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Background— Atrial fibrillation (AF) is common after cardiac surgery. Abnormal conduction is an important substrate for AF. We hypothesized that atrial inflammation alters atrial conduction properties. Methods and Results— Normal mongrel canines (n=24) were divided into 4 groups consisting of anesthesia alone (control group); pericardiotomy (pericardiotomy group); lateral right atriotomy (atriotomy group); and lateral right atriotomy with antiinflammatory therapy (methylprednisolone 2 mg/kg per day) (antiinflammatory group). Right atrial activation was examined 3 days after surgery. Inhomogeneity of conduction was quantified by the variation of maximum local activation phase difference. To initiate AF, burst pacing was performed. Myeloperoxidase activity and neutrophil cell infiltration in the atrial myocardium were measured to quantify the degree of inflammation. The inhomogeneity of atrial conduction of the atriotomy and pericardiotomy groups was higher than that of the control group (2.02±0.10, 1.51±0.03 versus 0.96±0.08, respectively; P P P =0.012). There also were significant differences in myeloperoxidase activity between the atriotomy and pericardiotomy groups and the control group (0.72±0.09, 0.41±0.08 versus 0.18±0.03 ΔOD/min per milligram protein, respectively; P P r =0.851, P Conclusions— The degree of atrial inflammation was associated with a proportional increase in the inhomogeneity of atrial conduction and AF duration. This may be a factor in the pathogenesis of early postoperative AF. Antiinflammatory therapy has the potential to decrease the incidence of AF after cardiac surgery.

BACKGROUND Since the atria are thin-walled structures, most studies that have examined the spread of activation in the atria have assumed that they behave electrophysiologically as a two-dimensional surface. It was the objective of this study to determine whether or not this assumption is true by simultaneously mapping the epicardial and endocardial activation sequences in the right atrium. METHODS AND RESULTS Identical precisely superpositioned epicardial and endocardial electrode templates with 250 unipolar electrodes each were used to map the isolated canine right atrium (n = 8) during continuous perfusion and superfusion with Krebs-Henseleit buffer. Data were recorded during control conditions (normal sinus rhythm), continuous pacing (S1S1 = 300 msec), and premature stimulation (S1S2 = effective refractory period + 5 msec). Pacing was performed at two sites, one located on the inferior crista terminalis and one lateral to the crista terminalis on a pectinate muscle. Tachyarrhythmias were induced by a single extrastimulus during the continuous perfusion of acetylcholine (10(-3.5) mol/L). Individual electrode sites were correlated with the gross anatomy and histology. Activation time differences were calculated between each two corresponding epicardial and endocardial sites. There were differences in the activation times between the epicardium and endocardium during all experimental conditions. However, the average difference for each condition was < 1 msec, suggesting that overall activation did not spread faster on either the epicardium or the endocardium, even though in certain regions one surface could lead the other. The dispersion of time differences was smallest during normal sinus rhythm and continuous pacing (SD = 5.6-5.8 msec) and largest after premature stimulation (SD = 6.3 msec for crista pacing, p < 0.05; SD = 8.1 msec for pacing lateral to the crista, p < 0.001). Differences in the activation sequence correlated with the underlying anatomic architecture. The largest differences in activation times between the epicardium and endocardium were associated with those regions of the atrium where pectinate muscles ran below the epicardial surface. The pectinate muscles in those areas were often discontinuous with the epicardial surface and facilitated the discordant epicardial-endocardial activation. The discordant activation was also found in regions where the atrial wall thickness was < 0.5 mm and correlated with transmural differences in fiber orientation. A tachyarrhythmia induced in the presence of acetylcholine, which demonstrated a focal activation pattern, was shown to have a reentrant loop that used free-running muscle bundles connecting the epicardial and endocardial surfaces, resulting in a three-dimensional pathway. CONCLUSIONS The findings of this study demonstrate that epicardial and endocardial activation can be discordant in specific regions and that discordance increases with abnormal activation sequences. Many of the differences in the epicardial and endocardial activation can be correlated with the heterogeneity of the anatomic architecture of the right atrium. The study also demonstrates that reentry can occur in a three-dimensional plane using the epicardial and endocardial surfaces connected by transmural muscle fibers.

Background— The critical mass hypothesis for atrial fibrillation (AF) was proposed in 1914. There has never been a systematic investigation defining the relationship between tissue geometry and AF. The purpose of this study was to determine the association among the probability of maintaining AF and the width, area, weight, effective refractory period (ERP), and wavelength in atrial tissue. Methods and Results— Isolated canine atria (n=20) were perfused with Krebs-Henseleit solution. Baseline ERPs were obtained with and without acetylcholine (10E-3.5 mol/L) using single extra-stimulus pacing while unipolar electrograms were recorded from 250 sites. The tissue was then partitioned using bipolar radiofrequency ablation, and the ERPs were measured again with and without acetylcholine. Any section of tissue that maintained AF was divided until the arrhythmia was no longer inducible. ERPs and conduction velocities were measured in all of the sections after each ablation, and the wavelengths were calculated. The probability of AF was found to be correlated with increasing tissue areas, widths, and weights ( P P Conclusions— The probability of sustained AF was significantly associated with increasing tissue area, width, and weight and decreasing ERPs and wavelengths. These data may lead to a better understanding of the mechanism of AF and, thus, help to design more-effective interventional procedures in the future.

Background— The Maze procedure restores normal sinus rhythm in the majority of patients. However, atrial tachyarrhythmias (ATA) are a common early complication after the operation. The purpose of this study was to define the incidence and natural history of ATA after the Maze procedure. Methods— Complete medical records from 200 patients who underwent the Maze procedures (I, II, and III) from 1987 to 2002 were examined for all episodes of early postoperative ATA that occurred during the first 30 days after the procedure. Two electrophysiologists independently reviewed all postoperative 12-lead electrocardiograms. Results— ATA occurred in 86 patients (43%) after the Maze procedure. Of the patients with ATA, 59% had atrial fibrillation (AF), 14% had atrial flutter (AFL), and 27% had both AF and AFL. Of the patients with AF or AFL, 20% and 5%, respectively, also had episodes of atrial tachycardia and supraventricular tachyarrhythmia. The peak incidence of early postoperative ATA was on postoperative day 8. The average duration of ATA was 5.7±5.0 days. Late recurrence of AF (>1 year postoperatively) occurred in 7.0% of patients who had early postoperative ATA and 8.8% of patients without early postoperative ATA ( P =0.8). Conclusions— ATA occurred in 43% of patients after the Maze procedure. The tachyarrhythmias occurred primarily within 8 days after surgery and resolved within 3 weeks in almost all patients. There was no relationship between the incidence of early postoperative ATA and the late recurrence of AF.

Background —The central common pathway, which is the target for ablation in reentrant ventricular tachycardia, can be localized by entrainment mapping techniques. However, localization of the pathway is not always possible because of the elevated pacing threshold and the low voltage and fractionated potentials at the pathway. We examined whether return cycle mapping after entrainment localizes the pathway without pacing at the pathway or recording the potentials from the pathway and determined the required electrode resolution to localize the pathway. Methods and Results —Epicardial mapping was performed with 253 unipolar electrodes during and after entrainment of 13 morphologies of ventricular tachycardia that were induced in dogs 4 days after infarction. The return cycle was calculated by subtracting the first activation time from the second activation time after the last stimulus and the return cycle distribution map was constructed for each stimulation site. The return cycle isochrones equal to the ventricular tachycardia cycle length converged on the lines of conduction block irrespective of the stimulation site, and the central common pathway was localized at the region between the intersections of the return cycle isochrones after entrainment from different stimulation sites. The potentials from the central common pathway were not required to localize the pathway, and the mapping accuracy did not change with or without analysis of the potentials from the pathway. According to the correlation between the electrode resolution and the mapping accuracy, an interelectrode distance of 8.5 mm was estimated as sufficient resolution for successful tachycardia termination during radiofrequency ablation guided by return cycle mapping. Conclusions —Return cycle mapping after entrainment localizes the central common pathway without pacing at the pathway or recording the potentials from the pathway. This new mapping technique could improve the success rate of the ablative procedures.

Background Atrial refractory periods and their spatial distribution are important determinants of atrial reentrant arrhythmias. The objective of this study was to demonstrate a correlation between the local atrial fibrillation interval (AFI) and local effective refractory period (ERP). Methods and Results To measure the local ERP and local AFI under stable conditions without hemodynamic, autonomic, or reflex influences, isolated perfused canine whole atria were used (n=8). The isolated atria were mounted on two endocardial electrodes. Bipolar electrograms were simultaneously recorded from 253 endocardial sites, and 16 to 20 randomly distributed electrodes were used to measure the local ERP by the extrastimulus technique. In all studies, several episodes of AF were induced by a single extrastimulus. The ERP and minimum AFI converged with increasing duration of AF. The convergence was more rapid if the total duration of AF analyzed came from multiple episodes of AF. The correlation coefficient between the local ERP and minimum local AFI was .92 (n=119, P Conclusions The minimum local AFI measured from at least 10 seconds of AF approximates the local ERP. Construction of a minimum local AFI map during AF can be used to predict the distribution of refractoriness and can be used to predict sites of functional block. Contrary to studies done in intact animals and patients, the AFI were longer than the ERPs, suggesting that reflex changes may shorten ERP in the intact heart.

BACKGROUND In humans, chronic ventricular tachycardia (VT) is usually associated with myocardial infarcts that involve the interventricular septum. In an effort to more closely mimic the anatomic substrate that gives rise to chronic VT in humans, we developed a canine model of VT in which the anterior septal coronary artery was ligated. The site of earliest activation, the subsequent activation sequence, and the mechanism of VT associated with the resultant ventricular septal infarct was then evaluated to determine if this model accurately reflected the characteristics of human VT. METHODS AND RESULTS Seventeen dogs underwent occlusion-reperfusion ventricular septal infarcts. Four to 7 days later, electrophysiological studies were performed. VT was initiated by programmed electrical stimulation and terminated by pacing at a cycle length of 50% to 75% of the VT cycle length. Electrophysiological studies were performed using a 256-channel mapping system. A total of 15 VT morphologies were mapped in 9 animals. Fourteen of 15 morphologies had septal subendocardial sites of earliest activation and 1 had a septal midwall site of earliest activation. VT ablation was performed using a nitrous oxide cryoprobe and confirmed the site of earliest activation by subsequently rendering VT noninducible. Electrophysiological studies demonstrated four distinct VT activation sequences: (1) circular reentrant (n = 7), (2) concentric spread (n = 5), (3) figure-of-eight (n = 2), and (4) septal midwall (n = 1). CONCLUSIONS This canine model of ventricular septal infarction produces VTs with sites of earliest activation and activation sequences similar to those in humans. A reentrant mechanism as the basis of these arrhythmias is supported by the following observations: (1) all VT was initiated and terminated with programmed electrical stimulation; (2) VT activation sequences were consistent with reentry; and (3) precise interruption of the sequence terminated the VT and rendered it noninducible.

Atrial depolarization was analyzed in 14 patients with the Wolff-Parkinson-White syndrome undergoing surgery to ablate accessory atrioventricular pathways associated with tachyarrhythmias. Bipolar potentials were recorded simultaneously from 156 atrial epicardial electrodes arranged in three templates to fit the anterior and posterior aspects of both atria. Spontaneous or sinus rhythms were recorded, as were atrial escape rhythms after overdrive pacing at rates of 150 and 200 beats/min. Atrial activation maps revealed different patterns of impulse initiation varying from typical unifocal sinus node impulse origin, unifocal extranodal impulse origin, and multicentric impulse origin from two to four widely distributed atrial pacemaker sites. In subjects demonstrating only unifocal impulse origin during control or sinus rhythm, other widely divergent pacemaker sites were recorded in other maps during subsequent rhythms. In addition to sites located at the upper superior vena cava-right atrium junction, pacemakers also dominated at sites anterior and inferior to the sinus node region during both control and escape depolarizations. Most of the subjects were found to have two or more pacemaker sites when maps of all control and postpacing conditions were analyzed. The right atrial pacemaker region encompassed a zone of 7.5 X 1.5 cm centered about the long axis of the sulcus terminalis posteriorly and the precaval band anteriorly. An unexpected finding was the participation of left atrial escape pacemakers. The functional behavior of both the control and escape pacemakers, as assessed by sinus node recovery time, was normal, indicating physiologic operation of the extranodal sites as part of an overall system of distributed pacemakers involved in the control of rate. Although functional assessment was limited in these initial patient studies, correspondence with similar observations in extensive previous canine studies supports the concept of a widely distributed atrial pacemaker complex in man.

Bipolar electrograms were recorded from five to six sites on the septal right bundle branch (RBB) using a multielectrode patch in ten mongrel dogs. Antegrade activation was recorded along the right bundle during sinus rhythm and during right atrial pacing at varying heart rates. Retrograde activation was produced by pacing from right ventricular epicardium. Right bundle conduction velocities varied from 1.4 to 3.3 m/sec (mean 2.0 m/sec) for antegrade conduction and from 1.8 to 2.7 m/sec (mean 2.1 m/sec) for retrograde activation. Varying degrees of conduction delay were elicited by premature stimulation and mechanical pressure to the right bundle. The conduction delays occurred over small segments of the right bundle branch with regeneration of normal propagation velocity distal to the region of block. The conduction delays were associated with fragmentation of the RBB electograms with initiation of delayed activation waves which traveled variable distances antegrade and retrograde. These data show that stress-induced longitudinal dissociation may produce delayed activation waves within the right bundle branch which may simulate re-entrant arrhythmias.

Isopotential body surface maps and the sequence of epicardial excitation were studied in children with three types of pure right ventricular hypertrophy; that is, secundum atrial defects, valvular pulmonic stenosis, and tetralogy of Fallot. Patients with similar types of hypertrophy demonstrated internal consistency as to the anatomy, sequence of epicardial excitation of the right ventricular free wall, and body surface potential distribution; however, these phenomena varied between the three groups for each type of hypertrophy. These studies indicate that diagnostic information is available on the body surface to distinguish: (1) right ventricular hypertrophy due primarily to dilatation (secundum atrial septal defects), (2) right ventricular hypertrophy with symmetrical increase in thickness throughout the right ventricle (valvular pulmonic stenosis with moderate to severe right ventricular hypertrophy), and (3) right ventricular hypertrophy proximal to infundibular narrowing (tetralogy of Fallot) from one another. The body surface events could be accounted for in part by the events measured at the epicardial surface.

The interatrial pressure-flow dynamics in patients with right-to-left shunting at the atrial level in the presence of right heart obstruction were studied. In tricuspid atresia most of the right-to-left gradient occurred during right atrial systole. This gradient, as well as the cineangiocardiograms, indicated that almost all systemic venous return was transferred from the right to the left atrium through the interatrial communication during right atrial contraction. Cine studies also suggesed that right atrial systole (1) contributed significantly to left ventricular filling and (2) produced regurgitant venous flow, especially into the hepatic veins. In two patients with secundum atrial defect and associated marked pulmonic valve stenosis, bidirectional shunting at the atrial level was defined by pressure gradient and cine and dye-dilution curve technics. The right-to-left gradient and shunt occurred during ventricular diastole with accentuation of this gradient by atrial contraction; the left-to-right interatrial flow and gradient occurred during ventricular systole when both A-V valves were closed. These studies indicate that, in the presence of an interatrial communication, increasing degrees of right heart obstruction not only produce right-to-left shunting but (1) do so primarily by right-to-left flow across the interatrial communication during ventricular diastole and (2) with complete right atrial obstruction, right atrial contraction plays a dominant role in the transfer of systemic venous return to the left atrium.

This study was conducted to determine the instantaneous pressure-flow relationships across secundum atrial septal defects. Simultaneous right and left atrial pressures and the pressure difference (determined with an analog computer) were recorded with matched catheter systems. Biplane cineangiocardiography was used to evaluate the timing of the shunts in various phases of the cardiac cycle. These studies indicated that the major left-to-right shunt and pressure gradient occurred over an interval encompassing late ventricular systole and early diastole. Also, there was augmentation of the left-to-right shunt during atrial contraction. Minute right-to-left shunting and pressure gradients occurred at two times in the cardiac cycle: (1) with the onset of ventricular contraction; and (2) during early ventricular diastole (heart rate, 80 to 100 beats/min). Detection of systemic right-to-left shunts by dye curves was enhanced by relatively slow heart rates (prolonged diastasis) which allowed the shunted blood to flow into the left venrticle. The effects of respiration during phasic changes in intrathoracic pressure resulted in an increasing left-to-right gradient during periods of increasing intrathoracic pressure and a fall in the left-to-right gradient across the defect during periods of decreasing intrathoracic pressure.

This study was conducted to determine the nature of intracardiac shunting in 50 patients between the ages of 3 and 15 years with isolated ventricular septal defects. Simultaneous right and left ventricular pressures and biplane cineangiocardiography were utilized to study the timing and the direction of flow across the defect. Patients with low to moderately elevated right ventricular pressures demonstrated left-to-right shunting across the defect throughout the cardiac cycle. When pressure in the right ventricle approximated that of the left, right-to-left shunting occurred across the defect into the left ventricle during isovolumic relaxation. All patients shared in common the following: (1) a predominant left-to-right gradient and shunt across the defect into the body of the right ventricle during diastole; and, (2) augmentation of the left-to-right gradient with resultant increase of the shunt into the right ventricle during isovolumic contraction immediately preceding opening of the aortic valve. In comparing patients with and without pulmonary hypertension, the major variations in the cardiac cycle occurred during the periods of ventricular ejection and isovolumic relaxation. These two periods are primarily affected by the changing relationships of the size of the defect, ratio of pulmonary to systemic resistance, and magnitude of net shunts.

The sequence of atrioventricular activation was studied in two human subjects with type B Wolff-Parkinson-White syndrome (WPW) and in a dog with spontaneous type A WPW. In all three subjects a focal spot of pre-excitation was demonstrated at the A-V margin of the right ventricle (RV). In the two human subjects with type B WPW, the area of pre-excitation was located on the anterior aspect of the RV and in the dog with type A the pre-excited area was located on the posterior aspect of the RV. A probable Kent bundle electrogram was recorded from the A-V margin in one of the human patients. Serial sections (7 µ) of a block taken from the region of pre-excitation in the dog revealed an anomalous A-V communication (Kent bundle). Propagation velocity across this pathway was estimated to be 0.3 mm/msec. Electrophysiologic data recorded from one of the human subjects at the onset and during an episode of supraventricular tachycardia demonstrated an atrioventricular-atrial sequence of excitation. The mechanism of initiation of the tachycardia was a ventriculo-atrial echo following a premature atrial contraction blocked in the anomalous pathway. Surgical separation of right atrium and RV at the site of pre-excitation normalized the activation and ECG and abolished the tachycardia in both patients. Ventricular fibrillation occurred repeatedly in the dog as a direct result of the rapid ventricular rate permitted by the Kent bundle subsequent to induced atrial fibrillation. Correlation of the activation sequence with the body surface potentials suggests an updated conceptual model for electrocardiographic typing of WPW. In a third patient, who demonstrated an atypical form of WPW, the region of pre-excitation could not be precisely defined and interruption of an accessory pathway was unsuccessful.

Ventricular activation was studied in 20 patients with ischemic heart disease at the time of surgery for myocardial revascularization. Because most of the activation studies in man were limited to recording of epicardial potentials, a canine model of chronic infarction was also studied. Pre- and postinfarction data were recorded in dogs and correlated with the anatomy of the lesions. Epicardial Q waves, when associated with delayed epicardial activation, were diagnostic of underlying infarctions in areas of the heart that did not normally exhibit Q waves. In areas normally containing Q waves, underlying infarction was associated with Q waves greater in duration than the normal range determined for those areas of the epicardium. The experimental model of chronic infarction showed epicardial delay to be due to slowed intramyocardial activation rather than to delay in Purkinje conduction. Correlations between electrical and anatomic data in two patients suggested that, within limits, the detailed relationships between infarction and activation established with the canine model could be applied to human infarction to understand the genesis of the epicardial potentials and the ECG. The technique was also felt to have a practical clinical application in selection of areas of myocardium for vascular implants or infarctectomy.

Bipolar potentials were recorded from intramural electrodes located within areas of acute myocardial ischemia in dogs. Alterations in bipolar potential electromotive force (EMF) and local activation times were measured at predetermined intervals up to 12 hours after coronary occlusion. Histochemical stains were used to correlate structural-biochemical changes with sites of electrophysiologic changes. In severely ischemic areas, bipolar potentials lost 50% of their preocclusion EMF within 30 min and 95% within six hours at which time all parameters stabilized. Lesser decreases in bipolar potential EMF were recorded in the peripheral areas of the infarct. Bipolar potential EMF increased at the junction of ischemic and normal myocardium. Activation time was delayed in ischemic areas but no correlation between the magnitude of delay and the degree of tissue ischemia could be established. Coronary reperfusion after 30 min, one hr, two hr and six hr of occlusion resulted in some return in bipolar potential EMF, decreasing as a function of duration between occlusion and reperfusion. Variation in the degree of ischemia of different zones of injury within an acute myocardial infarction, as well as a different response of those zones to the return of blood flow, was shown.

The present study was conducted to determine the instantaneous pressure-flow relationships across the ventricular septal defect in tetralogy of Fallot. Simultaneous right and left ventricular pressures and the pressure gradient were recorded with matched catheter systems. Biplane cineangiocardiography was used to evaluate the timing of the bi-directional shunts during various phases of the cardiac cycle. The instantaneous pressure differences between the two ventricles and the direction of the pressure gradient correlated well with the timing of the shunt across the defect. In 27 patients with moderate tetralogy of Fallot, a consistent pattern of bidirectional shunting was shown. The right-to-left shunt occurred at two places and two sites during the cardiac cycle; namely, during early ventricular ejection into the aorta, and during isovolumic ventricular relaxation directly across the ventricular defect into the left ventricle. Left-to-right gradients and shunting across the defect were found to occur during isovolumic ventricular contraction and during diastole. The results of this study suggest that further investigation of various cardiac defects may yield important information concerning shunting mechanisms.

The evolution of premature ventricular contractions (PVCs) in acute myocardial infarction was studied by recording bipolar potentials from the left ventricle before and after coronary artery occlusion in dogs. The potentials were recorded from 154 locations in the left ventricular wall as well as at the endocardial and epicardial surfaces. Desynchronization and marked slowing of previously uniform activation was noted and resembled abbreviated, local fibrillation. The dissociation of excitation was either simple, characterized by fragmentation into single delayed spikes, or complex, characterized by numerous spikes. Sustained, desynchronized activity, confined to local myocardial areas, was observed up to 215 msec after the onset of activation. These local areas of sustained excitation functioned as a source of re-entrant activity and were associated with PVCs. Histochemical stains of myocardium indicated a relationship between the inhomogeneous distribution of ischemia (stain) and the desynchronization of the electrical activity.

A combined electrophysiologic-anatomic study was performed in a dog with a congenital atrial septal defect (ASD) primum. Comparisons were made between the dog and electrophysiologic data obtained in four patients with ASD primum. The ECGs and VCGs in both the dog and patients revealed the characteristic features of superior orientation, counterclockwise rotation, and slow-rightward terminal forces in the frontal plane QRS. In both the dog and the patients, epicardial ventricular activation revealed early posterior LV wall excitation and later anterior left ventricular (LV) depolarization. Also, there was a marked delay in the activation of the RV in both dog and patients. In the dog, Purkinje (Pj) potentials were recorded from the endocardium of the anterior and posterior LV wall and the anterior RV wall. The endocardial-Pj activation times of these three regions were correlated with the measured lengths of the three major divisions of the conduction system supplying them. Premature activation of the posterior LV Pj and delayed activation of the anterior LV and RV Pj was observed. The marked asynchrony of Pj activation was due to a developmental asymmetry of the ventricular conduction system, characterized by markedly different lengths of the three major divisions. Purkinje conduction velocity was 1.5 m/sec, and there were no areas of block or slow conduction. The agreement between the dog and human data indicated an identical mechanism for patients with ASD primum. The terms left anterior-superior hemiblock and right bundle branch block are inappropriate descriptions of this lesion.

Recurrent supraventricular tachycardia is a frequent complication in patients with the Wolff-Parkinson-White (WPW) syndrome. Our patient was unusual in that the arrhythmia was the predominant rhythm, and it was felt that the sustained tachycardia was responsible for signs and symptoms of congestive heart failure. The arrhythmia could not be controlled adequately with digitalis, quinidine, diphenylhydantoin, or propranolol. Atrial or ventricular pacing also failed to prevent recurrent episodes of tachycardia. Physiological and pharmacological studies suggested that an anomalous pathway was responsible for the WPW abnormality and participated in a re-entrant circuit which sustained the episodes of tachycardia. Isopotential body surface mapping suggested anomalous ventricular excitation at the lateral aspect of the right atrioventricular groove. Epicardial mapping at the time of surgery was used to localize the earliest area of anomalous ventricular activation, and surgical transection of the atrioventricular junction at that point abolished the electrocardiographic features of WPW and the recurrent tachycardia. Five months after surgery neither the ECG features of WPW nor the tachycardia has recurred. The signs and symptoms of congestive heart failure have subsided, and the patient has returned to work.

The diagnosis of an intrathoracic goiter can, on occasion, be difficult to confirm. The Valsalva maneuver was found useful in making this diagnosis in 2 patients whose case histories are reported. Such goiters are termed plunging goiters. The phenomenon is discussed and the use of the Valsalva maneuver in demonstrating such lesions is emphasized.

The body surface potential distribution in two infants with myocardial infarction secondary to anomalous origin of the left coronary from the pulmonary artery demonstrated: (1) the persistence of a minimum in the area overlying the infarct during inscription of the prominent Q wave in V 6 , and, (2) the presence of a terminal maximum in an adjacent area overlying the infarct. The terminal maximum was considered to represent peri-infarction "block" resulting from persistence of wave fronts in the ischemic muscle surrounding the infarct as suggested by the studies of Durrer and associates. Postoperatively, there was persistence of the initial minima overlying the area of the infarct. Finally, there was disappearance or marked diminution in the terminal maximum overlying the area of the infarct following surgical enhancement of myocardial blood supply.