Normal Ventricular Activation Research Articles

Experimental study of assessment on ventricular activation origin and contraction sequence by Doppler tissue imaging.

To evaluate the possibility and accuracy of Doppler tissue image (DTI) on assessment of normal and abnormal ventricular activation and contraction sequence, 9 open chest canine hearts were analyzed by acceleration mode, M-mode, and spectrum mode DTI. Our results showed that: (1) Acceleration mode DTI could show the origin of activation and conduction sequence on line; (2) M-mode DTI revealed that the activation in mid-interventricular septum was earlier than that in mid-left ventricular posterior wall at sinus activation; (3) Spectrum DTI showed the ventricular endocardium was activated earlier than the ventricular epicardium in all segments at sinus rhythm. The earliest site of activation of the normal ventricular wall was at middle interventricular septum; the latest site was at basal-posterior wall; the contraction sequence was different at the different walls; (4) During abnormal ventricular activation, mid-left ventricular posterior wall was activated earliest in accordance with the pacing sites. Abnormal ventricular activation was slower than sinus activation, and the contraction sequence varied at different sites of ventricular wall. It is concluded that DTI can be used to localize the origin of normal or abnormal myocardial activation and to assess the contraction sequence conveniently, accurately and non-invasively.

Hemodynamic Benefits of Atrio-Biventricular Pacing in Open Chest Dogs

Background and Objectives:Ventricular pacing electrodes are customarily placed into the right ventricular muscle because it is easily accessible. However, detailed physiologic studies have demonstrated that the single stimulation of right ventricular sites causes dysynchronous ventricular contraction due to early depolarization of the right ventricle and a delayed depolarization of the left ventricle. In contrast, normal human ventricular activation, which is conducted by the Purkinje system, spreads transmurally from the endocardium to multiple paraseptal epicardial regions and results in more synchronous contraction of the ventricle. Therefore, the hypothesis that producing biventricular activation by simultaneously pacing ventricles across the septum may confer hemodynamic benefits greater than those of conventional right ventricular pacing. The purpose of this study was to evaluate the acute hemodynamic changes of the different pacing modes (right ventricular:RV, biventricular:BV, atrio-right ventricular:A-RV, and atrio-biventricular:A-BV pacing). Materials and Method:In 9 open chest dogs anesthetized with α-chloralose, sinus node crushing was accomplished and the hemodynamic data (QRS width, femoral arterial pressure:FAP, pulmonary arterial pressure:PAP, and cardiac output:CO) was acquired following 5 minutes of pacing at a fixed rate during each pacing mode. Results:The results were as follow:1) BV pacing significantly increased cardiac output as compared with RV pacing (p<0.01). BV pacing significantly shortened the QRS width as compared with RV pacing (p<0.01). 2) A-BV pacing significantly increased cardiac output as compared with A-RV pacing (p<0.01). A-BV pacing significantly shortened the QRS width as compared with A-RV pacing (p<0.01). 3) A-RV pacing significantly increased systolic pulmonary arterial pressure and cardiac output as compared with BV pacing (p<0.01). Conclusion:These results support the use of atrio-biventricular pacing to improve acute hemodynamic performance. (Korean Circulation J 2001;31(4):420-426)

On the estimation of the Laplacian electrocardiogram during ventricular activation.

Body surface Laplacian electrocardiogram (ECG) mapping using a set of disk electrodes is explored by both computer simulation and human experiments in 12 healthy subjects. The Laplacian ECG was estimated from body surface potentials using finite difference estimation algorithms. The performance of the finite difference Laplacian estimators was evaluated by both computer simulation and human experiments. The present experimental results show that the two types of finite difference Laplacian estimates are highly correlated and have a consistent spatial distribution over the anterolateral chest during normal ventricular activation. The present computer simulation and human experiment results suggest the feasibility of estimating the body surface Laplacian maps (BSLMs) from potentials using the finite difference algorithm over the anterior chest in male subjects. The noise levels of the BSLMs over the anterolateral chest were quantitatively compared to the noise levels in corresponding body surface potential maps (BSPMs) in 12 healthy subjects. The simulation and experiment results indicate that the noise to signal ratios in the BSLMs over the anterolateral chest during ventricular activation is about 5 times that of the BSPMs, when no signal processing is performed.

Simulation of ventricular arrhythmias using a re-entry model algorithm

The present study employs a computer simulation of the timing of normal and abnormal ventricular activation according to a re-entry model. A wide variety of arrhythmia patterns similar to those obtained in clinical settings may be simulated by using an algorithm which is based on parameters such as the sinus RR interval (RR), the refractory period, the coupling interval between normal activation and re-entry and the coupling interval between one re-entry and a subsequent re-entry (CV). By varying RR and CV the results of the simulation may show transition between different types of arrhythmia such as ventricular tachycardia, bigeminy, trigeminy and more widely separated ventricular ectopic beats such as in concealed bigeminy. The algorithm provides a basis for the study of re-entry, a major mechanism in the genesis of ventricular arrhythmias.

Programming Advanced Pacemaker Functions

The present generation pacemaker can, to an increasing degree, model the behavior of the normal conduction system. The level of sophistication has geometrically increased due to the use of microprocessors which enables the implementation of a multiplicity of new algorithms [1]. These include the ability to provide rate modulation along with diurnal variation in the resting base rate modeling the normal chronotropic response. The expected increase in the velocity of conduction through the AV node with physiologic increases in heart rate, the normal dromotropic response to endogenous catecholamines, is modeled by increasingly sophisticated rate responsive AV delay algorithms. The AV pacing behavior of the modern pulse generator not only supports the heart rate and maintains atrioventricular synchrony but can be set to allow for a normal ventricular activation sequence in the presence of intact AV nodal conduction yet provide an optimal, often shorter, AV interval in the presence of ~rst and higher degrees of AV block. In addition, dual-chamber pacemakers have recently been introduced which have the ability to monitor the presence or absence of capture on a beat-by-beat basis, run the output at the lowest level possible, automatically increase the output as needed and track and report the capture threshold over time.

The heart remembers.

Time for primary review 21 days. Cardiac memory was characterized by Rosenbaum et al. in 1982 as ST-T wave changes induced by ventricular pacing or arrhythmia that persist long after normal ventricular activation has resumed [1]. Rosenbaum's work enlarged upon the earlier studies of Chatterjee et al. [2]who reported persistent postpacing changes in T wave morphology. The key aspects of cardiac memory were that the magnitude and persistence of the postpacing T wave changes increased with the duration of abnormal ventricular activation (referred to as ‘accumulation’) (Fig. 1), and the subsequent normalization of the T wave occurred slowly, requiring hours to months, depending on the duration of the inciting stimuli. Fig. 1 (A) T wave changes in a human subject in complete heart block before and after siting a ventricular pacemaker, and then with the pacemaker turned off after 15 minutes and 3, 8 and 15 days after the onset of pacing. Note the progressive evolution of the T wave change (reprinted from reference [2], by permission). (B) Cardiac memory evolution over 21 days of ventricular pacing (VP). Depicted are leads I and aVR from one dog during control, during VP, and at the end of 1 hour after pacing was discontinued on days 7, 14, and 21. In both leads, evolution of the T wave is such that it tracks the vector of the paced QRS complex (reprinted from reference [15], by permission). (C) Frontal plane vectorcardiographic depiction of cardiac memory from the same dog presented in Figure 1B. A shows P, QRS, and T wave vectors in control, before the onset of pacing. B: The QRS and T vectors during ventricular pacing. C: The T wave vector alone (note enlarged scale as well as dotted line indicating the change in vector) during sinus rhythm in control … * Corresponding author. Tel.: +1-212-305-8754; fax: +1-212-305-8351; e-mail: emf3@columbia.edu

Hemodynamic importance of preserving the normal sequence of ventricular activation in permanent cardiac pacing

Pacing the right ventricle in the apex profoundly modifies the sequence of activation and thus the sequence of contraction and relaxation of the left ventricle. To evaluate the relative importance of preserving normal ventricular activation sequence and optimal atrioventricular (AV) synchrony in permanent pacing, we compared the effects of three pacing modes: AAI, preserving both normal AV synchrony and normal activation sequence; DDD, with complete ventricular capture that preserves only AV synchrony; and VVI, disrupting both, at rest and during exercise. Hemodynamic and radionuclide studies were performed in 11 patients who had normal intrinsic conduction and who were implanted on a long-term basis with a DDDR pacemaker for isolated sinus node dysfunction. AAI versus DDD and VVI significantly increased cardiac output at rest (6.6 ± 1.3 L/min vs 6 ± 0.9 L/min vs 5 ± 1 L/min; p < 0.01) and during exercise (13.5 ± 2 L/min vs 12.1 ± 2.2 L/min vs 14.4 ± 2.1 L/min; p < 0.01). Pulmonary capillary wedge pressure was lowest with AAI (15.4 ± 4.5 mm Hg), with an average reduction of 17% compared with DDD (19.6 ± 5 mm Hg; p < 0.01) and of 30% compared with VVI (25.8 ± 7 mm Hg; p < 0.01) during exercise. Identical benefits were observed for all other hemodynamic parameters: right atrial pressure, pulmonary artery pressure, left ventricular (LV) stroke work index, and systemic vascular resistances. LV ejection fraction was significantly higher in AAI than in DDD at rest (61% vs 58%, respectively; p < 0.05) and during exercise (65% vs 60%, respectively; p < 0.05). This improvement in LV systolic function resulted principally from the increase in septal ejection fraction. LV filling also was improved in AAI as demonstrated by a significant increase in peak filling rate at rest and during exercise. These data show the importance of preserving, whenever possible, not only normal AV synchrony but also normal ventricular activation sequence in permanent cardiac pacing.

Body surface Laplacian mapping of cardiac excitation in intact pigs.

Relating body surface electrocardiographic signals to regional myocardial events has been a major effort in cardiac electrophysiology. Conventional electrocardiographic means do not provide sufficient spatial resolution to resolve distributed cardiac electrical activity. The purpose of this investigation was to evaluate and study the validity of a new technique--body surface Laplacian mapping--in a well-controlled experimental setting, and to test the hypothesis that the body surface Laplacian map (BSLM) can resolve normal and abnormal ventricular depolarization patterns and localize the initial site of ventricular depolarization with high spatial resolution. In this study, BSLMs were constructed from direct measurements of the surface Laplacian of the body surface potentials using an array of 64 concentric bipolar Laplacian electrodes. BSLMs were compared to body surface potential maps (BSPMs) during normal and ectopic ventricular activation in intact anesthetized pigs. The BSLM displayed highly localized images of cardiac electrical activity, indicating its ability to resolve myocardial events. The BSLM in pigs identified the pacemaking focus overlying the known location of the epicardial pacing electrode, and imaged the activation sequence associated with exogenous ventricular pacing. In contrast, in all cases the BSPM revealed a diffuse distribution of activity over the chest. The present results suggest that the BSLM provides sufficient spatial resolution to relate body surface recordings to regional myocardial events and is able to detect ventricular depolarization patterns with greater resolution than the conventional BSPM.

Relative importance of activation sequence compared to atrioventricular synchrony in left ventricular function

This study evaluated the relative hemodynamic importance of a normal left ventricular (LV) activation sequence compared to atrioventricular (AV) synchrony with respect to systolic and diastolic function. Twelve patients with intact AV conduction and AV sequential pacemakers underwent radionuclide studies at rest and Doppler echocardiographic studies at rest and during submaximal exercise, comparing atrial demand pacing (AAI) to sequential AV sensing pacing (DDD) and ventricular demand pacing (VVI). Studies at rest were performed at a constant heart rate between pacing modes, and the exercise study was performed at a constant heart rate and work load. Cardiac output was higher during AAI than during both DDD and VVI (6.2 ± 1 vs 5.6 ± 1 and 5.3 ± 1 liters/min, p < 0.05). LV ejection fraction was likewise higher during AAI (55 ± 12 vs 49 ± 11 vs 51 ± 13, p < 0.05). VVI with or without AV synchrony was associated with a paradoxical septal motion pattern, resulting in a 25% impairment of regional septal ejection fraction. In addition, LV contraction duration was more homogenous during AAI. Peak filling rate during AAI and VVI was higher than during DDD (2.86 ± 1 and 2.95 ± 1 vs 2.25 ± 1 end-diastolic volume/s; p < 0.05). During VVI, the time to peak filling was significantly shorter than during both AAI and DDD (165 ± 34 vs 239 ± 99 and 224 ± 99 ms; p < 0.05). Doppler echocardiographic evaluation of cardiac systolic function (peak aortic blood velocity, mean aortic blood acceleration and systolic ventricular time integral) during rest and submaximal exercise showed improved LV performance with AAI compared to both DDD and VVI. VVI with or without AV synchrony resulted in an altered activation pattern of the left ventricle, associated with delayed onset, asynchronous contraction, interventricular septal motion abnormalities and an impaired LV systolic function. These changes persisted during submaximal exercise. Peak filling rate depended more on a normal LV activation pattern than on AV synchrony. It is concluded that normal ventricular activation is a prerequisite for optimal LV function. Pacing systems allowing a normal ventricular activation pattern (AAI or DDD with a long AV delay) are preferred for patients who have intact AV conduction but require artificial pacing.

Return Ventricular Rhythm: New Mechanism for Tachyarrhythmia

A case study is presented in which the electrocardiographic patterns during tachycardia showed ventricular premature depolarizations with retrograde conduction to the atria probably using a left-sided anomalous pathway and reentry to the ventricles with normal ventricular activation and duplication of the heart rate. This type of tachycardia is being labeled "return ventricular rhythm" and, as far as it is known, this is the first description of its mechanism.

Top-resolution frequency analysis of electrocardiogram with adaptive frequency determination. Identification of late potentials in patients with coronary artery disease.

Frequency analysis of the electrocardiogram with Fourier transform is a sensitive method of detecting late potentials. However, information about localization of late potentials is lost, frequency resolution is poor, and window functions have to be applied. We therefore analyzed multiple segments (25 msec long) of the surface electrocardiogram ("spectrotemporal mapping") with adaptive frequency determination (AFD), an autoregressive algorithm that is characterized by high-frequency resolution in very short segments without the use of window functions. Results were compared with those from Fourier transform and the Simson method. We studied 38 patients after myocardial infarction (MI) with sustained ventricular tachycardia (VT), 21 patients after MI without VT, and 18 healthy subjects. Frequency peaks could be clearly differentiated until a minimal interval of 6 Hz; with fast Fourier transform (Blackman Harris window) in a much longer segment (80 msec), the spectral peaks merged into one another at an interval of about 30 Hz. AFD revealed high-frequency components as narrow peaks in the range of 40-160 Hz in 28 of 38 patients (74%) after MI with VT. Because of the short segment size, exact localization of late potentials was possible; in most of the patients, the peaks occurred in segments inside the QRS complex and ended 20 +/- 10 msec after termination of the QRS complex. In patients after MI without VT, only four of 21 patients (19%) had spectral peaks in segments after the end of the QRS complex; however, 13 of 21 patients demonstrated microvolt potentials in segments within the QRS complex. These potentials did not extend beyond the end of normal ventricular activation. Only two of 18 healthy subjects showed abnormal AFD results. Patients with bundle branch block did not need to be excluded. AFD allowed good differentiation between late potentials and noise by a characteristic pattern of the spectral peaks. For the Simson method, patients with bundle branch block had to be excluded, and overall sensitivity was 42%. In five cases, the cause of failure of the Simson method could be identified as incorrect determination of the QRS limits due to noise. Thus, AFD is a promising method for detailed analysis of late potentials; it combines the advantages of frequency analysis (good differentiation between signal and noise and high-pass filters not necessary) and time domain analysis (localization of late potentials).

Atrial pacing for sick sinus syndrome

Atrial pacing is the most physiological way to pace patients with sinus node disease, as it provides both AV synchrony and a normal ventricular activation pattern. Long-term studies comparing atrial and ventricular pacing imply that atrial pacing results in fewer cardiac complications and, possibly, reduced mortality. Ventricular pacing should thus, if possible, be avoided in patients with sinus node disease. The potential risk of impending high-grade AV block during atrial pacing is low, with an annual incidence around 1% if patients are selected appropriately. Approximately 40-50% of patients with sinus node disease show signs of chronotropic incompetence during physical exercise, and are thus candidates for atrial rate responsive pacing. A preoperative evaluation of candidates for atrial pacing should include long-term Holter/telemetry, exercise test, carotid sinus stimulation, and an electrophysiological study excluding significant AV conduction disturbances.

Anatomically corrected malposition of the great arteries: Diagnostic difficulties and surgical repair of associated lesions

Four patients, aged 5 to 14 years, had repair of abnormalities associated with anatomically “corrected malposition,” a condition associated with mitral/ aortic discontinuity with atrioventricular and ventriculoarterial concordance, and with the aorta lying anterior and to the left of the pulmonary artery. All 4 patients had ventricular septal defect; in addition, 1 patient had coarctation, 2 patients had pulmonary infundibular stenosis, 1 patient had acquired pulmonary valve atresia, 1 patient had acquired fixed subaortic stenosis and 2 patients had left juxtaposition of the atrial appendages. The position of the great arteries suggest corrected transposition, but the true diagnosis is made from finding atrioventricular and ventriculoarterial concordance with wide mitral/aortic separation on the cross-sectional echocardiogram. The electrocardiogram shows normal ventricular activation. Three of the 4 patients had anticlockwise rotation of the heart, which displaced the apex. This made echocardiography difficult and caused a problem in visualizing the right-sided valved conduit and closing the VSD in conventional ways. One patient died at reoperation for an obstructed conduit. Mitral regurgitation developed after resection of subaortic stenosis in 1 patient. No arrhythmias occurred in the 3 surviving patients, followed for 1 to 5 years, but the risk of subaortic stenosis remains.

Effects of tachycardia with normal and ectopic ventricular activation on S-T segment potential and patterns in the dog

Tachycardia induced by atrial pacing in the dog increases the intensity of potentials recorded on the body surface during the ST-T interval. The effects of tachycardia caused by ectopic right or left ventricular stimulation on ventricular recovery potentials were studied in 30 dogs. Rate was increased in a stopwise manner from 90 to 250 beats per minute by atrial pacing (ten dogs), or by left atrial-right ventricular sequential pacing (ten dogs), or by left atrial-left ventricular sequential pacing (ten dogs). ECG effects were determined by construction of body surface isopotential maps from voltages registered from 84 torso electrodes using a P-R segment baseline. Ectopic stimulation intensified the repolarization maximum and shifted its location to correspond with sites of epicardial stimulation. These findings reflect a reduced cancellation of transventricular differences in recovery times, with earliest recovery occurring at earliest activated sites. Increasing rate with any one activation pattern linearly increased potential extrema magnitudes without further changes of spatial features. This singular response to tachycardia regardless of activation sequence is consistent with an increase in the apparent moment of a repolarization dipole without alteration of its orientation.

Endocardial mapping in humans in sinus rhythm with normal left ventricles: activation patterns and characteristics of electrograms.

Endocardial catheter mapping was performed in 15 patients in sinus rhythm who had no evidence of structural heart disease and normal left ventricles. Mapping was performed with the use of 10 mm interelectrode distance from various left ventricular endocardial sites. In 10 patients a quantitative analysis of electrographic amplitude, duration, and amplitude/duration ratio was performed. The normal left ventricular bipolar electrograms had an amplitude of greater than 3 mV, a duration of less than 70 msec, and an amplitude/duration ratio of greater than 0.045. Local activation times were also assessed in the 15 patients. This analysis revealed two endocardial breakthrough sites, one on the midinferior septum and a second on the anterior wall near the insertion of the anterior papillary muscle. We therefore have defined normal quantitative characteristics of left ventricular bipolar electrograms and the normal left ventricular activation sequence in the intact normal human left ventricle.

Relation between late potentials on the body surface and directly recorded fragmented electrograms in patients with ventricular tachycardia

The relation between low-amplitude, late potentials on the body surface and directly recorded electrograms in 8 patients with and 11 patients without ventricular tachycardia (VT) was studied. Bipolar X,Y,Z leads were signal-averaged and filtered with a digital technique. All patients had catheter endocardial left ventricular maps. The VT group had medically intractable VT and an endocardial excision was performed for control of VT. Before bypass, epicardial maps were obtained in the operating room. All studies were performed during normal sinus rhythm. Four patients without VT, each with a previous myocardial infarction, had fragmented endocardial electrograms recorded at 2.0 +/- 1.2 sites. The latest electrogram for each patient ended 87 +/- 8 ms after QRS onset, within the high-amplitude portion of the filtered QRS complex. All patients with VT had fragmented electrograms recorded at 6.1 +/- 3.1 sites/patient. Eighty-eight percent of the fragmented electrograms were endocardial. The latest fragmented electrogram for each patient ended 161 +/- 43 ms after QRS onset, significantly later than the fragmented electrograms from the patients without VT (p = 0.002). Six VT patients had low-amplitude, late potentials at the end of the filtered QRS complex. In these patients, the last 40 ms of the filtered QRS complex contained a higher proportion of fragmented electrograms compared with earlier segments of the QRS complex (68% versus 27%, p less than 0.001). Two patients with VT did not have late potentials. One patient with left bundle branch block had delayed left ventricular epicardial activation which masked the fragmented electrograms. The other had fragmented electrograms of brief duration which ended 80 +/- 12 ms after QRS onset, during the time of normal ventricular activation. It is concluded that the late potential corresponds to delayed, fragmented electrographic activity. Failure to record a late potential may arise from delayed ventricular activation at other sites from bundle branch block or fragmented electrograms of a brief duration.

Phase image characterization of ventricular contraction in left and right bundle branch block

The phase image is a computer-derived functional image, based on the analysis of the time versus radioactivity curve in each pixel location of the multiple gated blood pool scintigram. Within the ventricular regions of interest, the phase angle is roughly equivalent to the time of onset of counts reduction or to the time of onset of ventricular contraction and is expressed in degrees from 0 to 360 °. A gray scale-coded image of such a regional phase angle, the phase image, can be looked on as a map of sequential contraction. This method was applied in 33 patients without severe contraction abnormality including 16 patients with normal conduction, 9 with right bundle branch block and 8 with left bundle branch block. In patients with normal conduction the pattern of phase angle distribution, representing the pattern of ventricular contraction, was homogeneous and symmetric in both the left and right ventricles. Analysis in this normal group indicated a slight but significant difference between the mean (± standard deviation) phase angle of the left ventricle (8.5 ± 11.8 °) and that of the right ventricle (13.6 ± 12.9 °, p = 0.01). There was a slight, but nonsignificant difference between mean intrapatient left and right ventricular phase angle onset (1.9 ± 6.5 °). The mean phase angle of the right ventricle in patients with right bundle branch block (27.6 ± 14.2 °) and of the left ventricle in those with left bundle branch block (21.9 ± 14.0 °) was delayed compared with that in patients with normal conduction (p < 0.05 for both). The mean intrapatient difference between left and right ventricular mean phase angles in patients with normal conduction (−5.2 ± 6.8 °) was significantly different from that in patients with right (−21.8 ± 10.3 °, p < 0.001) or left (21.8 ± 6.8 °, p < 0.001) bundle branch block. The mean intrapatient difference between onset of left and right ventricular phase angles was also significantly different from normal in patients with right (−10.6 ± 7.5 °, p < 0.005) or left (18.7 ± 8.3 °, p = 0.01) bundle branch block. Although phase imaging is not without artifactual error, this study demonstrates that the phase image can characterize familiar conduction abnormalities. It presents the potential for application as a general noninvasive tool in the investigation of the timing and sequence of ventricular contraction in patients with normal or abnormal ventricular activation.

Effect of activation sequence on MVO2 before and after coronary ligation.

In pentobarbital-anesthetized, open-chest dogs with fixed heart rate, cardiac output, and systemic arterial pressure, ectopic ventricular activation originating from apical as compared to basilar regions of either ventricle was associated with small (3--5%) but significantly (P less than 0.005) lower myocardial O2 consumption (MVO2) and thus higher left ventricular (LV) efficiency without change in LV end-diastolic pressure (LVEDP), work index (LVWI), and LV dP/dt. Data obtained during epicardial and corresponding endocardial activation did not differ. During normal ventricular activation, MVO2 remained unchanged but LVEDP was significantly (P less than 0.005) lower, thus yielding higher LVWI and efficiency. MVO2 differences among ectopic sites were abolished after coronary artery occlusion, whereas data obtained during endocardial and epicardial on normal and ectopic activation were not affected. Thus, normal activation resulting in lower LVEDP is most efficient; apical ventricular activation is less efficient at the same MVO2P basilar is the least efficient, because both MVO2 and LVEDP are higher. Ventricular activation sequence changes do not constitute a substantial determinant of MVO2.

Determinants of ventricular septal motion. Influence of relative right and left ventricular size.

To test the hypothesis that the ventricular septum moves during systole toward the center of the ventricular mass (so that the end-diastolic position of the septum within the heart should determine both the direction and the magnitude of septal motion during systole), echocardiograms from patients with several different hemodynamic burdens were analyzed. A linear relation was noted between the end-diastolic intracardiac position of the ventricular septum and the direction and magnitude of systolic septal motion in 1) forty three patients with an atrial septal defect )regression coefficient r = 0.80), 2) fourteen patients with other causes of right ventricular volume overload (r = 0.82), 3) nineteen patients with left ventricular volume overload (r = 0.74), 4) ten patients with right ventricular pressure overload (r = 0.93), 5) ten patients with left ventricular pressure overload (r = 0.80), 6) twenty-eight normal subjects (r = 0.82). We conclude that, in the presence of normal ventricular activation and contraction, the direction and magnitude of sepatal motion during systole is determined by the intracardiac position of the septum at enddiastole.

Surgical correction of anomalous left ventricular pre-excitation: Wolff-Parkinson-White (type A).

This report describes two patients with the Wolff-Parkinson-White syndrome including episodes of supraventricular tachycardia and atrial fibrillation. Both patients had Type A electrocardiograms. Electrophysiological studies demonstrated pre-excitation and evidence that the site of pre-excitation involved the left ventricle. The effective refractory periods of the accessory pathway during atrioventricular conduction were 240 and 220 msec respectively. Epicardial mapping at the time of surgery showed that anomalous excitation began adjacent to the annulus of the mitral valve near a marginal branch of the left circumflex coronary artery. An incision which separated the atrial muscle from the annulus of the mitral valve at the region of anomalous excitation abolished the delta wave. Epicardial maps after surgery showed normal ventricular activation and follow-up studies have shown normal electrocardiograms and no arrhythmias.