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Nonischemic ventricular tachycardia most commonly arises in the right ventricular free wall and is frequently refractory to medical therapy. Many different types of surgical procedures have been employed to treat medically refractory nonischemic ventricular tachycardia arising in the right ventricle, but the results of these procedures have been less than optimal. The majority of these surgical procedures have been directed toward ablation of the site (or sites) of origin of the tachyarrhythmia and have failed because of the frequent occurrence of multifocal or polymorphic ventricular tachycardia in these patients. We first employed localized surgical isolation procedures to control nonischemic ventricular tachycardia arising in the right ventricular free wall in 1979. These localized procedures evolved into the development of a technique for isolating the entire right ventricular free wall from the remainder of the heart to control ventricular tachyarrhythmias arising from multiple sites in the right ventricle. Case histories are reported of two patients who underwent localized isolation procedures in 1979 as well as two patients who underwent total disconnection of the right ventricle in 1982. The follow-up period in these four patients ranges from 2 to 5 years and the control of their tachyarrhythmias has been uniformly successful. However, surgical isolation of the entire right ventricular free wall has resulted in progressive dilatation of the right ventricle as documented by serial echocardiography. The pathophysiology of the progressive right ventricular dilatation postoperatively is discussed in terms of etiology and prevention, and the indications for application of localized and total isolation procedures for nonischemic right ventricular tachycardia are outlined.

Cryothermia, a new technique for definitive treatment of the pre-excitation syndrome, is described in two patients. The first patient presented with a normal P-R interval with a delta wave and reciprocating tachycardia. Preoperative electrophysiologic study suggested a free-wall atrioventricular connection on the left posterior atrioventricular (A-V) groove. At surgery, epicardial mapping confirmed the site of pre-excitation on the posterior left ventricular (LV) wall. An electrogram arising from the accessory pathway (AP) was recorded at the site of earliest ventricular activation. Interatrial delay combined with an apparently long accessory pathway to the ventricle caused the P-R interval to appear normal. Local pressure abolished pre-excitation. The site of early ventricular activation was cooled to -60 degrees C with a specially designed cryoprobe. All evidence of pre-excitation and arrhythmias disappeared. The second patient presented with a refractory reciprocating tachycardia and was found to have an AP in the septum capable of only retrograde conduction. Retrograde conduction was abolished by applying a temperature of 0 degrees C to the anulus at this site during tachycardia. Conduction over the AP and reciprocating tachycardia returned with rewarming. Ablation of the AP was obtained by applying a temperature of -60 degrees C for 90 seconds on two occasions to the same area. The His bundle was not injured.

Eleven patients with an accessory pathway and reciprocating tachycardia were studied using both fixed rate atrial pacing and the atrial extrastimulus technique. Six of the patients had an accessory pathway that conducted in both the anterograde and retrograde direction; but the effective refractory period of their accessory pathway in the anterograde direction was relatively long and was greater than the longest coupling intervals that initiated atrial echoes. Five patients had an accessory pathway that conducted only in the retrograde direction. The extrastimulus technique could be used with stimulation sites near to and remote from the accessory pathway in 10 of the 11 patients. Atrial echoes were initiated by a single atrial extrastimulus at both sites in 7 of the 10 patients, and in each patient the upper limit of the echo zone was longer with stimulation at the site near the accessory pathway. In the other three patients atrial echoes were initiated only during stimulation at the site near the accessory pathway because either atrial refractoriness or atrioventricular nodal refractoriness was encountered before the echo zone was entered during stimulation at the site remote from the accessory pathway. Differences in the longest cycle length that initiated an atrial echo during fixed rate atrial pacing were similarly demonstrated in three patients. In these three patients, pacing at the site near the accessory pathway initiated echoes at a longer cycle length than pacing at the site remote from the accessory pathway. In three other patients the electrophysiologic characteristics of atrioventricular conduction prevented a demonstration of these differences. Catheter position is an important variable in the initiation of atrial echoes in patients with accessory pathways.

One hundred patients with proved accessory pathways of the Kent bundle type were studied with multiple intracardiac catheters. During the procedure 16 had atrial fibrillation. Two patterns of induction of atrial fibrillation were noted. In most patients an earlier than expected atrial deflection appeared in one of the atrial recordings and was followed by atrial flutter (cycle length less than 220 msec) or atrial fibrillation either immediately or after a brief period of acceleration of atrial rate. In a few patients, intraatrial conduction delay, manifested as 2:1 block or Wenckebach block from the right to the left atrium or vice versa, occurred before the onset of atrial fibrillation. The incidence of atrial fibrillation was not statistically related to any associated cardiac abnormalities. A significantly large incidence of ventricular fibrillation was recorded in patients who had documented atrial fibrillation either before admission or during the catheter study.

The Wolff-Parkinson-White syndrome is due to a congenital heart malformation that is the result of one or more persistent anomalous atrioventricular pathway(s). While supraventricular tachycardia is the most commonly associated arrhythmia, there is a wide spectrum of associated arrhythmias including fatal ventricular fibrillation. It is now known that surgical ablation of the anomalous pathway(s) can result in complete cure of arrhythmias in some patients. The purpose of this report is to describe the current methods used for the preoperative and operative electrophysiologic evaluation and surgical treatment in children with the Wolff-Parkinson-White syndrome, as illustrated by the case presentation of a normal eight-year-old patient who had ventricular fibrillation.

The conventional technique for mapping the sequence of epicardial activation uses a hand-held electrode moved over the heart to record from a number of epicardial sites one at a time, and requires 5-15 minutes to record from 50 or more sites distributed over the entire ventricular epicardium. This method is inadequate for arrhythmias that are transient or vary from beat to beat. To overcome these limitations the "sock electrode array," a contour-fitting sock containing 26 or 52 electrodes, has been developed. The nylon mesh sock is pulled over the heart and permits simultaneous recording of potentials from electrodes distributed over the entire ventricular epicardium. The electrograms are recorded and converted to digital form for computer generation of isochronous maps. Most of the epicardial activation sequence derived from the sock electrode were compared to those obtained by the hand-held electrode in six normal dogs during sinus rhythm and ventricular pacing. The sequence of local activation times acquired by both methods showed similar areas of early and late activation and comparable isochronous maps. The hand-held electrode technique required 10-15 minutes for data acquisition and another 15-30 minutes for analysis. The sock electrode array allowed electrograms from 26 epicardial electrodes to be recorded simultaneously during one cardiac cycle and computer generated isochronous maps could be displayed within 10 minutes. This method allows rapid recording and analysis of epicardial electrical phenomena and should meet the time constraints imposed during the intraoperative study of ventricular tachyarrhythmias in patients.

Because of the value of cryoablation of the atrioventricular (AV) conduction system in treatment of refractory cardiac rhythm disorders, the anatomic effects of cryoablation on the cardiac conduction system must be defined. In this report we summarize studies done on four patients who had intractable recurrent supraventricular tachyarrhythmias or or refractory atrial flutter-fibrillation. They were treated by cryoablation of the AV conduction system and died 8-360 days postoperatively. Serial sections of the AV conduction system were studied. Cryoablation produced lesions that completely destroyed most of the AV node in three cases, the penetrating portion of the His bundle in all four cases, and the branching portion of the His bundle in two cases. The right bundle branch was not involved markedly in any case. The lesions were discrete and sharply delimited; the patient who died 8 days postoperatively had hemorrhage, necrosis and slight inflammatory infiltrate; patients who survived for 49-360 days showed collagen deposition. The AV nodal artery and its branches showed slight to marked intimal thickening in three cases. Small, partly organized thrombi were present just behind the tricuspid valve in two patients. We conclude that cryoablation of the AV conduction system produced discrete cardiac lesions that did not markedly damage the tricuspid valve or aorta.

Paroxysmal supraventricular tachycardia (PSVT) is commonly caused by reentry within the atrioventricular (AV) node. This arrhythmia was abolished by operative dissection of the AV junction in a patient with disabling tachycardia that was not controlled by drugs. The operation was intended to create complete AV block, but AV conduction persisted after surgery. An electrophysiologic study 1 year after the operation revealed that the operation changed AV conduction in both the antegrade and retrograde directions, which may explain the absence of tachycardia. The patient has been free of arrhythmias for 18 months.

Neodymium:YAG laser photocoagulation was used in the intraoperative treatment of drug-resistant ventricular tachycardia (VT) in 17 consecutive patients. The cause of VT was previous myocardial infarction in 15, sarcoid in one, and idiopathic in one patient. Electrophysiologic studies were performed preoperatively, before hospital discharge, and 8 to 12 weeks and 1 year after surgery. At surgery, laser photocoagulation was performed on the normothermic heart during VT. Surgical mortality was 11.7%. There was one late nonarrhythmic death 35 days postoperatively. There were 55 VT morphologies. Laser successfully abated 52 of 55. Associated use of cryoablation was required in two of 55. One VT in the patient with sarcoidosis was not successfully ablated but was controlled by procainamide. In the long-term survivors with VT due to myocardial infarction the surgical cure rate was 100%, i.e., no spontaneous or inducible VT. Follow-up ranges from 6 to 18 months (mean 11.8 +/- 4.3). Nd:YAG laser photocoagulation is an effective addition to the operative treatment strategies for VT.

Antegrade (AERPAP) and retrograde (RERPAP) effective refractory periods of the accessory pathway were measured at multiple cycle lengths in 47 patients with the Wolff-Parkinson-White syndrome. In 20 patients the effect of changing cycle length on AERPAP could be determined. In 12 patients Aerpap decreased by 10-45 msec, in six it increased by 10-35 msec, and in two it was unchanged. In 13 of 15 patients in whom the effect of decreasing cycle length on RERPAP could be assessed, RERPAP decreased by 10-60 msec. In eight patients, the shortest AERPAP correlated well (r equals 0.83) with the shortest R-R interval of consecutive pre-excited beats in atrial fibrillation. However, predominantly normal conduction was observed in six of 28 patients with atrial fibrillation, probably because of concealment in the bypass. Therefore, induction of atrial fibrillation during electrophysiological evaluation may privide additional information. The RERPAP at the cycle length of the arrhythmia was shorter than the cycle length of reciprocating tachycardia in all but one of 21 patients. At the same or comparable cycle lengths, AERPAP was usually greater than RERPAP.

During reciprocating tachycardia in patients with accessory atrioventricular pathways, the observation of changes in ventriculoatrial (VA) intervals with bundle branch block (BBB) aberration has been used to localize the site of the pathway and prove the participation of the pathway in the tachycardia. In this report we present the changes observed during BBB in 93 patients with single atrioventricular pathways in whom the site of their pathways was subsequently proved at the time of their surgical interruption. In patients with left or right free wall pathways, the minimum VA interval (VA min) increased by 61 +/- 19 msec with ipsilateral BBB, whereas no change occurred with contralateral BBB. The smallest increase in the VA interval was 35 msec. In 14 patients, shortening of the AH intervals resulted in changes in overall cycle length that were less than 35 msec. Patients with septal pathways all had changes in VA min of 25 msec or less with either right or left bundle branch block (RBBB or LBBB), which suggests that a clear differentiation between septal and free wall pathways can be made on the basis of changes in VA min. In patients with anteroseptal pathways, VA min intervals frequently prolonged with RBBB (16 +/- 9 msec) but not with LBBB. In patients with posteroseptal pathways, VA min frequently prolonged with LBBB (13 +/- 8 msec) but not with RBBB. Therefore, the observed changes in VA min with BBB may serve as an important indicator of the site of an accessory pathway and may provide guidance in the choice of surgical therapy.

Forty-five patients with the Wolff-Parkinson-White syndrome and reciprocating tachycardia which utilized the atrioventricular (A-V) node for antegrade conduction and an accessory pathway for ventriculo-atrial (retrograde) conduction were studied. The extrastimulus technique in the right atrium and coronary sinus at multiple pacing cycle lengths was used. Three types of "echo zones" were defined by the relationship of the antegrade effective refractory period (ERP) of the accessory pathway, the longest coupling interval accompanied by an atrial echo, the ERP of the A-V node, and the functional refractory period of the atrium. Eighteen of 45 patients (40%) had more than one type of echo zone demonstrated by changing either pacing site or pacing cycle length or both. Pacing site and intraventricular conduction delay were found to have important effects on the longest coupling interval accompanied by an atrial echo in those echo zones in which the longest coupling interval accompanied by an atrial echo was less than the antegrade ERP of the accessory pathway. The echo zone is a useful concept to explain the physiology of the common reciprocating tachycardia in patients with the Wolff-Parkinson-White syndrome. However, the echo zone is profoundly affected by pacing site and pacing cycle length. When these variables are changed, many patients can be shown to have more than one type of echo zone. Studies of the echo zone have limited value as therapeutic guides.

Comparison of 2-dimensional (2-D) echocardiographic and right ventricular (RV) angiographic findings was performed in 10 patients with arrhythmogenic RV dysplasia. Diagnosis was based on accepted electrocardiographic and angiographic criteria. Nine patients underwent invasive electrophysiologic study, which confirmed RV source of ventricular tachycardia (VT) in 7. Biopsy findings of RV dysplasia were available in 3 patients. Two-dimensional echocardiography and angiography corresponded closely when diffuse RV enlargement and hypokinesia were present. Such diffuse findings were not invariably present. Localized abnormalities consisting of bulging or sacculation of the RV wall were noted by both techniques, even in the absence of diffuse changes. Echocardiographic evidence of localized disease predicted the presence of similar lesions at angiography, but agreement as to specific location was poor. Subjectivity in interpreting subtle RV abnormalities by either technique and the inherent differences in information provided by the 2 methods probably account for the inconsistencies. In the patient with suspected arrhythmogenic RV dysplasia, 2-D echocardiographic evidence of diffuse RV enlargement, otherwise unexplained, strongly supports the diagnosis and angiography may be avoided. Isolated local changes seen by echocardiography should increase suspicion of RV dysplasia, but complementary angiographic study is warranted.

Persistence of preexcitation in sinus rhythm with procainamide infusion has been reported to occur in patients with a short anterograde accessory pathway effective refractory period (AERPAP) and this test has been proposed as a reliable noninvasive method to identify patients with the Wolff-Parkinson-White syndrome who are at risk of sudden death. However, sudden death correlates best with a shortest preexcited RR interval during atrial fibrillation (SRRPE) of 260 msec or less. We infused 10 to 12 mg/kg procainamide to 56 patients to determine whether persistence or loss of preexcitation in sinus rhythm identified patients with SRRPEs of 260 or less or greater than 260 msec, respectively. Atrial fibrillation was induced in 53 patients. Of these, 32 patients had persistence of preexcitation with procainamide infusion and SRRPE in this group of patients was shorter than that in patients in whom preexcitation was lost (194 +/- 44 vs 235 +/- 55 msec, p less than .05). However, preexcitation persisted after procainamide infusion in only 31 of 46 (67%) patients with SRRPEs of 260 msec or less. Furthermore, 15 of 21 patients who lost preexcitation had SRRPEs of 260 msec or less and two of these patients had a history of ventricular fibrillation. The correlation between AERPAP and SRRPE was studied in a separate group of 79 patients with single accessory pathways. There was a significant (p less than .001) but poor (r = .58) correlation between these two variables. Thus, the procainamide test regarding accessory pathway refractoriness often cannot be extrapolated to SRRPE.(ABSTRACT TRUNCATED AT 250 WORDS)

This is a report of a 10-year-old child who underwent surgery for complex congenital heart disease consisting of corrected transposition of the great vessels, ventricular septal defect, patent ductus arterisus, severe left-sided atrioventricular (AV) valve insuffieicney (Ebstein's deformity) and Wolff-Parkinson-White syndrome. The site of his accessory AV connection was localized preoperatively at a left anterolateral site by isopotential body surface maps and by intracardiac electrophysiologic studies. He successfully underwent surgery for closure of the ventricular septal defect, ligation of the patent ductus arteriosus, replacement of the left-sided AV valve, and interruption of the accessory AV pathway. Unavoidable complete AV block acquired at surgery required subsequent permanent pacemaker therapy.

The family of tachycardias that are called long R-P' tachycardias represent a unique group of tachycardias which have been notably refractory to pharmacologic therapy in the past. On the surface electrocardiogram, the rhythms may be indistinguishable. It is only with careful electrophysiological evaluation in many cases that these rhythms can be sorted out. The differential diagnosis in these rhythms is important because with incessant tachycardia, ventricular dysfunction may be produced. In many of the instances of long R-P' tachycardias definitive and directed ablation of the tachycardia can be accomplished. New techniques involving catheter ablation and super-selective surgical dissection are now present which makes ablation of these tachycardias possible.