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Biomedical subjects

D M Mirvis

Publications and source records attributed to D M Mirvis.

At least 109 records · Page 6Linked to original sources
PubMed1985

Spatial variation of QT intervals in normal persons and patients with acute myocardial infarction.

The QT interval is a clinically important electrocardiographic measurement. This study attempted to determine 1) whether this interval was spatially distributed in a physiologically meaningful way on the torso of normal subjects, and 2) if these spatial patterns were altered in patients with acute myocardial infarction. To do so, 30 patients were studied within 72 hours of the onset of acute myocardial infarction (15 with an anterior and 15 with a posterior lesion) along with 50 normal control subjects. Electrocardiographic signals were registered from 150 torso electrodes; the QT interval in each lead was determined by a combined automated-manual method, and the durations displayed as "isointerval maps." In the normal subjects, the difference between the longest and shortest interval in each case was 59.4 +/- 12.9 ms. Long QT intervals were spatially located over the left lateral torso and short QT intervals were found over the right inferior chest. Acute infarction modified this distribution in relation to lesion location; the longest QT intervals were centrally positioned in anterior infarction and caudally located in inferior infarction. Thus, QT intervals in normal and abnormal states have distinctive spatial distributions that are consistent with known regional myocardial electrophysiology.

Adult↗
PubMed1985

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.

Action Potentials↗
PubMed1985

Electrocardiographic effects of experimental nontransmural myocardial infarction.

Clinical and experimental data have documented the ability of nontransmural myocardial infarction to produce abnormal Q waves on both the epicardial and body surfaces. We undertook this study to define the anatomic determinants of such Q wave development. Thirty dogs were studied before and after occlusion-reperfusion (26 dogs) or latex embolization (four dogs) of the left circumflex coronary artery. Occlusion was maintained for 60 to 240 min before reperfusion to produce nontransmural lesions of various sizes. Electrocardiographic data were registered from 84 torso electrodes by body surface mapping techniques before and 1 week after infarction. Infarct size was quantitated by computer analysis of heart slices stained with triphenyl tetrazolium chloride. Six dogs did not develop infarction. Of the remaining 24, 10 did and 14 did not develop significant changes in body surface Q wave duration and width. The incidence of Q wave changes was not different in dogs with nontransmural and those with transmural lesions. Infarct size (expressed as a percentage of the left ventricle infarcted), the percentage of endocardium subjacent to infarction, the average depth of necrosis, the percent of the four outer fifths of the ventricular wall infarcted, and the duration of occlusion were significantly (p less than .05) greater in dogs with than in those without Q wave changes. Logistic regression modeling demonstrated that only two anatomic parameters--percentage of left ventricle infarcted and average lesion depth--significantly and independently predicted Q wave development. A model including only these two variables accurately classified all 24 cases.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Reversible, highly localized alterations in fatty acid metabolism in the chronically ischemic canine myocardium.

Acute myocardial ischemia is accompanied by a marked decrease in the oxidation of fatty acids. Whether similar changes occur during chronic ischemia was studied in 13 beagles. In 10 dogs, an ameroid constrictor was implanted about the left circumflex artery; 3 others served as sham-operated controls. Mitochondrial and peroxisomal fatty acid oxidation of (1-14C)oleate were measured and compared in affected (posterobasal left ventricular endocardial [posterior LV endo]) and unaffected (anteroapical LV epicardial [anterior LV epi]) tissues of control and experimental dogs. Five experimental and 3 control dogs were killed after 3 weeks. The posterior LV endo sections of experimental dogs at 3 weeks showed increased fatty acid oxidation due to peroxisomal (KCN-insensitive) beta oxidation (p less than 0.01). The anterior LV epi sections showed no difference in fatty acid oxidation between sham-operated and experimental dogs. Five dogs were studied after 3 months; fatty acid oxidation of the posterior LV endo section was normal. Thus, under a slowly evolving state of myocardial ischemia, highly localized and reversible adaptive changes in fatty acid oxidation occur that enable the affected tissue to cope with a fatty acid load. When collateralization is accomplished, fatty acid metabolism reverts to normal.

Acyl Coenzyme A↗
PubMed1984

Electrocardiographic effects of myocardial ischemia induced by atrial pacing in dogs with coronary stenosis. II. Comparison of S-T segment and QRS changes in dogs with left circumflex arterial narrowing.

The effects of tachycardia on the QRS complex in the absence and in the presence of coronary arterial constriction are of possible clinical significance. To study the spatial and temporal distributions of these effects, a canine model simulating progressive coronary occlusion was studied. Tachycardia was induced by atrial pacing, coronary narrowing was produced by implantation of an ameroid constrictor about the left circumflex coronary artery and electrocardiographic effects were studied by isopotential mapping techniques at rates of up to 250 beats per minute, one to three weeks after constrictor implant. In five dogs. pacing without coronary constriction demonstrated the spatial and temporal dependence of QRS changes; tachycardia-induced changes varied from one torso site to another at any instant, and from one moment to another at any one torso location. Patterns in ten dogs with constrictors were dependent upon time after ameroid placement. Resting QRS and S-T segment distributions remained unchanged. One week after surgery, QRS and S-T segment patterns during pacing were as in controls. Two weeks after surgery, QRS patterns were as in controls but flat S-T segment depression resulted at high rates. After three weeks, QRS patterns during pacing were abnormal and S-T segment depression was observed. At each of the later times, the QRS response was similar at rates which did and which did not cause S-T depression. Thus, the effects of tachycardia on excitation and recovery forces in the presence of restricted coronary flow are independent of one another. This suggests that the two responses to ischemia may be due to different basic mechanisms and, hence, that their detection may reflect different myocardial abnormalities.

Animals↗
PubMed1984

Natural history of chronic mitral insufficiency: relation of peak systolic pressure/end-systolic volume ratio to morbidity and mortality.

The ratio of peak systolic pressure to end-systolic volume (PSP/ESV) is a measure of contractility that is relatively independent of loading conditions. To define the relation of this index to the natural history of chronic mitral insufficiency, follow-up studies were performed in 76 patients. All had isolated mitral insufficiency and were followed up for an average of 48 months. None underwent surgery. Cardiac volumes, ejection fraction and PSP/ESV ratio were calculated and Cox multiple regression analyses were performed to determine the relation of functional status, ejection fraction and PSP/ESV ratio to morbidity and mortality. Twenty-three patients died during follow-up; in 70% of those who died, the PSP/ESV ratio was reduced below the 20th percentile. However, as an independent predictor of mortality, this ratio was less sensitive (p greater than 0.05) than ejection fraction (p less than 0.01). Similarly, functional status change was predicted more accurately by ejection fraction (p less than 0.01) than by the PSP/ESV ratio (p greater than 0.05). Thus, although a decreased PSP/ESV ratio was associated with a higher mortality rate, other clinical and laboratory variables were superior to this index for determining morbidity and mortality in patients with isolated mitral insufficiency.

Adult↗
PubMed1983

Effects of thoracotomy on volume conductor properties of the canine torso.

The effects of left thoracotomy on the volume conductor properties of the canine torso were studied in ten dogs. Body surface isopotential distributions were examined before and serially (3, 7 and 14-15 days) after limited thoracotomy and pericardiotomy. Changes in QRS potentials were considered to reflect surgically-induced alterations in volume conductor properties. Results demonstrated that thoracotomy caused a generalized reduction in body surface potentials, quantitated as root-mean-square errors that were greatest soon after surgery and reached low levels (less than 200 uV) two weeks postoperatively. Although voltages were reduced, overall isopotential distributions remained similiar in form, with statistically significant correlation coefficients (greater than 0.7) three days after surgery; these values increased to high (greater than 0.85), stable levels by one week. These findings help define the nature and time course of ECG changes that may be attributed to thoracotomy without direct cardiac intervention.

Animals↗
PubMed1983

The electrogenesis of terminal QRS notches in normal subjects.

This study was undertaken to explore the mechanisms responsible for the low amplitude, low frequency notches commonly recorded at the end of the QRS complex. Such waves were registered in tracings from twenty-three of fifty normal volunteers evaluated. In fourteen cases, notches were localized to the lateral precordial leads (V3-6), in six they were limited to right precordial leads (V1-2) and in three, notches were found in both right and lateral lead records. Isopotential maps were constructed from potentials registered from one-hundred-fifty torso electrodes. Results demonstrated that: 1) notches in lateral precordial leads (V3-V6) were due to either movement of or changes in potential of early ventricular repolarization effects; and 2) notches in right precordial leads (V1-V2) were caused by migration of terminal ventricular activation currents. These findings document the necessity for study of factors that determine the spatial as well as the temporal and magnitude parameters of electrocardiographic waveforms.

Adult↗
PubMed1983

Electrocardiographic effects of myocardial ischemia induced by atrial pacing in dogs with coronary stenosis. I. Repolarization changes with progressive left circumflex coronary. artery narrowing.

The electrocardiographic effects of tachycardia in normal dogs and in dogs with progressive coronary stenosis were studied. In five animals, left atrial electrodes were surgically implanted and body surface isopotential patterns were recorded from 84 torso electrodes; pacing at rates of up to 250 beats/min increased recorded voltages registered during the ST segment but did not alter the spatial distribution of these potentials. In 10 dogs, an ameroid constrictor was also implanted about the left circumflex coronary artery. One week after surgery, pacing to rates of 250 beats/min had no effect on ST segment isopotential patterns. However, 2 and 3 weeks postoperatively, when significant coronary constriction was anticipated, pacing-induced ST segment depression was recorded along the inferior anterior and posterior chest surfaces. Abnormal negative voltages were more intense at 3 than at 2 weeks, but the distribution of these abnormalities was unchanged. This pattern was consistent with the location of ischemic myocardium. Calculation of early (10 to 40 ms) ST segment slopes demonstrated that downsloping forms were recorded over most of the area with abnormal ST segment voltages, but that horizontal or upsloping depression occurred at the margins of the abnormal zones. The findings suggest that this canine model may be a useful analog to clinical exercise stress testing to aid in evaluating the significance of clinical electrocardiographic patterns.

Action Potentials↗
PubMed1983

Differential electrocardiographic effects of myocardial ischemia induced by atrial pacing in dogs with various locations of coronary stenosis.

The spatial distribution of abnormal repolarization potentials caused by regional myocardial ischemia was determined in 45 dogs. Ameroid constrictors were placed around the left circumflex artery in 10, the left anterior descending artery in 10, and the right coronary artery in 10. Ten dogs without constrictors served as controls. Electrocardiographic events were determined from body surface isopotential distributions, which were computed from potentials sensed by 84 torso electrodes. In control dogs, pacing to heart rates of 230 to 250 beats/min increased the intensity of positive and negative surface extrema during the ST segment without altering their spatial features. Two weeks after placement of the ameroid constrictors, tachycardia induced abnormal negative potentials during the ST segment. Localization of these ischemic forces varied with the placement of the constrictor in a manner consistent with the affected perfusion territories. However, much of the torso surface was involved by all lesions, and only small zones of ST segment depression unique to specific lesions could be identified. In five additional dogs a constrictor was placed on the right coronary artery 3 months after implantation of a device on the circumflex vessel. ST segment patterns during pacing in dogs with two lesions were consistent with the sum of the two individual lesions. Thus, the regional nature of myocardial ischemia is detectable in the body surface isopotential distributions, but the degree of spatial overlap may limit the value of such techniques in extending the usefulness of clinical exercise-stress electrocardiography.

Action Potentials↗
PubMed1982

Evaluation of normal variations in S-T segment patterns by body surface isopotential mapping: S-T segment elevation in absence of heart disease.

S-T segment elevation is commonly observed in the electrocardiogram of normal persons. To study the possible origins of such patterns, 45 normal volunteers were examined. Electrocardiographic potentials were registered from 150 torso electrodes and processed to construct isopotential maps at 2 ms intervals throughout the QRS-T interval. The maximal potentials recorded from any of the 150 electrodes were 198 +/- 76.4 and 272.1 +/- 84.2 microV at instants 40 and 80 ms into the S-T segment, respectively. Maximal voltages recorded by the six standard precordial V leads at these respective time points were 109.7 +/- 57.0 and 163.6 +/- 66.9 microV. Torso maximal potentials were significantly stronger than were those sensed by V leads; the two were significantly correlated but predictability was limited. The duration of overlap between the onset of ventricular recovery and the end of the excitation was determined from isopotential maps and ranged rom 4 to 16 ms. There was no significant correlation (p greater than 0.05) between these values and either torso or V lead potentials at either 40 or 80 ms into S-T segment. These data suggest that (1) standard precordial leads do not accurately predict maximal torso potentials during the S-T segment, and (2) the degree of overlap between repolarization and depolarization is not a major determinant of precordial voltage. Hence, the rationale for use of the term "early repolarization" to describe this clinical condition is not substantiated.

Adolescent↗