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Cardiac mapping during sinus rhythm and during spontaneous or induced ventricular arrhythmias is a promising technique that offers a variety of potential strategies to improve our ability to locate abnormal areas in the heart that are the seat of arrhythmias. If surgical procedures are to become more limited in scope in an attempt to salvage myocardium, mapping will need to be used to a greater extent. However, it remains to be established which mapping technique will prove most sensitive and specific in detecting sites of arrhythmia, and whether the localizing method used allows a more directed surgical intervention to be successful.

The report relates experience with six patients with Kent bundles, five of whom had the Wolff-Parkinson-White syndrome, operated upon for tachyarrhythmias caused by the presence of the pathway. It was successfully divided in four patients, its antegrade conduction capacity interrupted in one, and a failure occurred in the sixth patient. In the three patients who had a Kent bundle with a short effective refractory period for antegrade conduction, the life-endangering potential of the Kent pathway was corrected. To emphasize the complexities of the tachyarrhythmias in Ebstein's anomaly, two patients have mild but controllable postoperative supraventricular tachyarrhythmias (SVT) due to a Mahaim pathway. The surgical problems encountered in these patients are reviewed.

Fifty patients have been operated upon for the tachyarrhythmias associated with Kent bundles. The indications for operation were supraventricular tachycardia (SVT) in 23 and life-threatening tachyarrhythmia in 27. Among the unusual variants noted were multiple Kent bundles that conducted only retrograde in 3. Forty-nine patients underwent attempted interruption of the bundle of Kent followed by His bundle division in 6. One had elective division of the bundle of His. The surgical problems occurred in 13 patients with posterior septal Kent bundles. A new approach is outlined for this group. Division of the Kent bundle was successful in 31 patients, but 2 deaths occurred from cardiomyopathy. Seven patients had successful control of SVT by His bundle interruption. One patient with postoperative retrograde conduction has the SVT controlled with drugs. Eight have postoperative delta waves, but their SVT is controlled with drugs. There were 3 failures.

In 34 successive patients with Wolff-Parkinson-White syndrome premature beats were induced from the right ventricular apex during reciprocating tachycardia (RT) at progressively shorter coupling intervals. The presence of an accessory pathway was confirmed by a reduction in the atrial cycle length (A-A interval) during which the premature ventricular beat was introduced. This retrograde preexcitation occurred at a time when the His-AV node pathway was refractory; i.e. there was premature activation of the atria over a pathway other than the His-AV node. 3 patients were excluded because of unsatisfactory or unstable H-H intervals. In the remaining 31 patients with constant preceding H-H intervals, the A-A interval shortened; (a) 35-65 msec in 4 patients with right-sided pathways and normal conduction during RT and by 110 msec in a 5th patient with a right-sided pathway, in whom bundle branch block aberration persisted during RT, (b) 45 msec in the single patient with both a right-sided and a septal accessory pathway, (c) 35-65 msec in 5 patients with septal pathways, and (d) 15-35 msec in only 4/20 patients with left-sided pathways and normal conduction during RT. Left-sided ventricular premature beats were introduced in 5 patients with left-sided pathways and normal conduction in RT. In 4/5, left-sided premature beats shortened the A-A interval 40-75 msec whereas right-sided premature beats at the same coupling interval failed to do so. In the fifth case, the left-sided premature resulted in a 65 msec abbreviation of the A-A interval compared to 30 msec from the right ventricular outflow tract and 15 msec from the right ventricular apex. In 5 patients with left-sided pathways, right ventricular premature beats were introduced during RT with left bundle branch block aberration, and shortened the A-A interval 30-50 msec in all of these, whereas right-sided premature beats in 4 of the 5 during normal conduction failed to do so. This technique is useful to confirm the participation of accessory pathways in reciprocating tachycardias associated with the preexcitation syndromes, and emphasizes the importance of the site of stimulation used relative to the location of the accessory pathway. Because of the possibility of multiple accessory pathways, stimulation of the left ventricle should be performed in patients undergoing surgery for preexcitation unless the left ventricle is already inplicated by right-sided studies.

The Wolff-Parkinson-White syndrome is an uncommon cardiac disorder due to the presence of an accessory atrioventricular pathway resulting in ventricular pre-excitation and supraventricular tachycardias. The recognition of the Wolff-Parkinson-White syndrome is important because of the potential for the development of extremely rapid ventricular rates during atrial fibrillation that may lead to ventricular fibrillation and sudden death. The diagnosis of the Wolff-Parkinson-White syndrome is obvious when classic delta waves and short P-R intervals are present, but the electrocardiographic manifestations of the syndrome may be subtle and vary considerably from patient to patient. Certain commonly used antiarrhythmic medications may be useful for the treatment of reciprocating tachycardia in these patients and yet prove to be ineffective--or even deleterious--in preventing excessively rapid conduction to the ventricles during atrial fibrillation. An appreciation of the functional properties of the accessory pathways in the Wolff-Parkinson-White syndrome and how they are affected by pharmacologic agents should result in improved recognition of this entity and more effective medical management of patients with a risk of sudden death.

Recent studies have emphasized the role of concealed accessory pathways in reciprocating supraventricular tachycardia. Diagnosis has generally required multicatheter electrophysiologic study. We recorded esophageal electrograms during study in 16 patients with reciprocating tachycardia due to reentry using an accessory atrioventricular pathway, and in 12 patients with reciprocating tachycardia due to reentry in the AV node. The interval from onset of ventricular depolarization to earliest atrial activation (V-AMIN), earliest atrial activity on the esophageal lead (V-AESO), and high right atrium (V-HRA) was measured. No patient with RT due to an accessory atrioventricular pathway had a V-AMIN or V-AESO less than 70 ms, or a V-HRA less than 95 ms. In contrast, 11 of 12 patients with reentry in the AV node had V-AESO intervals less than 70 ms. Esophageal recording during reciprocating tachycardia provides a simple screening procedure available to all practicing physicians to exclude the diagnosis of accessory atrioventricular pathways in the genesis of paroxysmal supraventricular tachycardia.

A case of pulmonary embolus arising from a popliteal vein aneurysm is reviewed. These aneurysms are believed to be developmental in origin; with the exception of embolic phenomenon, these venous anomalies are generally asymptomatic. To our knowledge, only six cases have been previously reported. Physical examination was not helpful, and noninvasive studies were of no value in detecting the aneurysm. Venography was the only reliable diagnostic test. Because popliteal vein aneurysms are a potential source of emboli, surgical intervention is recommended. Venous aneurysmorrhaphy or excision of the aneurysm with a venous bypass are the surgical procedures most often carried out. Aneurysmorrhaphy appears to be associated with an unacceptably high rate of thrombosis; excision with placement of a vein graft may be a more satisfactory alternative.

The incubation at 37 degrees C of rat-liver microsomal fraction followed by re-isolation of the treated microsomal vesicles results in a time-dependent increase in the activity of acyl-CoA:cholesterol acyltransferase. The rate of this increase was higher in the microsomal fraction from rats fed cholesterol-supplemented diet or starved overnight as compared with that in the microsomal fraction from rats fed standard diet. The presence of a plasma membrane preparation in the incubation mixture also resulted in a time-dependent increase in acyl-CoA:cholesterol acyltransferase activity at a rate that was dependent on the concentration of plasma membranes. During the incubation of the microsomal fraction in the presence of phosphatidylcholine liposomes, cholesterol is transferred from the microsomal to liposomal vesicles. This transfer followed first-order kinetics with respect to cholesterol concentration in the donor with a rate that increased with the concentration of liposomes in the incubation mixture. The presence of phospholipid was also associated with a decrease in the activity of the acyltransferase that was related to the concentration of phospholipid in the incubation mixture. The incubation of the microsomal fraction in the presence of phosphatidylcholine-cholesterol liposomes resulted in a time-dependent and concentration-dependent transfer of liposomal cholesterol to the microsomal fraction and the acyltransferase substrate pool. The measurement of the rate of transfer of liposomal cholesterol to the microsomal vesicles and to the acyltransferase substrate pool at various temperatures showed that activation energies for the two processes are similar. Similar to these various was also the activation energy for the increase in acyl-CoA:cholesterol acyltransferase activity due to preincubation in the absence of artificial membrane vesicles. The present results suggest that there is, under the present conditions, a time-dependent and temperature-dependent flow of cholesterol from plasma membranes to the acyltransferase substrate pool and that this flow is either diverted in the presence of phospholipid liposomes or increased in the presence of cholesterol-phospholipid liposomes.

3 patients with reciprocating tachycardia are described. In all 3, tachycardia was due to a reentrant mechanism. Anterograde conduction was via the AV node while retrograde conduction was over an accessory (Kent) pathway. In none of the 3 patients did this pathway sustain anterograde conduction despite pacing the atrium close to its location. With the advent of surgical modes of therapy, it is important to recognize such 'silent' bypasses. The observations which allow this diagnosis of unidirectional anterograde block in an accessory pathway and the exclusion of AV nodal reentry, the main differential diagnostic possibility, are discussed.

A variety of surgical interventions have evolved for the treatment of intractable or life-threatening arrhythmias unresponsive to conventional pharmacologic or pacemaker therapy. Supraventricular arrhythmias associated with rapid ventricular responses can be indirectly treated with ablation of the atrioventricular conduction system and insertion of a pacemaker. Ventricular tachyarrhythmias have previously been treated with sympathectomy, resection of tissue or revascularization. More recent approaches include the simple ventriculotomy, encircling endocardial ventriculotomy, cryosurgical ablation and insertion of the automatic implantable defibrillator. Refinement of methods to localize more precisely the origin of ventricular arrhythmias may allow design of more direct surgical procedures. The surgical treatment of arrhythmias related to the preexcitation syndromes remains the model of electrophysiologic surgery. It is now feasible to divide accessory pathways with a high degree of success and at low risk in selected patients.

This preliminary report describes 5 consecutive patients operated on for drug-resistant ventricular tachycardia (VT). All were successfully treated with laser photocoagulation ablation alone. The continuous-wave neodymium:yttrium-aluminum garnet (Nd:YAG) laser (wavelength, 1.06 micron) was chosen because of its capability for controlled deep tissue penetration, which can be adjusted by manipulating the power and exposure time of the beam. All patients had severe coronary artery disease. Preoperative left ventricular ejection fractions were low (0.18 to 0.29). Risk factors associated with increased failure rates by conventional surgical approaches were frequent: absence of discrete left ventricular aneurysm (5 patients) and multiple VT morphologies with disparate sites of origin (4 patients). All patients recovered fully. VT was not inducible prior to discharge, and no patient was placed on a regimen of antiarrhythmic drugs. Current direct surgical approaches to drug-resistant VT have markedly improved operative results compared with indirect procedures. However, failures and mortality remain high. Laser photocoagulation obviates some of the problems associated with conventional methods. It is similar to cryotherapy in that the structural integrity of affected tissues is maintained. In contrast to cryosurgery, however, laser photocoagulation is achieved more rapidly and with more precise myocardial destruction. One of the most promising features of laser coagulation is that it is administered to the perfused normothermic heart. Consequently, each morphological form of induced VT is observed to disappear as its area of origin is systematically located by mapping and then ablated.

Standard electrocardiograms from 87 consecutive patients with tachycardia of left bundle branch block configuration were analyzed retrospectively for features that might be characteristic of tachycardia utilizing a nodofascicular Mahaim fiber. The study group consisted of 13 patients with nodofascicular tachycardia, 34 with supraventricular tachycardia and aberrant conduction over the His-Purkinje system, 22 with ventricular tachycardia and 18 with antidromic tachycardia utilizing a right-sided accessory atrioventricular pathway. Six variables present during tachycardia of left bundle branch block configuration were predictive of a nodofascicular fiber: cycle length between 220 and 450 ms, QRS axis of 0 to -75 degrees, QRS duration 0.15 second or less, R wave in lead I, rS wave in precordial lead V1 and a precordial transition from a negative to a positive QRS complex after lead V4. All six criteria were present in 16 of the 87 patients. No patient with ventricular tachycardia satisfied these criteria, whereas 3 of 34 with supraventricular tachycardia, 1 of 18 with antidromic tachycardia and 12 of 13 with tachycardia using a nodofascicular fiber did. It is concluded that analysis of the surface electrocardiogram during tachycardia may suggest the presence of a nodofascicular fiber.

6 patients with reentrant supraventricular tachycardia were studied using the atrial extra-stimulus (S1-S2) technique. 3 patients had smooth curves of H1-H2 intervals plotted against A1-A2 intervals, and echoes occurred only in the relative refractory period of the AV node. These patients met traditional criteria for reentry within the AV node, but all 3 were found to have accessory pathways which functioned only in the retrograde direction. 3 other patients had discontinuous curves of H1-H2 intervals plotted against A1-A2 intervals, and the echo zone was confined to coupling intervals producing the longer of the two observed AV node responses. Accessory pathways could not be demonstrated in these latter 3 patients. In patients with accessory pathways the effect of changing atrial pacing site on the echo zone was studied. Pacing at a site remote from the accessory pathway shifted the echo zone to shorter coupling intervals. Some patients previously thought to have reentry within the AV node may have had accessory pathways which conducted only in the retrograde direction. The prevalence of this syndrome is unknown but is important because ablation of the accessory pathway is curative.

Follow-up was obtained in 33 of 35 patients with arrhythmogenic right ventricular disease (ARVD) from three centers, one in France, and two in the United States. The majority of patients are living but require antiarrhythmic drug therapy. Analysis of syncope as a prognostic factor for arrhythmic death in this series, as well as in patients with ARVD reported in the literature, suggests a more favourable long-term prognosis in those patients who did not have a history of syncope. ARVD may be due to a variety of pathological entities and the prognosis of patients who have different aetiologies may well be distinct from one another.

Twelve patients with evidence of Mahaim fibers are reported, six with nodoventricular (NV) fibers and six with fasciculoventricular (FV) fibers. All patients with NV fibers had left bundle branch block morphology, and a sustained reentrant tachycardia with this morphology was proved in each case. In three of the six, ventriculoatrial dissociation occurred during tachycardia. We postulate that the mechanism of this tachycardia is a macroreentry circuit using the NV fiber for the antegrade limb and the His-Purkinje system with a portion of the atrioventricular node for the retrograde limb. ECGs of patients with FV fibers were varied, suggesting a functional relation to the right or left side of the septum. No direct relationship of FV fibers to observed arrhythmias could be found.

Intermittent preexcitation, block in the accessory pathway after intravenous injection of ajmaline or procainamide, and block in the accessory pathway during exercise usually exclude a short antegrade refractory period of an accessory pathway in patients with the Wolff-Parkinson-White syndrome. This report describes three patients with these findings suggestive of a relatively long antegrade effective refractory period of the accessory pathway in whom life-threatening ventricular response occurred during atrial fibrillation. In the first patient with a pattern of intermittent preexcitation, rapid ventricular response with wide QRS was present during atrial fibrillation. In the second patient in whom preexcitation disappeared after intravenous injection of ajmaline or procainamide as well as during exercise testing, atrial pacing showed 1:1 conduction over the accessory pathway at a cycle length of 220 msec and the shortest R-R interval during induced atrial fibrillation was 190 msec. The third patient, with no evidence of preexcitation during sinus rhythm, presented antidromic reciprocating tachycardia and atrial fibrillation with life-threatening ventricular response, the minimal R-R interval being 220 msec. Noninvasive tests in the preexcitation syndrome lack sufficient prognostic sensitivity. The evaluation of ventricular response during induced atrial fibrillation represents the most reliable means of identifying such patients at risk.

Electrophysiological characteristics of atrioventricular (A-V) conduction and refractoriness were examined in 12 patients with Lown-Ganong-Levine (LGL) syndrome referred for assessment of the following arrhythmias: (group I) regular narrow QRS tachycardia 6/12 (50%), (group II) atrial fibrillation (AF) 2/12 (17%), group III) ventricular tachycardia (VT) 4/12 (33%). A-V node refractory periods were shorter, and enhanced A-V conduction more frequent (7/12, 58% vs 7/28, 25%) in LGL patients compared to similar studies in 28 normal controls. During laboratory study reciprocating tachycardia (RT) due to re-entry within the A-V node occurred in 4/12 (33%) LGL patients, and exhibited a shorter cycle length (294 +/- 60.4 msec) than did the same arrhythmia in 11/28 (39%) controls 372 +/- 51.8 msec, P less than 0.05). Similarly, RT utilizing a concealed accessory pathway had a shorter cycle length (228 +/- 3.5 msec) in 2/12 (17%) LGL patients than in 11/28 (39%) controls (314 +/- 24.3 msec, P less than 0.001). In AF, the shortest R-R intervals in 4/12 (33%) LGL patients (2 group I, 2 group II) were shorter than in 15/28 (54%) control patients (254 +/- 42.2 msec vs 325 +/- 64.2 msec, P less than 0.05). The mean R-R internvals did not differ significantly (LGL 372 +/- 89 msec vs control 428 +/- 82.6 msec). This study suggests that the characteristics of A-V conduction and refractoriness may permit development of more rapid heart rates during certain arrhythymias in LGL patients compared to normal controls. Furthermore, the occurrence of VT in patients with LGL sydrome indicates that symptomatic arrhythmias require specific diagnosis.

Epicardial mapping was used as a standard to investigate how well the limb leads, both alone and in conjunction with 5 select epicardial electrodes, can verify reproducibility in a common, open-chest canine model of ventricular tachycardia (VT). Reproducible VT was defined as 2 or more episodes of monomorphic VT with similar rates, limb lead tracings and epicardial maps. In this study, 21 dogs underwent 2-hour occlusion of the left anterior descending coronary artery followed by reperfusion. Three days later, programmed stimulation was used to induce VT that was analyzed with limb leads I, II and III and 27 simultaneously recorded, bipolar epicardial electrodes. Thirteen dogs had VT of which 11 had polymorphic VT (varying QRS morphology). Twelve dogs yielded at least 1 form of monomorphic VT. Eight had 2 or more distinct forms of monomorphic VT (pleomorphism). Four of these 8 dogs had pleomorphic VT that was not apparent from the limb lead tracings, but was recognized from the epicardial activation maps constructed from the 27 epicardial recordings. To provide a method of distinguishing various VTs without the need of full epicardial mapping, 5 of the 27 epicardial electrodes were selected. These were positioned over the midanterior and midposterior right and left ventricles, and the left ventricular apex. By analyzing electrogram morphology and activation time, VT reproducibility could be as accurately identified with these 5 electrodes as with epicardial mapping derived from 27 electrodes. In conclusion, multiple VT morphologies are common in this open-chest canine model. Limb lead recordings alone are inadequate for analysis of VT reproducibility.(ABSTRACT TRUNCATED AT 250 WORDS)

Records from patients with the Wolff-Parkinson-White syndrome were reviewed with particular emphasis on the occurrence of bundle-branch block aberration during reciprocating tachycardia and the significance of this observation with respect to accessory pathway location. Increase by greater than 25 ms in the ventriculoatrial interval during reciprocating tachycardia with bundle-branch block, when compared to reciprocating tachycardia with normal intraventricular conduction, occurred only with right or left free wall accessory pathways. No patient with a septal accessory pathway proven by epicardial mapping showed a ventriculoatrial interval prolongation greater than 20 ms during bundle-branch block aberration. Measurement of ventriculo-atrial interval during bundle-branch block abe-ration also helped to diagnose accessory pathways AH and HV intervals as well as ventriculo-atrial times, may give midleading information. In one patient increase in cycle length during left bundle-branch block was the result of prolonged HV interval rather than prolonged ventriculo-atrial interval. In another patient cycle length remained the same during bundle-branch block while the ventriculo-atrial interval increased by an increment identical to the decrease in AH interval.

We present a patient with Wolff-Parkinson-White syndrome who died of a myocardial infarction 19 months after clinical electrophysiologic studies. These studies suggested the presence of a left atrioventricular accessory pathway that sustained conduction well in the retrograde direction but only intermittently in the antegrade direction. Postmortem examination of the heart revealed three accessory atrioventricular pathways in proximity to each other in the posterolateral atrioventricular region. One pathway showed complete fibrosis and two showed patchy fibrosis. The fibrosis suggests an anatomic basis for the impaired antegrade conduction observed in life.

Since the original description by Dessertenne, predominantly European literature has reported the features of the unusual ventricular arrhythmia "les torsades de pointes." Named because of the way the polarity of the QRS complexes seems to spiral around the baseline of the ECG, this arrhythmia is virtually always associated with prolongation of the Q-T interval. Its importance lies not in its unusual structure but in the potentially fatal outcome if conventional treatment is administered. Antiarrhythmic drugs that further prolong the Q-T interval frequently aggravate the arrhythmia and are contraindicated. Overdrive pacing, preferably atrial, is the treatment of choice with attention to any correctable causes of associated Q-T prolongation. Electrophysiologic studies so far favor a re-entrant cause for the arrhythmia, but the exact mechanism and its true relation to both conventional ventricular tachycardia and ventricular fibrillation remain to be defined.

A cryosurgical instrument was used to ablate atrioventricular conduction. The procedure was carried out in 20 dogs and subsequently in three patients with drug resistant, life-threatening supraventricular tachycardias. In patients, the cryosurgical unit lowered the temperature of the His bundle area to 0 degrees C, effecting complete but reversible heart block. Rewarming resulted in resumption of normal atrioventricular conduction. The His bundle region then was cooled to -60 degrees C; complete heart block was produced with two or more 90-120 second freezes. Postoperative evaluations revealed persistent atrioventricular conduction block. The lesion showed no tendency to rupture, form aneurysm, or interfere with valvular function. In the clinical cases, postoperative studies demonstrated a stable pacemaker arising proximal to the branching portion of the His bundle. A potential application of the cryosurgical technique might be ablation of sites of dysrhythmia (i.e., ectopic foci, re-entry circuits, accessory pathways).

We evaluated the electrophysiologic effects of disopyramide phosphate in 12 patients with the Wolff-Parkinson-White syndrome. Electrophysiologic studies were performed during a control period and after administering i.v. disopyramide (four bolus doses of 9.5 mg/kg over 40 minutes superimposed on a continuous infusion at 1.0 mg/kg/hour). All patients were then restudied after 3 days on oral medication in doses of 800-1200 mg/day. In all patients we tried to induce reciprocating tachycardia and atrial fibrillation. The cycle length during reciprocating tachycardia was not changed by i.v. disopyramide, but increased after oral disopyramide, from 331 +/- 53 (+/- SD) to 370 +/- 68 msec (p less than 0.01). This increase occurred predominantly as a result of prolongation of retrograde conduction time in the accessory pathway. Despite prolonging cycle length during reciprocating tachycardia, disopyramide did not prevent its induction. The shortest and mean RR intervals during atrial fibrillation were used to assess antegrade refractoriness of the accessory pathway. Intravenous disopyramide prolonged the shortest RR from 169 +/- 18 to 226 +/- 24 msec (p less than 0.0001) and the mean RR from 255 +/- 58 to 329 +/- 62 msec (p less than 0.005). Oral disopyramide prolonged the shortest RR interval from 169 +/- 18 to 248 +/- 36 msec (p less than 0.0001) and the mean RR from 255 +/- 58 to 360 +/- 93 msec (p less than 0.001). After oral disopyramide, the episodes of atrial fibrillation were shorter and self-terminating. No acute hemodynamic side effects were observed, but five patients developed gastrointestinal or anticholinergic side effects on oral disopyramide. Seven patients elected to have surgical interruption of their accessory pathways and five have been successfully treated with oral disopyramide for 14-33 months. Disopyramide appears to have beneficial electrophysiologic effects in patients with Wolff-Parkinson-White syndrome. Prolongation of refractoriness in the accessory pathway markedly slows the ventricular response during atrial fibrillation and therefore prevents the development of life-threatening arrhythmias.

Forty-two patients with life-threatening or disabling atrial arrhythmias are discussed. Fifteen had Kent bundles as the basis for the reentry tachycardia, while 27 had arrhythmias that originated in or above the atrioventricular (AV) node. Nineteen of the latter had an AV node that conducted atrial impulses rapidly to the ventricle. These patients were classified as having enhanced conduction through the AV node, a diagnosis based on clinical and electrophysiological studies. Initially, the technique employed for His bundle interruption was, either separate or in combination, blind suture, electrocauterization, and incision of the septal portion of the right atrium. The technique later adopted was sharp division of the atrial septum at its attachment to the right fibrous trigone. Cryothermia was used in 31 patients. There were four failures. In the group in whom sharp division was used. there were two failures among 11 patients. Two patients, however, had to have a second operation. Following AV node-His bundle interruption, a junctional rhythm resulted and a pacemaker was always installed. Our studies indicate that interruption of atrial to ventricular conduction is a satisfactory operation for atrial arrhythmias that are disabling or life threatening and that are refractory to vigorous medical therapy. Cryothermic ablation is the preferable technique. However, if this is not successful, then division is required of the AV nod-His bundle junction by interruption of the insertion of the atrial septum into the right fibrous trigone.

The major hypothesis in the present study was that differences between high-risk and low-risk children in performance on standardized tests of cognitive ability would be explained, in part, by differences in attentiveness to auditory stimuli and differences in task orientation. The data collected revealed the anticipated higher standardized test scores for low-risk children. Within the high-risk sample, few differences were found between children who attended an intervention day-care program and those who did not. Measures from a laboratory task and a free-play observation suggested that attention is a key factor in understanding the high-risk child's development and also that differences in attention between high- and low-risk children can be reliably obtained as early as 3 years of age. A lessened attention span was demonstrated by high-risk children to both auditory and visual stimuli if either were complex or demanding.

The purpose of this study was to ascertain the origin of the atrial electrogram recorded on the esophageal lead. The atria and esophagus were mapped during reciprocating tachycardia in 11 patients with the Wolff-Parkinson-White syndrome and one patient with atrioventricular nodal reentry, and during right ventricular pacing in four additional patients. The esophagus was mapped by recording atrial electrograms at 1-cm intervals throughout the esophagus beginning at the most distal area where atrial depolarization was seen. The retrograde atrial activation time recorded on the esophageal lead in its distal position occurred at the same time as atrial septal depolarization in all patients. In 14 of 16 patients, the distal esophageal ventriculoatrial (VA) conduction time was also the shortest esophageal VA conduction time recorded. In two of five patients with left lateral accessory pathways, the shortest esophageal VA conduction time was noted during pullback of the lead from the esophagus instead of at the most distal area. The most likely explanation for this was an unusual anatomic relationship between the esophagus and left atrium in these two patients. We conclude that 1) the most distal esophageal atrial electrogram probably records posterior paraseptal atrial depolarization; 2) it is unusual to record clearly identifiable left atrial activation in the esophagus; and 3) the esophageal lead is not useful in locating left-sided accessory pathways.

A regular wide QRS tachycardia was electrocardiographically documented in 32 patients aged 1 month to 18 years. The mechanisms of the tachycardia were evaluated using standard multicatheter electrophysiologic techniques. These mechanisms included (1) orthodromic reciprocating tachycardia with bundle branch aberration (seven patients), (2) antidromic reciprocating tachycardia using single (three patients), or multiple (three patients) atrioventricular connections (Kent bundles), (3) atrial flutter with ventricular preexcitation over accessory connections (eight patients), (4) reciprocating tachycardia using a nodoventricular connection (Mahaim fiber) (five patients), and (5) ventricular tachycardia (six patients). Regular side QRS tachycardias are not rare in pediatric patients. Their mechanisms can be quite complex, and electrocardiographic analysis with respect to QRS configuration, heart rate, or the presence or absence of ventriculoatrial dissociation is not sufficient for diagnostic purposes. Our results show that considerable understanding of the mechanism of regular, wide QRS tachycardias can be obtained by multicatheter electrophysiologic study. Understanding the mechanism is essential in order to make rational use of available therapeutic options.

Patterns of ventriculoatrial conduction have been used to distinguish retrograde conduction over an accessory atrioventricular pathway from that over the normal atrioventricular conduction system. Ventriculoatrial conduction at a constant interval during incremental ventricular pacing and during progressive prematurity of ventricular extrastimuli has been considered characteristic of conduction over an accessory pathway. We describe three patients with the Wolff-Parkinson-White syndrome who had progressive or sudden increments in ventriculoatrial conduction over an accessory pathway during fixed-rate ventricular pacing or during introduction of ventricular extrastimuli. Such properties have been considered characteristic of conduction over the normal atrioventricular conduction system. We conclude that retrograde conduction over accessory pathways may resemble conduction over the normal atrioventricular conduction system.

The AA. describe a technique for interrupting the A-V conduction using a direct-current shock delivered from a cardioversion unit to the A-V junctional tissue by means of a conventional electrode-catheter. The method was used in 2 patients with refractory supraventricular tachycardias. After the procedure both patients received a programmable A-V sequential pacemaker. The first patient, with cardiomyopathy and intermittent W-P-W syndrome, had a 2-year history of iterative reciprocating tachycardia and occasional episodes of atrial flutter-fibrillation. The second patient, with coronary heart disease, had recurrent episodes of atrial flutter for at least 2 years. In patient 1 the shock caused a suprahisian first-degree block. Atrial pacing at 580 ms cycle length provoked a 2:1 block and ventricular pacing showed no retrograde conduction. The patient, who is not pacemaker-dependent, is now free from reciprocating tachycardia and, during atrial flutter-fibrillation episodes, the ventricular rate varies from 62 to 75 bpm. In patient 2 the shock caused a persistent complete A-V block and neither antegrade nor retrograde conduction was observed during atrial and ventricular pacing. During a long episode of atrial flutter, there was a complete A-V block with a ventricular rate between 40 and 48 bpm. The follow-up is 9 months in both patients. We conclude that the technique used, which does not require open heart surgery, can be effectively used in patients with disabling supraventricular tachyarrhythmias resistant to drug treatment.

Ventricular fibrillation was induced in eight of 10 open-chest dogs by reperfusion after a 15-minute occlusion of the proximal circumflex coronary artery. Simultaneous recordings were made from 27 epicardial electrodes spaced over both ventricles. Analysis of the initial 1.5--2.5 seconds of the transition from sinus rhythm or ventricular tachycardia to fibrillation revealed that ventricular activation occurred in an orderly, rapidly repeating sequence in all hearts. Each activation from arose near the border of the ischemic-reperfused region and passed across the nonischemic portion of the ventricles to the opposite side of the heart as a single, organized wavefront. As the arrhythmia progressed, the time between the appearance of successive activation fronts on the epicardium decreased. Concurrently, the time for each activation front to traverse the ventricles increased. The stimulation increase in rate of appearance and decrease in conduction velocity for each successive cycle resulted in overlapping cycles in which a new activation front arose from the ischemic-reperfused region before the previous front terminated over the right ventricle. The overlap between successive activation fronts increased as the arrhythmia continued. Thus, ventricular activation during the transition to ventricular fibrillation arose near the border of the ischemic-reperfused region and was organized as it passed across the nonischemic tissue, but the body surface ECG appeared disorganized because of variable spacing between successive, coexistent activation fronts.

This report relates the surgical experience with 79 patients with arrhythmias who had 82 left free wall accessory pathways of atrioventricular conduction of the Kent type. The current operation for the interruption of the pathway consists of two steps. First, the localization of the pathway is done by mapping the epicardial excitation sequence of the atria and the ventricles. This is followed by a set group of maneuvers needed to divide the pathway, which is not visible or palpable. First, an endocardial atrial incision is made just above the anulus fibrosus extending 1.5 to 2.0 cm on each side of the pathway's crossing point. Then, a wide separation of the coronary sulcus fat from the atria and ventricles is done. Finally, superficial fibers of the ventricular myocardium are separated from the anulus fibrosus. The surgical problems such as the possible coronary sinus origin of a pathway and the proximity of pathways to the left fibrous trigone are discussed, both from the electrophysiological and the surgical standpoints. The overall success rate for interruption of left free wall pathways has been 90% with no failure in the last 34 patients.

The effect of atrial pacing and recording site and ventricular pacing site on assessment of conduction over the accessory pathway (AP) was examined in a group of patients with the Wolff-Parkinson-White syndrome. The importance of initial localization of the AP by recording the sequence of retrograde atrial activation during circus movement tachycardia is demonstrated. Inability to record or pace near the AP may lead to significant errors in the assessment of the antegrade and retograde conduction properties of the AP. During ventricular pacing, retrograde atrial fusion was consistently demonstrated with laterally located APs.