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Biomedical subjects

M J Burgess

Publications and source records attributed to M J Burgess.

At least 19 recordsLinked to original sources
PubMed1991

Effects of sudden changes in cycle length and pacing site on canine cardiac surface QRST isoarea maps.

The effects of changes in paced cycle length alone and changes in both paced cycle length and site of pacing on canine cardiac surface QRST isoarea maps were studied. The correlations between QRST isoarea maps acquired during right ventricular pacing at 900 ms and 700 ms averaged 0.97. The correlations between maps acquired during RV pacing at 900 ms and 500 ms averaged 0.94. The root mean square value of QRST areas progressively decreased as cycle length was decreased from 900 ms to 700 ms and then to 500 ms. This suggests that the pattern of distribution of repolarization properties remained the same and the magnitude of difference in repolarization properties decreased as cycle length was decreased. The correlation coefficients of QRST isoarea maps acquired during RV pacing at 900 ms and those acquired during left ventricular pacing at 700 ms and 500 ms averaged 0.74 +/- 0.01 and 0.68 +/- 0.03, respectively. These correlations were lower than those associated with a change in pacing cycle length alone. Root mean square differences in QRST areas recorded during changes in both pacing site and pacing cycle length were greater than the differences associated with change in cycle length alone. This suggests that changes in activation sequence altered repolarization properties more than they were altered by changes in cycle length alone. QRST isoarea maps have been proposed for assessing arrhythmia vulnerability. The results of this study provide a framework for interpreting QRST isoarea maps acquired during supraventricular tachycardias, premature ventricular complexes, and sustained ventricular tachycardias.

Animals↗
PubMed1991

Modulation of collision-induced changes in canine heart repolarization by cycle length.

The possibility that cycle length modulates the electronic effect of activation sequence on repolarization was investigated in experiments using isolated canine cardiac Purkinje strands, in situ canine ventricular myocardium, and computer simulations. Action potential durations and refractory periods during one-way propagation were compared to those obtained during action potential collision. In both the computer simulations and the Purkinje strand experiments, collision decreased action potential duration more at long cycle lengths than at short cycle lengths. Comparably, collision of activation fronts in ventricular myocardium was associated with greater reductions in refractory period during pacing at long cycle lengths than at short cycle lengths. Theoretic considerations indicate that the magnitude of electrotonic effects of activation sequence on repolarization are directly related to action potential height and the square root of membrane resistance during repolarization and are inversely related to conduction velocity. In computer simulations and Purkinje strand experiments, changes in conduction velocity and action potential height elicited by decreasing cycle length could not fully account for the cycle length dependence of collision-induced changes in repolarization. Time-varying membrane resistance of a single cell was calculated in the simulations by briefly hyperpolarizing the membrane and determining the change in total ionic current. Membrane resistance during repolarization was less at short cycle lengths than at long cycle lengths. The results suggest the cycle length dependence of collision-induced changes in repolarization results largely from the effect of cycle length on membrane resistance during action potential repolarization, with changes in action potential height and conduction velocity playing a lesser role.

Action Potentials↗
PubMed1990

Determination of transmural location of onset of activation from cardiac surface electrograms.

Methods of estimating depth of origin of ventricular activation from cardiac surface electrograms were evaluated in experiments on eight dogs. The ventricles were paced via multielectrode needle arrays placed transmurally in from four to six locations in the wall of the left ventricle. A multiplexed data-recording system was used to simultaneously record from 64 unipolar cardiac surface electrodes during pacing at each multielectrode needle site. The four indexes evaluated were the maximum and average gradients of activation isochrones around the site of earliest epicardial activation, the QRS area at the site of earliest epicardial activation, the interval between the QRS onset computed from all 64 epicardial surface electrograms, and the time of the minimum dV/dt in the electrogram displaying the earliest epicardial activation time (t(ee)-t(rmso) interval). Correlation coefficients between depth of stimulation and average and maximum gradients of isochrones, QRS area at the site of earliest epicardial activation, and t(ee)-t(rmso) interval were 0.985 or higher. These methods, particularly those involving gradients of isochrones, should be useful for evaluating electromaps of patients undergoing surgery for ablation of tachyarrhythmias.

Analysis of Variance↗
PubMed1988

Activation sequence at the onset of arrhythmias induced by localized myocardial warming and programmed premature stimulation in dogs.

The effect of localized shortening of ventricular repolarization on arrhythmia vulnerability was studied in 10 pentobarbital anesthetized dogs. An area of the anterior right ventricle was warmed by directing a light beam through a condenser lens assembly and a rectangular aperture. Arrhythmia vulnerability was assessed with low-amplitude programmed stimulation. Activation sequence maps were constructed from electrograms recorded simultaneously from 40 epicardial sites and 24 endocardial sites in and surrounding the warmed area. Recordings were taken during regular atrial and ventricular drives and during programmed stimulation in control periods and during myocardial warming. Spontaneous activity could not be induced with low-amplitude programmed stimulation during control periods in any dog. During myocardial warming arrhythmias were induced in every dog. Most induced arrhythmias had features consistent with local reentry. However, activation sequence at the onset of some arrhythmias strongly resembled that of superventricular activation and was consistent with reentry involving the His-Purkinje system. The findings provide evidence that a localized area with short ventricular repolarization is an abnormality sufficient to increase arrhythmia vulnerability and also that even in this relatively simple setting there can be multiple mechanisms for arrhythmias.

Animals↗
PubMed1988

Effects of coronary occlusion on cardiac and body surface PQRST isoarea maps of dogs with abnormal activation simulating left bundle branch block.

The possibility of detecting myocardial infarction in the presence of left bundle branch block by analysis of cardiac and body surface PQRST isoarea maps was studied in nine open-chest and six closed-chest dogs. Recordings were taken during supraventricular drive or right atrial plus right ventricular pacing in control periods and at intervals for up to 10 hr after left anterior descending coronary artery occlusion. Right ventricular pacing was used to simulate left bundle branch block. Myocardial infarction was documented with triphenyl tetrazolium staining. The PQRST areas during supraventricular drive and right atrial plus right ventricular pacing were highly correlated to each other both before and after coronary occlusion. The PQRST isoarea maps after coronary occlusion showed a strong pole overlying the ischemic area on the cardiac surface in open-chest animals and over the left anterior thorax in closed-chest animals. The PQRST pole was positive during the first 1 to 2 hr of occlusion and became negative after several hours. The findings demonstrate that localized abnormalities due to ischemia and infarction are manifest in body and cardiac surface PQRST isoarea maps of both supraventricular complexes and right ventricular paced complexes. The findings suggest that PQRST isoarea maps may aid in identification and localization of ischemic or infarcted myocardium in the setting of abnormal activation such as left bundle branch block.

Animals↗
PubMed1988

Relation of cardiac surface QRST distributions to ventricular fibrillation threshold in dogs.

The relation between ventricular fibrillation threshold (VFT) and cardiac surface QRST area distributions was studied in eight pentobarbital-anesthetized dogs. Unipolar epicardial electrograms were recorded from 64 sites evenly distributed on the right and left ventricles. Localized areas of short repolarization properties were produced by directing five intensities of light onto the surface of the anterior right ventricle through apertures of three sizes. VFT, measured at the center of the lesion, decreased during warming and had a high negative correlation to the change (warming-control) in QRST area (delta QRST1) in the electrogram recorded from the center of the lesion. This correlation was independent of lesion size. For the six experiments, the correlation coefficients for 400-, 800-, and 1,600-mm2 lesions averaged -0.95, -0.94, and -0.96, respectively. The correlation between VFT and delta QRST1 without regard to lesion size averaged -0.88. VFT also had a negative correlation to root mean square (RMS)delta QRST because of warming. RMS delta QRST was calculated from the change in QRST areas (warming-control) in all 64 electrograms. The correlation between VFT and RMS delta QRST was dependent on lesion size. For all experiments, the correlation between VFT and RMS delta QRST averaged -0.97, -0.93, and -0.93 for 400-, 800-, and 1,600-mm2 lesions, respectively. The correlation between VFT and RMS delta QRST without regard to lesion size, however, was considerably lower, -0.59. The results of this study provide the first direct evidence that VFT is correlated with cardiac surface QRST area distributions.

Animals↗
PubMed1988

Nonuniform epicardial activation and repolarization properties of in vivo canine pulmonary conus.

The relation between nonuniform epicardial activation and ventricular repolarization properties was studied in 14 pentobarbital anesthetized dogs and with a computer model. In 11 dogs, isochrone maps of epicardial activation sequence were constructed from electrograms recorded from the pulmonary conus with 64 electrodes on an 8 X 8 grid with 2-mm electrode separation. The heart was paced from multiple sites on the periphery of the array. Uniformity of epicardial activation was estimated from activation times at test sites and their eight neighboring sites. Acceleration shortened and deceleration prolonged refractory periods. The locations of acceleration and deceleration sites of activation differed during drives from various sites, and differences in uniformity of activation during pairs of drives were correlated to differences in refractory periods (r = 0.76, range 0.59-0.93). In three additional experiments, transmural activation sequence maps were constructed from electrograms recorded from needle-mounted electrodes placed upstream and downstream to epicardial activation delays. Activation proceeded from epicardium to endocardium upstream to the delays and from endocardium to epicardium downstream to the delays. A computer simulation of two-dimensional action potential propagation based on the Beeler-Reuter myocardial membrane model provided insights to the mechanism for the results of the animal experiments. The two-dimensional sheet modeled the transmural anisotropic histology of the canine pulmonary conus and corresponded to previous reports and histology of specimens from five experiments. Simulated activation patterns were similar to those found in the experimental animals. In addition, action potentials were electronically prolonged at sites of deceleration and shortened at sites of acceleration, results comparable to the animal experiments. Our findings demonstrate that the location of areas of nonuniform epicardial activation is dependent on drive site and that nonuniform activation electronically modulates repolarization properties. Therefore it seems likely that the site of origin of ectopic ventricular complexes, especially in ischemic myocardium where activation is nonuniform, could be an important determinant of whether ectopic activity initiates sustained tachyarrhythmias.

Action Potentials↗
PubMed1987

Effects of cardiac sympathetic nerve stimulation on regional coronary blood flow.

The purpose of this study was to examine the effects of cardiac sympathetic nerve stimulation on regional coronary blood flow following beta-blockade. In 17 anesthetized dogs treated with propranolol (2 mg/kg iv) regional myocardial perfusion was measured (microspheres) during control and during stimulation of the ventrolateral, ventromedial, or recurrent cardiac nerve (8-10 V, 4-ms pulses at 10 Hz for 30 s). Ventrolateral nerve stimulation produced 25.5 +/- 3.4 and 23.5 +/- 3.1% (mean +/- SE) decreases in coronary blood flow in the posterior and lateral quadrants of the left ventricle. These changes were significantly greater than the 8.5 +/- 2.9, 11.5 +/- 3.0, and 3.7 +/- 2.8% decreases in the anterior and septal left ventricle and right ventricle, respectively (P less than 0.01). Ventromedial nerve stimulation produced 18.6 +/- 2.8, 15.4 +/- 2.8, and 10.1 +/- 3.2% decreases in flow in the anterior, septal, and lateral left ventricle, respectively. These changes were significantly greater than the 5.3 +/- 3.8 and 9.9 +/- 3.6% decrease in the posterior left ventricle and right ventricle (P less than 0.01). Recurrent cardiac nerve stimulation produced 16.4 +/- 2.1, 15.6 +/- 2.2, and 13.6 +/- 2.5% decreases in flow in the anterior and septal left ventricle and right ventricle, respectively. These changes were significantly greater than the 5.2 +/- 3.2 and 5.4 +/- 3.0% changes in the posterior and lateral quadrants (P less than 0.01). Ventrolateral nerve stimulation resulted in a small but significant increase in the endocardial-to-epicardial blood flow ratio in the posterolateral left ventricle.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1986

Determination of activation and recovery sequences and local repolarization durations from distant electrocardiographic leads.

Experiments using an isolated heart, perfused by a support dog were done to compare estimates of activation times, recovery times and activation recovery intervals from cardiac surface electrograms to estimates from distant electrocardiographic leads and to known features concerning normal activation and recovery sequences. The isolated heart was suspended in a tank with 600 electrodes located at sites 0.5 cm to 7.5 cm from the surface of the heart. In some experiments up to 330 electrodes, spaced 2.5 mm to 5 mm apart on a nylon matrix, were placed on the cardiac surface. Recordings were made during atrial and ventricular drives at cycle lengths of 400 msec to 700 msec. The minimum QRS and maximum T derivatives and the interval between them were taken as the estimates of activation times, recovery times and activation recovery intervals respectively. Maps of activation sequence, and the distribution of activation recovery intervals were constructed from cardiac surface data and from data recorded at various distances from the heart. Regions of earliest and latest activation and recovery times, range between the earliest and latest activation and recovery times and the average activation recovery interval could be determined from data recorded at distances from the heart comparable to the distance between the cardiac and thoracic surfaces. The results indicate that electrocardiographic signals, recorded with regionally sensitive distant leads, contain considerable detail concerning local activation and recovery sequences and the distribution of repolarization properties. This information should be useful in the evaluation of patients and in guiding drug therapy.

Action Potentials↗
PubMed1985

Effects of activation sequence on ventricular refractory periods of ischemic canine myocardium.

Refractory periods were measured in pentobarbital-anesthetized dogs during control periods and one to one and a half hours after distal left anterior descending coronary artery occlusion. The refractory period test site was on the anterior surface of the left ventricle in the distribution of the artery to be occluded. Measurements were made during drive of the refractory period test site, drive of a distant site on the pulmonary conus and during fusion drive in which drive of the test site was delayed with respect to drive of the pulmonary conus. Refractory periods were longer during test site drive than during pulmonary conus or fusion drives in both the control periods and following coronary occlusion. However, the effects of driving mode on refractory periods were greater following coronary occlusion than in the control periods. The findings are likely secondary to different magnitudes of change in electrotonic interactions associated with changes in activation sequence in ischemic and nonischemic myocardium. The greater dependence of repolarization properties in ischemic than nonischemic tissue suggests that inhomogeneity of these properties could be modified considerably by the site of origin of ectopic ventricular complexes.

Action Potentials↗
PubMed1985

Effects of age, sex, and body habitus on QRS and ST-T potential maps of 1100 normal subjects.

Body surface potential maps provide more detailed regional cardiac electrophysiologic information than the standard electrocardiogram. We performed a large-scale study of a normal population to form a comparison base for evaluation of the clinical utility of this technique. We analyzed body surface maps from 1113 normal subjects from 10 to 80 years old to detail map features as a function of age, sex, and body habitus. Maps were analyzed by visual inspection and by a spatial and temporal data reduction technique that allows statistical comparison of map features. On average, both QRS and ST-T potentials decreased with increasing age. Potential pattern distributions remained constant from 10 to 40 years. Beyond age 40, larger numbers of maps from normal subjects showed depolarization patterns consistent with delayed activation of the left anterior fasicle, despite normal 12-lead electrocardiograms. Only minor QRS potential amplitude and distribution differences were noted when male and female subjects were compared within groups of similar age and body habitus. Male subjects consistently showed greater average T potential amplitudes. Slender body habitus was associated with a more horizontal "zero" potential line. In female subjects over age 40 there were more extensive low-level negative potentials recorded over the precordium during the ST segment than in men. This study defines the range of normal body surface potential maps in a large clinically normal population and provides a basis for qualitative and statistical comparison with map features of patients with disease.

Adolescent↗
PubMed1979

Relation of ventricular repolarization to electrocardiographic T wave-form and arrhythmia vulnerability.

The normal sequence of ventricular recovery proceeds from epicardium to endocardium, but on the epicardium the pattern of ventricular recovery is similar to the pattern of activation. Data concerning ventricular repolarization have been obtained from analyses of electrocardiographic recordings, suction potential recordings, a limited number of recordings of transmembrane action potentials, and from measurements of refractory periods. Normal ventricular repolarization has now been characterized in sufficient detail that it can be used with theoretic models to derive T waves with forms that correspond closely to recorded T waves. These models provide insights concerning the body surface manifestations of the electrophysiologic events of ventricular repolarization and should contribute to a more physiologic approach to interpreting T wave abnormalities in clinical electrocardiograms. A relationship between inhomogeneity of ventricular refractory period duration and arrhythmia vulnerability has also been documented. Because inhomogeneity of ventricular repolarization is a factor in both T wave-form and arrhythmia vulnerability, methods of analysis of the T wave for determining patients at risk of developing arrhythmias should be possible. One such analysis is presented. The method has been tested on experimental animals before and after interventions designed to increase arrhythmia vulnerability and in a limited number of patient studies. The results to date are encouraging and suggest that in the future electrocardiographic examination will be used as a prognostic tool in addition to its already established diagnostic function.

Action Potentials↗
PubMed1979

Clinically practical lead systems for improved electrocardiography: comparison with precordial grids and conventional lead systems.

The use of limited leads for estimating total body surface potential distributions was investigated as a practical solution to the problem associated with extensive electrocardiographic sampling used in surface potential mapping. Two practical, limited lead sets of 32 leads each were derived and contrasted to a set of 30 precordial leads similar to those used in ST-segment and QRS mapping for estimating infarct size, and to a set of nine leads simulating those used in conventional 12-lead examinations. The two arrays, one of which excluded posterior sites for use in recumbent patients, showed little difference in ability to estimate 192 lead measured maps (average rms voltage error of 35 muV and average correlation coefficient of 0.97). The 30- and 9-lead arrays consistently showed twice the voltage (72 muV) and poorer pattern estimation (average correlation coefficient of 0.91) than either of the 32 lead arrays. These findings indicate the need for 20-35 properly located electrodes for accurate total body surface potential estimation. They also show that there is no difference in the abilities of a 30-lead precordial array and conventional leads to estimate maps.

Arrhythmias, Cardiac↗
PubMed1978

Effects of bilateral and unilateral stellate stimulation on canine ventricular refractory periods at sites overlapping innervation.

The efffects of unilateral right, unilateral left, and bilateral stellate stimulation on ventricular refractory periods at sites of overlapping cardiac sympathetic innervation were studied in 11 pentobarbital anesthetized dogs. The stellates were stimulated with 10 Hz pulses 4 msec in duration with intensities strong enough to produce T wave changes in a vertical ECG lead and just below the intensity at which control of drive of the ventricle at a 400-msec cycle length was lost. Refractory periods shortened more with left stellate stimulation, 17.8 +/- 5.9 msec (mean +/- SD) than with right stellate stimulation, 10.3 +/- 5.1 msec, P less than 0.001. During bilateral stimulation, shortening of refractory periods was no greater whether stimulation was applied first to the left and then right stimulation was added, 19.7 +/- 6.9 msec, or the stimulation was applied first to the left and then right stimulation was added, 18.3 +/- 6.5 msec. The shortening of refractory periods with bilateral stellate stimulation was not significantly different from that with left stellate stimulation alone. The results of this study suggest that ventricular recovery properties in areas of overlapping cardiac sympathetic innervation are less influenced by increases in tone of the right sympathetics than by increases in left sympathetic tone. In addition, the findings indicate that a bilateral increase in cardiac sympathetic tone has no greater effect on recovery properties than the effects of the left cardiac sympathetics alone.

Animals↗
PubMed1978

Electrotonic interaction during canine ventricular repolarization.

Canine ventricular refractory periods were measured during test site drive, during drive of single ectopic sites, during fusion drive from two ectopic sites, and during fusion drive from an ectopic site and the test site. Refractory period duration was dependent on the driving modes employed. Refractory periods were 2.63 +/- 0.73%, 3.42 +/- 0.87%, 3.54 +/- 100%, and 4.68 +/- 1.36% (mean +/- SD) shorter during drive of single ectopic sites 2, 4, 6, and 40-60 mm, respectively, from the test site than during test site drive. During fusion drive from two ectopic sites, refractory periods were an average of 2.44 +/- 1.04 msec (mean +/- SD) less than during drive from a single ectopic site (P less than 0.005). When fusion of activation, induced by ectopic and test site drive, was located within 4 mm or less of the test site, refractory periods during fusion drive were also significantly shorter than during test site drive (P less than 0.05). Refractory periods were as much as 10 msec shorter when fusion occurred within 1 mm of the test site than their durations during test site drive. The differences in refractory periods measured during various driving modes were most likely due to electrotonic interactions during ventricular repolarization and are explicable on the basis of the intracellular distribution of potentials to be expected with each driving mode.

Animals↗