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Biomedical subjects

M L Marcus

Publications and source records attributed to M L Marcus.

At least 217 records · Page 12Linked to original sources

Computer simulation of the precordial QRS complex: effects of simulated changes in ventricular wall thickness and volume.

The cardiac electric field generated by depolarization of the human ventricle is simulated with a computer model which utilizes 1,500 dipoles. The configuration of the ventricles utilized in the model assumed that the cross-sectional shape of the left ventricle was circular and the right ventricular free wall was a portion of an ellipse. The torso was assumed to be homogeneous and infinite. The activation sequence was based on the measurements of Durrer. The depolarizational wave was simulated by dipole layers. The output of the model is presented as a standard multilead precordial ECG. The ECG complexes generated by the model closely resemble the precordial QRS complexes of normal man. Simulated increases in wall thickness (1 to 2.2 X control) were associated with changes in the calculated precordial QRS complexes which were characteristic of left ventricular hypertrophy. Voltage (R in V5 or V6 and S in V1) and QRS duration increased linearly as a function of calculated left ventricular mass. Increases in ventricular activation time were related nonlinearly to changes in left ventricular mass and did not occur in the absence of a simulated increase in wall thickness. The effects of simulated changes in left ventricular volume (0.6 to 3.0 X control) on the QRS complex were mainly dependent on the resultant increase in left ventricular mass. This model may be useful in simulating the precordial QRS complexes that result from isolated or combined changes in ventricular volume or wall thickness or other disorders of the heart. Furthermore, it may be useful whenever a simulation of a QRS generator is needed.

Cardiac Volume↗

Effects of time on volume and distribution of coronary collateral flow.

Changes in the volume and distribution of collateral blood flow were studied during the 1st h after coronary occlusion in nine open-chest dogs. Labeled microspheres (7-10 mum) were injected into the left atrium prior to and 20 s, 5 min, and 60 min after acute occlusion of the midcircumflex coronary artery so that myocardial perfusion to small segments of the entire left ventricle could be measured. The segmental perfusions were classified as normally perfused, severely hypoperfused, moderately hypoperfused, and borderline hypoperfused. Standard hemodynamic measurements were obtained and relative coronary vascular resistance to the normally perfused and hypoperfused zones was calculated. The principal conclusions of the study are as follows: 1) during the 1st h after coronary occlusion the collateral flow to the hypoperfused myocardium increases substantially; 2) the increase in collateral flow is distributed fairly evenly to various hypoperfused zones and is associated with a marked decrease in coronary vascular resistance; and 3) as a result of this influx in collateral flow the size of the hypoperfused area decreases and the relative proportion of severely hypoperfused segments within the hypoperfused area decreases.

Animals↗

Total and regional cerebral blood flow measurement with 7-10-, 15-, 25-, and 50-mum microspheres.

Cerebral arteriovenous shunting of 7-10-, 15-, 25-, and 50-mum labeled microspheres was studied in 12 anesthetized dogs. Approximately 8% of the 7-10-mum spheres were shunted to cerebral venous blood, whereas less than 2% of the 15-, 25-, and 50-mum spheres were shunted. Cerebral vascular dilatation induced by hypoxia or hypercapnia did not alter the shunting. The calculated total cerebral flow was 10-15% lower with 7-10-mum microspheres as compared with simultaneous flows measured with the larger microspheres which also suggests that 7-10-mu spheres were shunted through the brain. The calculated distribution of cerebral flow was similar with 7-10- and 15-mum spheres but markedly altered when 50-mum spheres were used. Repeated injections of 15-mum spheres were used. Repeated injections of 15-mum microspheres given under stable conditions yielded total cerebral blood flows which averaged +/- 6% of their respective mean and the regional distribution of flow was highly reproducible. These data suggest that, in dogs, 15-mum spheres are an appropriate size to use to measure cerebral blood flows, since shunting is minimal, the distribution is not artifactually distorted, and the measurements are reproducible.

Animals↗

Effect of intra-aortic balloon counterpulsation on the motion and perfusion of acutely ischemic myocardium. An experimental echocardiographic study.

The effect of intra-aortic balloon counterpulsation (IABC) on the motion and perfusion of ischemic left ventricular posterior myocardium was studied in 30 open-chest dogs, using ultrasound to register motion and 7-10 mu radioactive microspheres to determine perfusion. Circumflex coronary artery ligation produced acute aneurysmal bulging during isovolumetric contraction and diminished ischemic wall velocity during systolic ejection. Myocardial perfusion was determined in five dogs; perfusion of the area supplied by the ligated coronary artery fell from a control value of 72.9 +/- 13.8 (SE) to 30.0 +/- 2.3 cc/100 g/min (P less than 0.05) at 5 minutes after coronary occlusion. IABC was then administered for one hour, with a fall in aortic systolic pressure (112 +/- 6 to 105 +/- 7 mm Hg, P less than 0.05) and rise in peak aortic diastolic pressure (94 +/- 6 to 102 +/- 7 mm Hg, P less than 0.05). Despite this the ischemic area showed no change in perfusion (measured at the same time): 30.0 +/- 2.3 to 28.0 +/- 2.4 cc/100 g/min. Little change in wall motion occurred: aneurysmal bulging decreased modestly (4.5 +/- 0.3 to 3.6 +/- 0.3 mm, P less than 0.05), but ischemic wall velocity did not increase. After cessation of counterpulsation and one hour of coronary reperfusion aneurysmal bulging disappeared and wall velocity improved. The addition of norepinephrine (eight dogs) or nitroprusside (seven dogs) to intraaortic balloon counterpulsation did not cause a significant further improvement in the response of the dyskinesis during the period of ischemia. We conclude that IABC has little effect on ischemic dyskinesis, probably due to its failure to improve perfusion of the acutely ischemic myocardium.

Acute Disease↗

Limitations of thallium-201 myocardial perfusion scintigrams.

The reliability of myocardial perfusion scintigrams with thallium-201 (201Tl) for detecting areas of hypoperfusion was assessed in 16 closed-chest dogs. Variable areas of ischemia were produced either by occluding or stenosing the left anterior descending coronary artery. Cardiac scintigrams taken in four projections were compared with regional myocardial perfusion maps. Segmental concentrations and segmental perfusions were quantitated by counting the emissions from 201Tl and the microspheres in each of 96 segments of the left ventricle. In addition, studies with a phantom were performed. The results indicate: 1) The emissions from 201Tl and from microspheres correlated well in ischemic segments (r = 0.93 +/- SE 0.02). 2) Seven of twelve ischemic hearts had definitely abnormal scintigrams and in each of these the hypoperfused zone was greater than 4.9 grams and perfusion was decreased by more than 45%. 3) In the phantom, abnormal scintigrams could be detected in the presence of lesser deficits than in the dogs. The limitation of the thallium perfusion scintigrams will be the inconsistent detection of small perfusion deficits.

Animals↗

Relationships between myocardial perfusion, myocardial necrosis, and technetium--99m pyrophosphate uptake in dogs subjected to sudden coronary occlusion.

The quantitative relationship between abnormalities seen on technetium-99m pyrophosphate (99mTc-PYP) infarct scintigrams and the size of the myocardial infarction is unclear. We evaluated two possible determinants of 99mTc-PYP accumulation: myocardial perfusion measured with 7-10 mu microspheres and the extent of necrosis determined histologically. Hemodynamics and myocardial perfusion to small segments of the left ventricle were measured prior to, 5-10 min, and 44-48 hours following sudden occlusion of the left anterior descending coronary artery in ten awake dogs. 99mTc-PYP was injected i.v. following the third injection of microspheres and the animals were killed 2 hours later. The important findings were as follows: 1) there is a close relationship between the extent of myocardial necrosis observed and the perfusion of segments 5-10 min following coronary occlusion; and 2) that segmental myocardial perfusion is an important determinant of 99mTc-PYP accumulation by myocardial segments which contain areas of necrosis. Although the present data preclude statistical analysis of the relationship between the level of necrosis in a segment and the accumulation of 99mTc-PYP by that segment, the two do not appear to be related, a finding which would discourage use of intensity of 99mTc-PYP images for infarct size. The distribution of an abnormality on the scintigram may provide an estimate of infarct size. However, the geometry of the infarct and the resolving power of the scanning equipment will significantly limit this in many clinical situations.

Animals↗

Effects of acute coronary occlusion on the motion and perfusion of the normal and ischemic interventricular septum.

To establish the effect of local and remote myocardial ischemia on interventricular septal motion, 27 open-chest dogs were studied using ultrasound and radioactive microspheres. In 14 dogs the left anterior descending coronary artery was ligated. If the ultrasound beam traversed ischemic septum (proximal LAD occlusion), significant (P less than 0.05) declines in systolic septal velocity (26.4 +/- 2.9 to 6.4 +/- 1.8 mm/sec), and excursion (2.6 +/- 0.3 to 0.7 +/- 0.2 mm) occurred, and systolic thickening was reduced. Similar significant changes were seen when the ultrasound beam traversed nonischemic septum adjacent to the ischemic area (distal LAD occlusion). In 13 additional dogs, circumflex coronary ligation produced posterior ischemia. The mean septal velocity for this group increased significantly (21.8 +/- 2.6 to 26.5 +/- 3.3 mm/sec), as did the septal excursion (2.5 +/- 0.2 to 3.1 +/- 0.4 mm). We conclude that acute LAD occlusion causes a reduction in systolic velocity, excursion, and thickening of both the involved ischemic and the adjacent nonischemic septum. When myocardial ischemia was produced in a part of the ventricle remote from the septum, septal velocity and excursion increased.

Animals↗

Effect of stimulation of carotid chemoreceptors on total and regional cerebral blood flow.

This study was performed to determine whether stimulation of the carotid chemoreceptors increases total or regional cerebral blood flow and whether activation of arterial chemoreceptors contributes to cerebral vasodilation during systemic hypoxemia. In anesthetized and ventilated dogs, carotid chemoreceptors were stimulated with nicotine or hypoxic and hypercapnic blood. To measure total and regional cerebral blood flow, we used labeled 15-mu microspheres. Stimulation of chemoreceptors did not increase cerebral blood flow or produce significant redistribution of cerebral blood flow, even though the chemoreflex was intact in these animals (as manifested by vasoconstriction in muscle, kidney, and small bowel) and the cerebral vessels dilated in response to systemic hypercapnia. In other studies in anesthetized, ventilated dogs and rhesus monkeys, cerebral vasodilator responses to systemic hypoxemia were observed before and after denervation of carotid and aortic chemoreceptors. Systemic hypoxemia produced large and equivalent increases in cerebral blood flow before and after chemodenervation. We conclude that stimulation of carotid chemoreceptors does not produce cerebral vasodilation and that chemoreceptors do not contribute significantly to cerebral vasodilation during systemic hypoxemia.

Animals↗

Three dimensional geometry of acutely ischemic myocardium.

The distribution of coronary flow to small segments of the entire left ventricle (96 per dog; average weight = 0.78 g) was studied in 28 open-chested dogs utilizing 7-10 mu labeled microspheres. Although the flow to large areas of the ventricle was nearly evenly distributed, there was considerable heterogeneity of flow to small adjacent segments of myocardium (average standard deviation of the flow distributions was 17.3 +/- 3.2% of mean lfow). Approximately one-half of the measured heterogeneity of flow could be attributed to various extraneous factors, and one-half appears to be due to inherent heterogeneity of flow in the left ventricular myocardium. In ten of 28 dogs, the mid-circumglex coronary was suddenly occluded, and five minutes thereafter the distribution of left ventricular flow was determined with microspheres labeled with a different isotope. The ischemic regments were separated into three groups: severely ischemic, moderately ischemic, and borderline ischemic. The three dimmensional geometry of the acutely ischemic myocardium was analyzed, and four general conclusions were reached. 1) The percent distribution of severely ischemic segments, moderately ischemic segments, and borderline ischemic segments within an ischemic region varies from animal to animal. 2) Subendocardial segments were more frequently and more severely affected than neighboring mid-wall or epicardial segments. 3) No evidence of an "hyperperfused zone" of myocardium surrounding the ischemic area was found. 4) The flows to segments immediately adjacent to the severely ischemic segments were heterogeneous. Therefore, the concept of a geometrically defined "buffer zone" of moderately ischemic myocardium surrounding and separating severely ischemic from normally perfused myocardium no longer seems realistic.

Animals↗

Temporal heterogeneity of myocardial blood flow in anesthetized dogs.

Temporal variation in perfusion to small segments of the myocardium was studied in 19 opened-chest dogs. In six control dogs, three or four differently labeled 7-10 mu microspheres were injected simultaneously into the left atrium to assess the variability in measured myocardial perfusion due to the microsphere technique. In 13 other dogs, microspheres were injected four times at 5 minute intervals while various hemodynamics parameters (mean aortic pressure, peak systolic pressure, heart rate, left ventricular end-diastolic pressure, and Vmax) were stable (less than 10% variation in any one parameter). The left ventricles were divided into 96 segments, the mean weight+/- SD of each segment was 0.95+/-0.17 grams. The flow to each segment was expressed as a percent of the mean flow of the three or four measured flows to that segment, and the difference between the largest and the smallest percent of each segment was taken as a measure of the variability of flow to that segment. The average variability of segmental flow (mean +/-SD) when the three to four differently labeled microspheres were injected was 14.0+/-4.7; and the variability when differently labeled microspheres injected sequentially was 31.0+/-10.8% (P less than 0.001). Furthermore, in the sequentially injected animals the magnitude of temporal variation was similar in various subdivisions of the ventricle (layers, walls, apex to base). The mean and standard deviation of the variability of flow to the endo, mid, and epicardial layers were 28.7+/-10.2, 30.0+/-11.3 and 34.5+/-12.4%, respectively. These changes may reflect either spontaneous or local autoregulatory changes in precapillary sphincters or arterioles.

Animals↗

Correlation between echocardiographically demonstrated segmental dyskinesis and regional myocardial perfusion.

In order to evaluate the relationship between regional myocardial perfusion and segmental dyskinesis, 22 open chest dogs were studied using ultrasound to register cardiac wall motion and radioactive labeled microspheres to determine myocardial perfusion. In six dogs, motion and perfusion were correlated at two levels of partial circumflex coronary artery occlusion followed by complete occlusion. A good correlation between declining myocardial perfusion of all the ischemic segments and development of aneurysmal bulging (during isometric contraction) was seen: r = minus 0.80. A similar correlation between myocardial perfusion and endocardial wall velocity (during systolic ejection) was observed: r = 0.92. In nine dogs, the effect of 45 minutes of complete coronary occlusion followed by 30 minutes of reperfusion was evaluated with respect to perfusion and motion. After coronary reperfusion myocardial perfusion of the ischemic area returned to control levels (from 32.6 +/- 3.5 to 130.3 +/- 13.3 ml/100 g/min), but aneurysmal bulging during isometric contraction persisted. Endocardial wall velocity during systolic ejection showed a variable response to reperfusion, achieving values ranging from 32% to 162% of the preocclusion levels. In seven dogs the ultrasound beam was reflected off nonischemic myocardium adjacent to areas of ischemia resulting from coronary occlusion. Despite preservation of normal myocardial perfusion in these nonischemic areas wall motion abnormalities were evident: endocardial wall velocity declined from 25.8 +/- 5.8 to 14.0 +/- 4.9 mm/sec (P less than 0.01), and aneurysmal bulging in three animals. These changes may be due to transient undetected ischemia in the segments struck by the ultrasound beam, or to passive alteration of the motion of the normally perfused areas by the severe dyskinesis of the adjacent ischemic myocardium.

Animals↗

Demonstration of Ebstein's anomaly by simultaneous catheter-tip localization of the tricuspid valve visualization: A new method.

The diagnosis of Ebstein's anomaly has traditionally been made by angiocardiography and confirmed by simultaneous intracardiac electrocardiographic and pressure recordings. These techniques may result in false positive or negative tests. A new method is proposed, whereby the right coronary artery is used an an angiographic marker for the tricuspid annulus and a pressure catheter simultaneously marks the position of the tricuspid valve. In the right anterior oblique position the tip of the pressure catheter should be just under the right coronary artery as the tricuspid leaflets close in systole, indicating the normal relationship of the tricuspid leaflets and annulus. In Ebstein's anomaly the tip of the catheter extends well past the coronary artery in systole, demonstrating the characteristic displacement of the attachments of the tricuspid valve downward toward the right ventricular apex.

Adult↗