone for refractory monomorphic sustained ventricular tachycardia due to inferior wall infarction.

The efficacy of cryosurgery alone was evaluated in 15 patients with refractory monomorphic sustained ventricular tachycardias related to inferior wall infarction. Patients were 64 +/- 9 (SD) years old and had a mean left ventricular ejection fraction of 39.2 +/- 11.2%. Thirty different tachycardias were mapped with the origin localized to the septum or inferior wall in 20 (67%), near the mitral valve anulus in 6 (20%) and at the base of the posterior papillary muscle in 4 (13%) tachycardias. Endocardial cryoablation of these sites was performed with 6 to 13 (mean 9.2 +/- 1.8) cryolesions per heart. No mitral valve replacement was performed. There was one postoperative death as a result of sepsis. Cryoablation abolished inducible ventricular tachycardia in 11 patients. Of the other three patients, the tachycardia in two was controlled with a single antiarrhythmic agent that had previously failed to suppress inducible ventricular tachycardia. Thus, clinical success was obtained in 13 (93%) of 14 patients. The remaining patient received an automatic implantable cardioverter defibrillator. Ejection fraction remained unchanged or improved after surgery in 14 patients (93%). There have been no late deaths, recurrence of sustained ventricular tachycardia or significant mitral regurgitation during a mean follow-up period of 19 +/- 7 months. These results compare quite favorably with those previously reported for subendocardial resection alone, and indicate that cryosurgery is highly effective, does not result in deterioration of left ventricular function and preserves mitral valve competence when cryoablation of the posterior papillary muscle is necessary.

Isoproterenol reversal of antiarrhythmic effects in patients with inducible sustained ventricular tachyarrhythmias.

Seventeen patients (16 men and 1 woman) were challenged with isoproterenol after their initially inducible sustained ventricular tachyarrhythmia (monomorphic tachycardia in 14 patients and fibrillation in 3) was completely suppressed by class I antiarrhythmic drugs. Coronary artery disease was documented in 11 patients, dilated cardiomyopathy in 2 and no structural heart disease in the remaining 4 patients. The initial presentation was aborted sudden cardiac death (five patients), syncope (eight patients) and symptomatic nonsustained ventricular tachycardia (four patients). The antiarrhythmic drug that rendered the initial ventricular tachyarrhythmias noninducible was class IA in 11 cases, class IC in 5 and combined class IA and IB in 1. The original ventricular tachyarrhythmia became reinducible in 10 patients (group A) and remained noninducible in 7 patients (group B) after isoproterenol infusion at a rate necessary to achieve a 20% increase in heart rate. Despite the results of isoproterenol challenge, all patients were maintained on their electrophysiologically guided antiarrhythmic regimen. During a mean follow-up period of 13 +/- 9 months, 3 of the 10 patients in group A experienced clinical recurrence of tachyarrhythmia; no recurrence was noted in group B. In conclusion, reinducibility of ventricular tachyarrhythmia after beta-adrenergic stimulation seems to identify a subgroup of patients at high risk of subsequent arrhythmic events. Beta-adrenergic blockade or surgical therapy may be indicated in some patients with a positive isoproterenol challenge.

Electrophysiologic mechanisms of orthodromic tachycardia initiation during ventricular pacing in the Wolff-Parkinson-White syndrome.

Orthodromic tachycardia is the most common arrhythmia in patients with Wolff-Parkinson-White syndrome. It is often initiated during incremental ventricular pacing that requires the onset of retrograde block along the normal pathway (that is, atrioventricular [AV] node-His-Purkinje system) with concomitant retrograde atrial activation by way of the accessory pathway. However, the site of retrograde block, that is, the AV node versus the His-Purkinje system, during incremental ventricular pacing and, hence, the mechanism of orthodromic tachycardia initiation have not been systematically elucidated. The mechanisms of orthodromic tachycardia induction were studied in 17 patients with Wolff-Parkinson-White syndrome using a specially designed pacing protocol. A beat by beat analysis indicated that the retrograde His-Purkinje system block was the most common initiating mechanism of orthodromic tachycardia in 14 of the 17 cases. In two cases, AV node block preceded the onset of orthodromic tachycardia, whereas the data in the remaining case suggested that both mechanisms were operative but at different pacing cycle lengths. The orthodromic tachycardia induction with His-Purkinje system block occurred within the first two cycles in most cases. When orthodromic tachycardia initiation was delayed beyond the first two cycles of the ventricular train it represented either a 2:1 block in the His-Purkinje system; a linking phenomenon in the His-Purkinje system; or a block in the AV node. These data have methodologic, mechanistic and therapeutic implications for patients with the Wolff-Parkinson-White syndrome.

Echocardiographic demonstration of decreased left ventricular dimensions and vigorous myocardial contraction during syncope induced by head-up tilt.

Two-dimensional echocardiography was performed during a head-up tilt test in 11 control subjects (group I) and 18 patients with recurrent unexplained syncope. In four patients (group II), the head-up tilt test was negative at baseline and after isoproterenol infusion. Syncope was induced during baseline head-up tilt in nine patients (group III) and after isoproterenol challenge in five (group IV). The echocardiographic variables assessed were left ventricular end-systolic and end-diastolic areas and percent fractional shortening. At the end of head-up tilt, end-systolic area decreased by 4.5 +/- 1.3 and 3.0 +/- 1.2 cm2 in groups III and IV, respectively, compared with 0.5 +/- 0.7 and 0.2 +/- 0.1 cm2 in groups I and II, respectively (p less than 0.04). Similarly, end-diastolic area decreased by 5.5 +/- 2.6 cm2 in group III compared with 2.7 +/- 1.9 and 1.75 +/- 0.4 cm2 in group I and II, respectively (p less than 0.04). Additionally, at the end of the baseline study, fractional shortening was significantly greater in group III and group IV (43 +/- 5%) than in groups I and II (p less than 0.01). In conclusion, syncope induced by head-up tilt is associated with vigorous myocardial contraction and a significant decrease in left ventricular end-systolic dimensions. This left ventricular hypercontractility may play an important role in the pathogenesis of syncope induced by head-up tilt.

Functional characteristics of human macro-reentry: a study of "pre-excited" circuits by extrastimulus method.

The effect of improved conduction in areas of delay was tested during macro-reentry within the His-Purkinje system, in an attempt to separate the role of conduction delay from that of prematurity of the extrastimulus as the key determinant of reentry. Using the right ventricular extrastimulus technique (S1S2 method), both the critical His-Purkinje system delays and the zone of S1S2 intervals causing His-Purkinje system reentry were determined. Then, using a previously described technique of atrioventricular (AV) sequential pacing during the basic drive, the potential site of His-Purkinje system conduction delay was (anterogradely) excited earlier (pre-excitation), as compared with the control S1S2 method. This produced a decrease in retrograde His-Purkinje system delay (S2H2), as compared with the same S1S2 interval during the control method. Changing the degree of pre-excitation at each S1S2 interval allowed for determination of the critical (or shortest) S2H2 delay necessary for His-Purkinje system reentry at each coupling interval. Of importance was the observation that the critical delay was not specific for each case but varied with the prematurity of S2. For example, the critical S2H2 delay required for reentry was actually less at shorter S1S2 intervals as compared with longer S1S2 intervals (from 206 +/- 25 to 187 +/- 20 ms, p less than 0.01). These data suggest that manifestation of reentry is a complex interplay between degree of prematurity and conduction delay. The so-called critical conduction delay can be readily modified by altering the site of block, which in turn may be dependent on prematurity of the extrastimulus.

Ventricular tachycardias arising from the aortic sinus of valsalva: an under-recognized variant of left outflow tract ventricular tachycardia.

OBJECTIVES: To describe a normal heart left bundle branch block, inferior axis ventricular tachycardia (VT), that could not be ablated from the right or left ventricular outflow tracts. BACKGROUND: Whether these VTs are epicardial and can be identified by a specific electrocardiographic pattern is unclear. METHODS: Twelve patients with normal heart left bundle branch block, inferior axis VT and previously failed ablation were included in this study. Together with mapping in the right and left ventricular outflow tracts, we obtained percutaneous epicardial mapping in the first five patients and performed aortic sinus of Valsalva mapping in all patients. RESULTS: No adequate pace mapping was observed in the right and left ventricular outflow tracts. Earliest ventricular activation was noted in the epicardium and the aortic cusps. All patients were successfully ablated from the aortic sinuses of Valsalva (95% CI 0% to 18%). The electrocardiographic pattern associated with this VT was left bundle branch block, inferior axis and early precordial transition with Rs or R in V2 or V3. Ventricular tachycardia from the left sinus had rS pattern in lead I, and VT from the noncoronary sinus had a notched R wave in lead I. None of the patients had complications and all remained arrhythmia-free at a mean follow-up of 8 +/- 2.6 months. CONCLUSIONS: Normal heart VT with left bundle branch block, inferior axis and early precordial transition can be ablated in the majority of patients from either the left or the noncoronary aortic sinus of Valsalva.