Body Surface Isopotential Maps Research Articles

Electrocardiographic changes in diabetes mellitus.

Diabetes mellitus (DM) has been known for many years to be associated with poor cardiovascular prognosis. Due to the sensitive neuropathy, the coronary artery disease in diabetic patients is frequently asymptomatic. Also twelve leads resting ECG can be within normal limits even in an advanced stage of coronary artery disease. Therefore in addition to the standard ECG other electrocardiographic procedures started to be studied in order to find some typical signs of myocardial damages caused by DM. Repeatedly reported results showed in DM patients without cardiovascular complications the tachycardia, shortening of the QRS and QT intervals, increase of the dispersion of QT interval, decreased amplitudes of depolarization waves, shortened activation time of ventricular myocardium and a flattening of T waves confirmed by the lower value of maximum and minimum in repolarization body surface isopotential maps. Most of these changes are even more pronounced in patients with cardiac autonomic neuropathy. Comparison with similar ECG changes in other diseases suggests that the electrocardiographic changes in DM patients are not specific and that they are particularly caused by an increased tone of the sympathetic nervous system what was indirectly confirmed by the heart rate variability findings in these patients.

Resolution of pace mapping stimulus site separation using body surface potentials.

Several studies have related 12-lead ECG waveform during ventricular tachycardia to ECG waveform during ventricular pacing to identify ablation sites for therapy of ventricular tachycardia. QRS isopotential maps and QRS isointegral maps derived from body surface isopotential maps have also been correlated with left ventricular pacing sites with the same objective. The comparison process used is subjective and only semiquantitative. Improved accuracy of catheter placement may improve success rates of ablation therapy. This animal study was performed to determine the spatial resolution with which left ventricular pacing sites could be distinguished by body surface isopotential mapping. Potentials were recorded from 64 evenly spaced thoracic leads. Hexapolar or octapolar pacing catheters with 2-mm interelectrode spacing were placed percutaneously in the left ventricle in each of six dogs, and bipolar endocardial pacing was performed using each pair of adjacent electrodes. QRS isopotential maps of each pacing site for each catheter placement were cross-correlated by computer. Difference maps for each pair of pacing sites were calculated lead by lead and time instant by time instant, and root-mean-square voltage differences were calculated. Results indicated that correlation coefficients and root-mean-square error of voltage differences monotonically decrease and increase, respectively, with stimulus site separation. Both measures were significantly different (P < .05) for separations of 4 mm or more. A method of quantitative comparison of body surface potential maps can be used in normal hearts to localize ventricular pacing sites within a 4-mm range. The method may have utility in determining potential ablation sites for therapy of ventricular tachycardia or preexcitation syndromes.

Noninvasive localization of accessory pathways by magnetocardiographic imaging.

The magnetocardiogram (MCG) is a newly developed method that helps localize a cardiac current source. To test the clinical accuracy of a 7-channel biomagnetic system in the localization of early ventricular depolarization sites, the MCGs of 14 patients with Wolff-Parkinson-White (WPW) syndrome were recorded in a radiofrequency-shielded room. The locations of early ventricular depolarization sites were classified by standard 12-lead electrocardiograms (ECGs) and body surface isopotential mapping. The accessory pathways of 3 patients with WPW syndrome were located in the right free wall and in 11 patients in the left free wall. The three-dimensional (3-D) dipole location was computed every 2 ms from the onset of the QRS complex by the least-square method. These 3-D dipole locations were projected onto a gated magnetic resonance image in order to visualize the propagation of the calculated ventricular source. The results were compared with those obtained by body surface isopotential mapping, and electrocardiographic and electrophysiologic studies. The location of the deduced current dipole at 20 ms correlated well with the location of the accessory pathway by the body surface mappings in 12 of the 14 patients with WPW syndrome. The MCG is capable of precisely determining the 3-D location of a current source in a noninvasive manner and may be of potential benefit in the treatment of WPW syndrome by catheter ablation.

Body Surface Signal-Averaged P Maps in Normal Subjects and Patients with Valvular Heart Disease

A signal-averaging technique was applied to 87-lead body surface mapping in 25 normal subjects and 14 patients with valvular heart disease to estimate spatial changes in atrial depolarization. Both in normal and patient groups, the maximum of the P isopotential map was located in the lower sternal region during the early phase of the P wave, then it gradually moved leftward, and finally reached the left lateral side. In 44% (14/25) of normal subjects and in all patients examined, maxima were simultaneously present: around 50 and 90 ms after the onset. These double maxima were considered to indicate the presence of two excitation wavefronts over the atria. The leads with the highest voltage were observed around the left anterior chest in the normal subjects and around the left lateral chest or the back side of the chest in the patients' group. The level of the highest voltage was larger, and the time when the highest voltage was attained was more delayed compared to those with normal subjects. Our results demonstrated that spatial propagation of atrial depolarization derived from the body surface isopotential map is more informative than that of standard 12-lead electrocardiogram or vectorcardiogram and provide insights into the electrophysiological events related to structural alterations in valvular heart disease.

Signal-averaged body surface mapping for the assessment of low-amplitude potentials: Detailed maps during early ventricular activation in normal subjects

Body surface isopotential maps around early ventricular activation were investigated in 30 normal subjects by the use of the authors' signal-averaged body surface mapping system. The number of beats averaged was 96–154 (mean, 127). Two distinct patterns were recognized in the appearance of a maximum at the onset of ventricular activation: the maximum in the first type (n = 16) was located on the right anterior chest; the maximum in the second type (n = 14) was on the central or left anterior chest. The site of the earliest ventricular activation was considered to be different in each of these types. During early ventricular activation, 25 subjects (83%) had two minima: one was on the left lateral chest and the other was on the left back. The two minima probably reflect two different receding activation fronts in the ventricles. The data in the present study are important to the understanding of the early ventricular activation process, as well as the diagnosis of heart diseases in which this process is disturbed.

Body surface isopotential mapping of the entire QRST complex in the Wolff-Parkinson-White syndrome. Correlation with the location of the accessory pathway

Body surface potential maps were recorded during sinus rhythm and during atrial pacing at the time of electrophysiologic studies in 42 patients with Wolff-Parkinson-White syndrome. The locations of the accessory pathways were determined by epicardial mapping during surgery in 34 patients and by multicatheter endocavitary electrophysiologic studies in eight additional patients. During delta wave inscription, the shape and extension of areas of the negative and positive potentials on the thorax correlated better with the preexcitation site (69% of patients) than with the localization of the minimum potential alone (45.2% of patients). Typical potential distributions were present from the beginning of the delta wave and remained stationary during the first half of the QRS complex. During marked preexcitation, the superposition of atrial activity on the delta wave produced a mixed pattern in the earliest maps. However, these alterations of early delta thoracic potential distribution did not persist longer than 30 msec. The spread of the negative potentials during the last half of the QRS complex also characterized each localization: right-sided preexcitation reproduced the depolarization sequence of left bundle branch block, left-sided preexcitation reproduced that of right bundle branch block, and posterior pathways resembled left anterior fascicular block. Anterior left ventricular and more anterior left lateral ventricular preexcitations mimicked a right bundle branch block-left posterior fascicular block pattern. There was good correlation between the body surface potential map obtained during the ST segment and the site of the right-sided preexcitation. However, in left-sided preexcitations, ST patterns concordant with delta wave patterns were found less frequently than in right-sided preexcitations. With multiple pathways there was a lack of agreement between the body surface potential maps obtained during the delta wave and those obtained during the second half of the QRS complex. In conclusion, analysis of body surface potential maps obtained during the entire QRST sequence can furnish additional clues that may be useful in predicting the location of the accessory pathways and the presence of multiple pathways.

Signal-averaged body surface mapping for the assessment of low-amplitude potentials. Relation between ventricular depolarization and repolarization in normal subjects.

To examine the relation between ventricular depolarization and repolarization, body surface isopotential maps at the end of the QRS complex were studied in 32 normal subjects using a signal-averaged body surface mapping system. The number of beats averaged was 96-154 (mean 126.2). In this study, there were 8 types of isopotential map patterns at the end of the QRS complex. Mean +/- SD of QRS duration, appearance time of repolarization, and disappearance time of depolarization were 82.0 +/- 8.7 msec, 71.8 +/- 10.5 msec, and 79.7 +/- 9.4 msec, respectively. Time duration of overlapping depolarization and repolarization was 8.6 +/- 6.4 msec. The early repolarization was widely distributed on the left anterior chest and the upper sternal region. These results demonstrated the difference between the appearance time of repolarization and the disappearance time of depolarization for each lead. We concluded that it is difficult to evaluate ECG waves in the terminal portion of the QRS complex with the dipolar theory only.

Abnormalities of early depolarization in patients with remote anterior myocardial infarction and ventricular septal hypoperfusion: Diagnosis of septal MI by BSM

The authors conducted this study to find the difference in body surface isopotential maps in 46 patients with previous anterior infarction with and without septal involvement. Thallium-201 myocardial-perfusion imaging identified 25 patients with septal infarction (group P) and 21 without (group N). In contrast to group N, group P had a prominent minimum on the anterior chest during the early phases of the QRS. According to the results obtained, the following criteria for identifying patients with septal infarction (group P) were proposed (1). Criterion 1: The absolute value of the voltage of the minimum is equal to or greater than that of the maximum at 5 ms after the onset of the QRS; (2) Criterion 2: During the early portion of the QRS the voltage of the minimum reaches −0.10 mV at the same time or earlier than the maximum reaches 0.10 mV. Both criteria had higher sensitivities (100% and 100%), specificities (71.4% and 90.5%), and predictive accuracies (87.0% and 95.7%) than either Franklead vectorcardiograms or standard 12-lead electrocardiograms in the study population. Thus, body surface isopotential mapping is considered to be useful for the diagnosis of septal involvement in patients with previous anterior myocardial infarction.

Body surface isopotential maps during the first week of life

One hundred body surface isopotential maps for 30 normal infants, ages three hours to seven days, were evaluated. Ventricular activation and recovery were examined. In the early and mid phase of QRS, the maximum moved from the center of the anterior chest to the lower right portion of the anterior chest. In the late phase, the maximum appeared on the back. The niche appeared earlier in normal newborn infants (19.6 +/- 3.9 msec) (mean +/- S.D.) than in normal children (25.7 +/- 4.6 msec) (P less than 0.001). The location of the maximum at the time of peak positive potentials gradually shifted leftward during the first week of life. The 100 T wave maps were classified into three types. During the first day of life, the T wave maps showed type I or II, changing to type II or III a few days after birth. All T wave maps were type III a week after birth. The ratio of type III gradually increased with age. We found that the QRS maps were different from those of normal children and that T wave maps changed within the first week of birth.

Detection of experimental right ventricular infarction by isopotential body surface mapping during sinus rhythm and during ectopic ventricular pacing

Electrocardiographic (ECG) effects of experimental, isolated right ventricular infarction were studied in 10 dogs during sinus rhythm as well as during ectopic right and left ventricular pacing. Infarction was produced by injecting latex into the right coronary artery and ECG consequences were examined by body surface isopotential mapping methods using an 84 electrode torso array. During sinus rhythm, subtraction of preinfarction from postinfarction maps demonstrated that right ventricular necrosis produced abnormal negative potentials over the right hemithorax during the early, middle and late portions of the QRS complex. These patterns corresponded to loss of R waves and deepening of preexistent or development of new Q and S waves in waveforms from this region. Patterns during ectopic ventricular stimulation were compared with mean maps derived from 13 control dogs. Both left and right ventricular pacing after right ventricular infarction resulted in a right-sided abnormal minimum, similar in location to that observed during sinus rhythm, throughout the QRS complex. Thus, right ventricular necrosis does produce QRS complex changes over the right torso that are analogous to those produced by left ventricular infarction, and the dominant pattern of an abnormal right-sided minimum was present regardless of the ventricular activation pattern. This latter finding suggests that the region of right ventricular necrosis provided a supplementary path for current to reenter the heart regardless of the current source, so that an overlying electrode would record negative voltage with all activation patterns.

Myocardial infarction size and location: A comparative study of epicardial isopotential mapping, thallium-201 scintigraphy, electrocardiography and vectorcardiography

Based on epicardial isopotential mapping (the Ep Map), which was calculated from body surface isopotential mapping (the Body Map) with Yamashita's method, using the finite element technique, we predicted the location and size of the abnormal depolarized area (the infarcted area) in 19 clinical cases of anterior and 18 cases of inferoposterior infarction. The prediction was done using Toyama's diagnostic method, previously reported. The accuracy of the prediction by the Ep Map was assessed by comparing it with findings from thallium-201 scintigraphy (SCG), electrocardiography (ECG) and vectorcardiography (VCG). In all cases of anterior infarction, the location of the abnormal depolarized areas determined on the Ep Map, which was localized at the anterior wall along the anterior intraventricular septum, agreed with the location of the abnormal findings obtained by SCG, ECG and VCG. For all inferoposterior infarction cases, the abnormal depolarized areas were localized at the posterior wall and the location also coincided with that of the abnormal findings obtained by SCG, ECG and VCG. Furthermore, we ranked and ordered the size of the abnormal depolarized areas, which were predicted by the Ep Map for both anterior and inferoposterior infarction cases. In the cases of anterior infarction, the order of the size of the abnormal depolarized area by the Ep Map was correlated to the size of the abnormal findings by SCG, as well as to the results from Selvester's QRS scoring system in ECG and to the angle of the maximum QRS vector in the horizontal plane in VCG.(ABSTRACT TRUNCATED AT 250 WORDS)

肥満者の体表面心臓電位図

肥満者の体表面心臓電位図

Regional blood flow correlates of ST segment depression in tachycardia-induced myocardial ischemia.

Tachycardia produces subendocardial ischemia and ST segment abnormalities after coronary obstruction. To determine whether a quantitative relationship exists between these ST shifts and transmural blood flow, 19 dogs were studied. Coronary obstruction was produced by ameroid constriction of the left circumflex artery, and tachycardia was generated by atrial pacing at 90 to 210 beats/min. ST shifts were studied by body surface isopotential mapping with an 84-electrode torso grid, and blood flow was quantitated by serial radiolabeled microsphere injections. Isopotential maps at each paced rate, 40 msec into the ST segment, were classified as normal or ischemic based on spatial patterns of voltages. Pacing after 3 weeks of ameroid constriction reduced endocardial/epicardial flow ratios in 11 dogs from 1.16 +/- 0.22 at rest to 0.41 +/- 0.18 at 210 beats/min. Abnormal ST depression developed in these dogs at a rate of 184.0 +/- 16.5 beats/min. Endocardial/epicardial ratios with ST depression (0.45 +/- 0.15) were lower than at those without ST depression (1.05 +/- 0.19; p less than .01). Logistic regression analysis demonstrated that ST depression corresponded to an endocardial/epicardial ratio of 0.67 or less (p less than .01). With this model, 95.5% of data sets were correctly classified. Neither heart rate nor perfusion bed size were significant independent predictors of an ischemic electrocardiographic response. The magnitude of abnormal ST segment shift was significantly correlated (r = .87) with the transmural flow ratio. Thus development of electrocardiographic changes indicative of ischemia corresponds to a predictable degree of flow redistribution and the magnitude of the ST shift is correlated with the intensity of the flow abnormality.

健常成人の体表面心臓電位分布図-QRS波について-

健常成人の体表面心臓電位分布図-QRS波について-

心房中隔欠損症(二次孔開存)の体表面電位図

心房中隔欠損症(二次孔開存)の体表面電位図

健常高齢者の体表面電位図の検討 QRS・T波について

健常高齢者の体表面電位図の検討 QRS・T波について

体表面電位図による左室肥大判定に関する研究

The purpose of this study was to compare body surface isopotential maps with echocardiographically-obtained IVST, PWT, LVDd and LV mass in 45 cases of hypertention (HT), 25 of aortic regurgitation (AR), 20 of hypertrophic cardiomyopathy (HCM) and 45 normal subjects. In most cases, Rmax (the highest point of maximum) was located at V4 and V5, though occasionally above, below or left of V4 and V5. Smax (the highest point of minimum) was located below V2 and V3. The Rmax voltage and Smax voltage were significantly greater in the three disease groups. The Rmax voltage correlated roughly to the LVmass (r=0.55), as did the Smax voltage (r=0.67). Though there was no correlation between IVST and the time reflecting septal activation (time for Rmax to move to the left midclavicular line) in maps, the time in HCM was much longer compared to that in HT. Furthermore, the maximum voltage of the R wave in the left back leads (left scapular line) correlated to PWT (r=0.69, p<0.01).These results indicate the usefulness of bedy surface isopotential maps for presuming underlying disorders of LVH and for estimating the left ventricular posterior wall thickness.

心筋梗塞の体表面心臓電位図に関する研究 -QRS departure mapと左室,冠動脈造影所見との対比-

心筋梗塞の体表面心臓電位図に関する研究 -QRS departure mapと左室,冠動脈造影所見との対比-

Effects of experimental myocardial infarction on the ST segment response to tachycardia

Prior studies have shown that tachycardia results in ST segment depression in dogs with chronic, gradual coronary occlusion. This response was compared with that produced by acute, total occlusion of the left anterior descending artery. Ten dogs served as controls; in another 10 dogs, an ameroid constrictor was implanted about the left anterior descending artery. This artery was acutely ligated in a third set of 10 animals, and in a final set of 10, the distal left anterior descending coronary vasculature was embolized by latex injection. Tachycardia was produced by atrial pacing from rates of 90 to 250 beats/min using implanted atrial electrodes. Electrocardiographic signals registered from 84 torso electrodes were used to construct body surface isopotential maps during the ST segment. In normal dogs, pacing increased repolarization potentials without shifts in spatial features. New and abnormal anterior negativity, correlating with significant ST depression, appeared at rates of 170 beats/min or faster in dogs with ameroid constriction. However, in both groups with acute occlusion that produced transmural myocardial infarction, tachycardia resulted in increases in anterior ST elevation and reciprocal ST depression. Specific findings demonstrated the lead dependency of the response to tachycardia and the greater than normal increase in potential magnitudes after infarction than in control cases. The similarity of the response with acute occlusion and with embolization suggested that the response to tachycardia after infarction was not dependent on coronary collateral function but may represent a direct electrophysiologic effect of rate. Thus, these acute occlusion models simulate exercise-induced ST segment elevation as it may be seen clinically.

Electrocardiographic correlates of myocardial ischaemia induced by atrial and ventricular pacing in dogs with coronary stenosis.

We determined the electrocardiographic response to pacing-induced tachycardia in 45 dogs. Pacing was performed using left atrial, left atrial-right ventricular sequential or left atrial-left ventricular sequential modes at rates of 90 to 250 beats X min-1. Body surface isopotential maps in 15 dogs with normal coronary circulations defined the normal response to rate; surface potential extrema during the S-T segment increased in strength with increasing rate but spatial features remained constant. In the other 30 dogs, an ameroid constrictor was placed around the left circumflex coronary artery. Two weeks after implantation, atrial pacing to rates of 190 beats X min-1 or greater resulted in flat, S-T segment depression, with new and abnormal negative voltages registered over the inferior and left posterior torso. However, with either form of ventricular pacing, tachycardia with coronary obstruction did not alter the S-T segment response seen in control animals, in either intensity or spatial parameters. We interpret these findings to suggest that: in normal dogs, tachycardia produced a common electrocardiographic effect regardless of activation pattern; and tachycardia in the presence of coronary constriction results in subendocardial myocardial ischaemia that, with atrial pacing, reverses the normal transmural S-T segment potential gradient and causes body surface S-T segment depression, but with primary ventricular stimulation, the subendocardial ischaemia does not alter the transventricular repolarisation gradients sufficiently to generate body surface S-T segment shifts.