Marandapalli R. Sridharan

Electrocardiographic changes in cerebrovascular hemorrhage

The electrocardiographic abnormalities found in localized cerebrovascular hemorrhage which have been documented by computerized tomography (CT) scans are described. Frontal lobe hemorrhages are associated especially with the electrocardiographic abnormalities of QT prolongation and neurogenic T waves. Brain stem hemorrhage seems to be associated with noncardiogenic pulmonary edema, and sudden development of atrial fibrillation. It is proposed that the cause of ECG abnormalities in association with lesions in the vicinity of area 13 on the orbital surface of the frontal lobe, or around the circle of Willis, results from alterations in sympathetic and parasympathetic tone mediated by fibers from the orbito-frontal area to the heart via the stellate ganglia.

Electrocardiographic J wave of hypercalcemia

In 1920, Krausl reported electrocardiographic changes in experimental animals with hypercalcemia; we believe that his Figure 1 showed an ST-junctional deflection resembling the J wave of hypothermia. Except for a 1922 article by the same author, we have found no further reports that suggest J waves in hypercalcemia in either experimental animals or humans.2 The electrocardiographic descriptions of hypocalcemia and hypercalcemia have focused on the slope and duration of the ST segment.3 We have repeated the induction of hypercalcemia in the dog and observed that at serum calcium (Ca) levels of 24.6 mg/dl and higher, the QRS widened, largely because of the appearance of a new deflection where the

The influence of electrode placement in the reconstruction and analysis of body surface potential maps from limited thoracic arrays

Despite their capacity to indicate abnormality outside the scope of routine electrocardiography, body surface maps remain extensive, time-consuming research procedures. By contrast, a 35-electrode grid which sums precordial ST segment deviations has received wide attention as a clinical monitor of acute myocardial infarction. First, this study examined the feasibility of recovering essential data from a small electrode array to construct maps equal to those obtained from a much larger array. Such a small-array technique would offer economy, easy application, plus the comprehensiveness and clinical correlation of the large system. Second, the relationships between map, small-array and a 35-component equivalent multipolar generator were explored for a transformation system which both expands the small-array data to map displays and reduces such data to non-redundant waveforms. Comparisons were made between direct maps and those derived from two 35-electrode sets on normal subjects and patients with myocardial infarction or cardiomyopathy. Electrode placement did not conform to the conventional rectangular grid; for one, the electrodes encircled the thorax symmetrically; in the other they were statistically selected for signal information content. We found 1) symmetrical electrode placement and analytic reconstruction of maps from multipolar lead components consistently reproduced known maps well (.91 correlation, 120 microvolts error); but 2) empirical electrode placement and statistical prediction of known maps averaged .99 correlation and 20 microvolts error for the normal training population and .97 and 60 microvolts for the abnormal test sample. Worsening occurred when placement and prediction methods were mixed; however, maps reconstructed by the empirical-statistical approach reduced to a reasonable approximation of equivalent generator scalar leads.

Analysis of PR subintervals in normal subjects and early studies in patients with abnormalities of the conduction system using surface his bundle recordings

Utilizing several different approaches to noise reduction, satisfactory beat by beat His bundle activity was recorded from the chest surface in 41 (80%) of 52 normal subjects. Surface atrial to His intervals (PAH) and His to ventricular intervals (HV) were measured in this group and compared with subintervals of the PR segment recorded endocardially from 47 persons with normal electrophysiologic findings. A recent modification in the selection algorithm allows on-line identification of the four of five possible recording sites for utilization in a spatial summation. The ability to record in less favorable circumstances has been improved to the extent that records of suitable clarity for measurement were also obtained in 17 (77%) of 22 individuals with conduction system abnormalities. Comparison of the surface and endocardially acquired data in the normal group reveals no statistically significant difference in the surface acquired PAH and endocardially acquired high right atrial to His (HRAH) intervals, nor in the HV intervals. In a small subset of patients data were acquired by both techniques and no significant differences were found. Thus, when programmed stimulation or endocardial mapping is not required to answer specific clinical questions, in the majority of persons it is possible to record meaningful subintervals from the body surface from each cardiac cycle. Additionally, in instances in which surface P wave activity is obscure in the routine electrocardiogram, this technique enhances atrial electrical activity.

Use of body surface maps to identify vessel site of coronary occlusion

Body surface mapping is more sensitive than conventional electrocardiography for various cardiac regions. In this pilot study, the authors used isoarea maps of early (the first 40 msec), late (the next 40 msec), and total (early and late, or 80 msec) QRS complex to determine the site of coronary occlusion in patients with known coronary artery disease. In the absence of conduction abnormalities or axis deviation in the 12-lead electrocardiogram, isoarea body surface map data of single-vessel disease were unremarkable; however, isoarea departure maps (ie, the average isoarea map of normal population extracted from the study group) were characteristic. Early departure isoarea maps were revealing in all three coronary artery disease groups, with a large negative potential noted over the anterior thorax, midline for the right coronary artery, left anterior in the left anterior descending artery, and further laterally for the left circumflex artery groups. The late isoarea departure map was distinct in the left circumflex artery group with positive potentials leftward, anterolaterally. Discriminant function analysis revealed a high predictive accuracy for the left anterior descending artery group. Thus, isoarea departure maps hold promise for predicting the site of coronary occlusion in this training set of patients.

The determination of the human ventricular gradient from body surface potential map data

We have analyzed the Wilson ventricular gradient in terms of body surface potential maps and of the reduction of such surface patterns to equivalent dipoles or vectors. While the ventricular gradient traditionally was treated as first a scalar, then a vector concept, we found that the three entities (QRS area, T area, QRST area) did not reduce to vectors with a common location. However, conventional vector addition (QRST area = QRS area + T area) did precisely apply. Further we found considerable more-than-vector or extra-dipolar information remaining for all three entities after removal of the dipole effect. This suggests that maps of these entities should be considered the boundaries of complex electrical fields rather than simple surface effects of vectors.

The Comparative Predictive Accuracy of Spectral Turbulence Analysis and Time‐Domain Analysis for Sustained Monomorphic Ventricular Tachycardia in Postinfarction Patients with Conduction Defects

Signal‐averaged electrocardiograms obtained in 86 postinfarction patients with right bundle branch block (RBBB), left bundle branch block (LBBB), or intraventricular conduction defect (IVC‐D), underwent time‐domain analysis (TDA) and spectral turbulence analysis (STA) to determine which approach provided the more effective marker for patients with sustained monomorphic ventricular tachycardia. TDA parameters included the root mean square value of the last 40 ms of the vectormagnitude complex and the duration of the low amplitude signal below 40 μV STA utilized a summation lead (X + Y + Z) and quantitated four parameters: interslice correlation mean, interslice correlation standard deviation, low slice correlation ratio, and spectral entropy. High‐pass filters of 40 Hz and 25 Hz were used to study the total patient population with noise levels ≤1 μV and a subset of 67 patients with noise levels ≤ 0.5 μV, The techniques compared their effectiveness as measured by their positive predictive values (PPV), negative predictive values (NPV), sensitivity (Sn), and specificity (Sp). In RBBB, STA was uniformly a more powerful tool utilizing either filter at both noise levels. In LBBB, STA was consistently more powerful at both noise levels at 40 Hz and, generally, more powerful at 25 Hz with isolated exceptions. In conduction defects in which QRS was > 100 ms but < 120 ms, TDA was equal to or more effective than STA, with the exception of PPV and Sp at 40 Hz at 1‐μV noise level and the Sp at 0.5 μV. The addition of ejection fraction data to STA score resulted in further overall improvement in performance, but above conclusions were unchanged.

A basis for determining body surface potential patterns attributable to single-site coronary arterial occlusion**

The authors focus on computational separation of the individual patterns of occlusion of the major segments of the right coronary artery. The raw patterns of occlusion throughout 15 standard subdivisions of the coronary arterial tree and body surface isoarea maps for 8 consecutive 10-msec intervals of QRS were examined in 200 patients with known coronary artery disease. Mean patterns of occlusion and of potential distribution were formed into 15 groups according to which patients showed greater than or equal to 90% occlusion of the respective segments. By diagonalization of the occlusion matrix, individual potential map patterns were obtained to represent the effect of isolated occlusion of each segment. While these patterns appeared consistent with the known anatomy of ventricular myocardial perfusion, further correlative study will be needed. The authors suggest that the use of such prototypical patterns of single-site obstruction may be helpful in forming and assessing recognition patterns in the clinical setting of multiple-site, multiple-vessel disease.

Evaluation of the association of mitral valve prolapse in patients with Wolff-Parkinson-White type ECG and its relationship to the ventricular activation pattern

The association of mitral valve prolapse (MVP) and Wolff-Parkinson-White (WPW) syndrome was examined using simultaneous two-dimensional and M-mode echocardiography. Twelve-lead electrocardiograms (ECGs) and two-dimensional echocardiograms (2DEs) were recorded in 24 patients with WPW. The location of the accessory pathway was predicted from the ECG as being in one of 10 possible sites correlating the delta wave polarity with epicardial mapping. Nineteen of the 24 patients had conduction via the accessory pathway and five were conducting normally during the recording of the echocardiogram. Mitral valve prolapse was found in 13 of 19 patients conducting via the accessory pathway. The only WPW patient with mitral valve prolapse during normal conduction had a chest deformity which has an independent association with mitral prolapse. No association was found between the prediction of the accessory pathway and the presence of mitral prolapse. We concluded that consideration should be given to the possibility that some patients demonstrating MVP do so as the result of the altered sequence of ventricular activation, rather than as the result of a structural abnormality.

Combined effects of graded hyperkalemia on activation and recovery

We have demonstrated the progressive transmission delay in the A-V conduction system in graded hyperkalemia against a background of otherwise normal cations, and known blood gas relationships. This extends and further quantitates the work of others. We were unable to demonstrate sinoventricular conduction, as atrial activity was consistently recordable when surface P-waves disappeared. The His bundle appears to be the least susceptible conduction system structure to hyperkalemia. Finally, we have postulated the possible mechanism for the genesis of the sine wave, including loss of electrical gradient with resulting phase difference of QRS and T, associated with maintenance of His bundle activity with progressive, distal, Purkinje blockade.