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Biomedical subjects

M L Marcus

Publications and source records attributed to M L Marcus.

At least 127 records · Page 7Linked to original sources
PubMed1984

Does visual interpretation of the coronary arteriogram predict the physiologic importance of a coronary stenosis?

To assess visual interpretation of the coronary arteriogram as a means of predicting the physiologic effects of coronary obstructions in human beings, we compared caliper measurements of the degree of coronary stenosis with the reactive hyperemic response of coronary flow velocity studied with a Doppler technique at operation, after 20 seconds of coronary arterial occlusion. In 39 patients (44 vessels) with isolated, discrete coronary lesions varying in severity from 10 to 95 per cent stenosis, measurement of the percentage of stenosis from coronary angiograms was not significantly correlated (r = -0.25) with the reactive hyperemic response. Results were the same for obstructions in the left anterior descending, diagonal, and right coronary arteries. Underestimation of lesion severity occurred in 95 per cent of vessels with greater than 60 per cent stenosis of the diameter by arteriography. Both overestimation and underestimation of lesions with less than 60 per cent stenosis were common. These results, together with the high interobserver and intraobserver variability of standard visual analysis of angiograms, suggest that the physiologic effects of the majority of coronary obstructions cannot be determined accurately by conventional angiographic approaches. The need for improved analytical methods for the physiologic assessment of angiographically detected coronary obstructions is apparent.

Angiography↗
PubMed1984

Angiographic evidence that reciprocal ST-segment depression during acute myocardial infarction does not indicate remote ischemia: analysis of 23 patients.

Although reciprocal ST-segment depression from the remote noninfarcting ventricular wall during acute myocardial infarction (MI) is a common clinical finding, the significance of this electrocardiographic pattern is unclear. Previous retrospective studies have suggested that these findings may reflect either remote wall ischemia, multivessel coronary artery disease (CAD), extensive MI or a benign electrical phenomenon. Prior studies have lacked angiographic data obtained at the time of these acute electrocardiographic changes. In this study we prospectively evaluated 23 patients with acute MI. Left ventricular wall motion, coronary anatomy and the ECG were all assessed over a short period during the acute phase of the MI. Segmental wall motion was used as a sensitive indicator of ischemia. Seventeen patients had acute anterior MI, of whom 47% had reciprocal ST-segment depression; 6 patients had inferior MI, with 3 showing reciprocal ST depression. The mean degree of ST-segment elevation from the infarcting wall tended to be greater in patients with reciprocal ST-segment depression than in those without such reciprocal ST depression (2.8 +/- 0.4 vs 1.9 +/- 0.3 mm, p = 0.06). Patients with and without reciprocal ST-segment depression had similar degrees of segmental dysfunction in the infarct wall. However, no abnormalities in segmental wall motion in the remote wall were seen regardless of the presence or absence of remote wall ST-segment depression. In addition, the presence or absence of ST-segment depression did not predict the extent or degree of CAD.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Validation of a third-generation Doppler system for studies of detailed aortic flow.

A multigated, third-generation Doppler velocity system has been developed and validated for detailed studies of aortic hemodynamics. The Doppler system employs a single 3-mm, 5-MHz crystal applied to the aorta at a fixed angle with respect to the flow axis and is capable of measuring velocity profile, blood vessel diameter, and integrated volume flow on a continuous, real-time basis. This represents a major developmental advance over existing first-generation, continuous-wave and second-generation, single-gated pulsed Doppler systems. Validation studies have been performed in vitro and in dogs. Aortic diameter was measured simultaneously with the volumetric Doppler system and with sonomicrometer probes. During changes in aortic diameter between 8 and 18 mm (n = 18), produced by temporary pulmonary artery occlusion or epinephrine infusion, quantitative agreement between the Doppler and sonomicrometer probes was found (r = 0.96). Velocity profile measurements and axial velocity values made with the Doppler system compared favorably with hot-film anemometry studies in vitro and in vivo. Although the current system is nondirectional, measurements of phasic aortic volume flow and absolute-time-averaged changes in flow rates showed an excellent correlation with chronically placed electromagnetic flow probes over a broad range of flow rates in vivo (1-5 l/min, n = 36, r = 0.95). This third-generation Doppler system should prove useful in clinical and research studies of detailed aortic hemodynamics.

Animals↗
PubMed1984

Coronary venous outflow persists after cessation of coronary arterial inflow.

During single long diastoles we simultaneously measured coronary arterial blood flow and coronary venous outflow. When vasomotor tone was intact, approximately 20% of the total volume of diastolic coronary venous outflow appeared after cessation of inflow. During maximal coronary dilation, approximately 40% of the total volume of diastolic coronary venous outflow appeared after cessation of inflow. Theoretically, coronary capacitance could enable persistence of diastolic coronary venous outflow during zero coronary artery inflow. Intramyocardial coronary capacitance calculated from these data was 0.10 ml X mmHg-1 X 100 g-1 with vasomotor tone intact and 0.21 during maximal coronary dilation. These results indicate that the diastolic coronary arterial stop-flow pressure cannot be equated with cessation of flow throughout the coronary vasculature due to the significant contribution of intramyocardial capacitance. We also found that the arterial pressure at which coronary outflow stopped (10-14 mmHg) was substantially less than that at which coronary artery inflow ceased (19-31 mmHg), yet slightly above right atrial pressure (5-9 mmHg). These studies indicate that coronary venous outflow stops at a lower pressure than arterial inflow. Furthermore, the cessation of venous blood flow in the coronary system during long diastoles occurs at pressures only a few mmHg above right atrial pressure.

Animals↗
PubMed1984

Rethrombosis after reperfusion with streptokinase: importance of geometry of residual lesions.

We tested the hypothesis that lesion rethrombosis after streptokinase reperfusion is related to luminal size of the residual stenosis. Two independent techniques of analyzing coronary angiograms, quantitative coronary angiography and computer-based videodensitometry, were used to estimate the size of the residual lumen immediately after discontinuation of streptokinase. These techniques were selected because they provide independent estimates of cross-sectional area of a lesion with high degrees of reproducibility and minimal observer variability. Twenty-four patients who had undergone successful reperfusion with streptokinase were studied. Seven patients had lesion rethrombosis documented either on a repeat angiogram, at autopsy, or, in one case, by the fact that the patient had an acute transmural infarction resulting in death. Vessel patency was documented by repeat coronary angiography 8 to 14 days after initial streptokinase reperfusion in the other 17 patients. As assessed by quantitative coronary angiography, seven of 13 patients (54%) with minimal luminal cross-sectional areas of less than 0.4 mm2 had rethrombosis. None of the 11 patients with lumens greater than 0.4 mm2 had rethrombosis. In the 17 patients with vessels that remained patent the size of the residual lesion at repeat catheterization was compared with its size immediately after reperfusion with streptokinase. Over the intervening 8 to 14 day interval, an average percentage increase in minimal cross-sectional area of 116 +/- 34% was observed. In seven patients minimal luminal cross-sectional area more than doubled. Integrated optical density, an index of the severity of coronary stenosis derived from computer-based videodensitometry, was also useful in identifying a subgroup of patients at high risk for rethrombosis of lesion.(ABSTRACT TRUNCATED AT 250 WORDS)

Computers↗
PubMed1984

The value of lesion cross-sectional area determined by quantitative coronary angiography in assessing the physiologic significance of proximal left anterior descending coronary arterial stenoses.

The results of previous work from this laboratory have shown a poor correlation between percent stenosis (determined visually with calipers) and the coronary reactive hyperemic response (an index of maximal coronary vasodilator capacity) determined during cardiac surgery. This study was performed to determine whether other parameters of lesion severity could predict the reactive hyperemic response and thus the hemodynamic significance of coronary stenoses in human beings. Twenty-three patients with lesions in the proximal left anterior descending coronary artery were studied. To account for differences in expected vessel size, patients with large diagonal branches (greater than one-half the diameter of the left anterior descending artery) arising before the lesion were excluded. Computer-assisted quantitative coronary angiography was used to measure percent diameter stenosis, percent area stenosis, and minimal stenosis cross-sectional area. With a pulsed Doppler velocity probe, reactive hyperemic responses were recorded after a 20 sec coronary occlusion of the left anterior descending artery at cardiac surgery before cardiopulmonary bypass and were quantified by the peak/resting velocity ratio (normal greater than 3.5:1). Percent area stenosis ranged from 7% to 54% for vessels with normal reactive hyperemic responses and from 27% to 94% for vessels with abnormal reactive hyperemic responses. With both percent diameter stenosis and percent area stenosis there was substantial overlap between vessels with normal and abnormal reactive hyperemic responses. In contrast, nine of nine vessels with normal reactive hyperemic responses had lesion minimal cross-sectional areas of greater than 3.5 mm2 and 13 of 14 vessels with abnormal reactive hyperemic responses had minimal cross-sectional areas of less than 3.5 mm2.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Augmented responses to vasoconstrictor stimuli in hypercholesterolemic and atherosclerotic monkeys.

We examined effects of hypercholesterolemia and atherosclerosis on vasoconstrictor responses to norepinephrine and serotonin. Responses were compared in normal, atherosclerotic, and hypercholesterolemic but non-atherosclerotic cynomolgus monkeys. The hindlimb was perfused at constant flow so that changes in perfusion pressure indicated changes in vascular resistance. We measured the pressure gradient from the iliac to the dorsal pedal artery so that responses of the large artery segment could be determined. Serotonin decreased total hindlimb resistance in normal and hypercholesterolemic monkeys, but increased total resistance in atherosclerotic monkeys. There was a greater than 10-fold increase in constrictor responses of large arteries to serotonin in atherosclerotic monkeys, compared with normal and hypercholesterolemic monkeys. In contrast, we found that vasoconstrictor responses to norepinephrine are normal in atherosclerotic monkeys and increased in hypercholesterolemic monkeys prior to development of atherosclerosis. Hypercholesterolemia augmented responses of small vessels to norepinephrine. We conclude that, during early stages of hypercholesterolemia in cynomolgus monkeys, vasoconstrictor responses to norepinephrine are increased in small vessels. At a later stage, as atherosclerosis develops, responses to norepinephrine return to normal, but vasoconstrictor effects of large arteries to serotonin are greatly potentiated.

Animals↗
PubMed1983

Relations between 2-dimensional echocardiographic wall thickening abnormalities, myocardial infarct size and coronary risk area in normal and hypertrophied myocardium in dogs.

Systolic wall thickening abnormalities are sensitive indicators of ischemia and infarction. One purpose of this investigation was to assess the relation between coronary risk area, infarct size and wall thickening abnormalities (dyskinesia) using 2-dimensional echocardiography (2-D echo) in a closed-chest conscious dog model of acute myocardial infarction. The second purpose was to study the effects of systemic hypertension (SH) and left ventricular (LV) hypertrophy on these relations. Our hypothesis was that the infarct size and the extent of 2D echocardiographic dyskinesia would be quantitatively different in SH-LV hypertrophy, a condition in which coronary vascular reserve is diminished. Permanent circumflex coronary occlusion was performed in 15 conscious normal dogs and in 14 dogs with LV hypertrophy secondary to renal hypertension. Two-dimensional echocardiograms were obtained before, 20 minutes after and 2 days after coronary occlusion. The systolic wall thickening along 12 equidistant radii was analyzed in short-axis images. Percent dyskinesia on 2-D echo was defined as the percentage of radii showing systolic thinning. Infarct size was determined pathologically and risk area was determined angiographically. For a given risk area, coronary occlusion resulted in a larger infarction in dogs with SH-LV hypertrophy than in normal dogs (p less than 0.05). Two-dimensional echocardiographic dyskinesia correlated well with infarct size both at 20 minutes (r = 0.92) and 2 days (r = 0.94); dyskinesia modestly overestimated the infarct size and underestimated the risk area. The relations were similar in both normal and SH-LV hypertrophy groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Abnormalities in the coronary circulation that occur as a consequence of cardiac hypertrophy.

Myocardial ischemia is frequently observed in patients with cardiac hypertrophy even when the conduit coronary arteries are normal. Recent studies indicate that impaired coronary reserve in hypertrophied hearts probably occurs because growth of the coronary bed does not keep pace with increases in cardiac mass. The imbalance between vascular proliferation and muscle growth is probably most severe when cardiac hypertrophy is produced by pressure overload. Experimental studies also suggest that abnormalities intrinsic to pressure-hypertrophied heart muscle (decreased capillary density; decreased coronary reserve; electrophysiologic abnormalities) adversely affect the response of the enlarged heart to sudden coronary occlusion. When animals with hypertension and left ventricular hypertrophy are subjected to sudden coronary occlusion, the incidence of sudden cardiac death is increased severalfold and infarct size is substantially augmented. These observations suggest that abnormalities in the coronary microcirculation that accompany cardiac hypertrophy play a significant role in the pathogenesis of the complications associated with cardiac hypertrophy.

Animals↗
PubMed1983

Detection of acute myocardial infarction in closed-chest dogs by analysis of regional two-dimensional echocardiographic gray-level distributions.

We hypothesized that acute myocardial infarction could be detected in standard two-dimensional echocardiograms of closed-chest dogs by evaluating regional echo amplitude distributions using computerized image analysis. We tested this hypothesis by performing standard, 2.4 MHz two-dimensional echoes before and 2 days after circumflex coronary occlusion in seven closed-chest dogs. Control and infarcted regions of interest were studied in digitized stop-frame images. Average gray level was calculated for each region of interest, and the shape of the gray-level distribution was analyzed by calculation of skewness and kurtosis and by qualitative features of shape. Average gray level increased significantly from the pre- to postocclusion images in the infarcted regions (16.7 +/- 4.2 vs. 32.4 +/- 4.4 units, P less than 0.01), but not in the control regions (17.4 +/- 4 vs. 22.3 +/- 5.5., P = NS). Average gray level could not distinguish between infarcted and normal regions within the postocclusion images (36 +/- 5.2 vs. 33.6 +/- 5.8, P = NS). Three independent observers qualitatively evaluated histogram shape and correctly identified 7/7 MI regions (100% sensitivity) and 14/20 normal regions (70% specificity). Quantitatively, infarct regions exhibited a significant decrease in kurtosis from pre- to postocclusion images (7.1 +/- 4.0 vs. 5.2 +/- 2.9, P = NS). Within postocclusion images, infarcted regions displayed a significantly lower kurtosis than did normal regions (0.27 +/- .47 vs. 2.5 +/- 1.0, P less than .01). We conclude that acute myocardial infarction may be detected in closed-chest dogs by analyzing regional echo amplitude data from standard two-dimensional echocardiograms.

Animals↗
PubMed1983

Hemodynamic sequelae of regression of experimental atherosclerosis.

Regression of experimental atherosclerosis is characterized by decreased intimal thickness and luminal enlargement, but intimal fibrosis becomes more dense. We tested the hypothesis that fibrosis of arteries during regression might limit vasodilator capacity and restrict hemodynamic improvement despite luminal improvement. We studied limb, coronary, and cerebral hemodynamics in 11 normal cynomolgus monkeys, 10 monkeys given an atherogenic diet for 20 mo and 8 monkeys given a regression diet for an additional 18 mo. The atherogenic diet induced lesions of moderate severity (50-60% stenosis); owing to characteristic vessel growth during the atherogenic period, luminal size did not decrease correspondingly. Regression monkeys showed typical changes of regression with luminal enlargement but increased fibrosis. The iliac artery was perfused at constant blood flow and maximal vasodilatation was produced with papaverine. Blood flow was measured with microspheres during maximal vasodilatation in the coronary bed (adenosine) and cerebral bed (hypercapnia). In normal monkeys, minimal vascular resistances were 1.95 +/- 0.19 mm Hg/ml/min X 100 g (mean +/- SE) (limb), 0.13 +/- 0.01 (coronary), and 0.44 +/- 0.02 (cerebral). In atherosclerotic monkeys minimal resistance increased (P less than 0.05) 108, 62, and 166% in the limb, coronary, and cerebral beds, respectively. In regression monkeys, minimal resistance increased from values found in atherosclerotic animals in the limb (+22%), decreased inconsistently in the coronary bed (-19%), and decreased significantly in the cerebral bed (-44%, P less than 0.05). Thus morphologic regression was accompanied by significant hemodynamic improvement during maximal dilatation only in cerebral vessels. We conclude that increases in luminal size during regression of atherosclerotic lesions may not be associated with increases in vasodilator capacity, as intimal fibrosis may limit physiologically important hemodynamic improvement.

Animals↗
PubMed1982

Decreased coronary reserve: a mechanism for angina pectoris in patients with aortic stenosis and normal coronary arteries.

The pathogenesis of angina pectoris in patients with aortic stenosis and normal coronary arteries remains uncertain. Using a specially designed Doppler probe, we measured the maximal velocity of coronary blood flow in the left-anterior descending coronary artery at the time of elective open-heart surgery in 14 patients with aortic stenosis and left ventricular hypertrophy (13 had angina) and in 8 controls without left ventricular hypertrophy. The ratio peak velocity of coronary blood flow, after a 20-second occlusion, to resting velocity was decreased by more than 50 per cent (P less than 0.05) in the patients with aortic stenosis. In 7 of the patients this ratio was decreased by more than 75 per cent. Studies of the velocity of coronary blood flow in vessels perfusing the right ventricle in these patients showed only mild abnormalities. These data demonstrate a selective and marked decrease in coronary reserve to the hypertrophied left ventricle in patients with severe aortic stenosis. The impairment in coronary reserve is probably an important contributor to the pathogenesis of angina pectoris in these patients.

Aged↗
PubMed1982

Pial artery diameter and blood flow velocity during sympathetic stimulation in cats.

The effects of sympathetic stimulation on the cerebral circulation in cats are in dispute. One unexplained observation is that sympathetic nerve stimulation constricts pial arteries but does not decrease cerebral blood flow (CBF). To reconcile these findings, we studied effects of sympathetic nerves on cerebral vessels using a new method that permits virtually continuous measurement of pial artery diameter and blood flow velocity, and calculation of change in CBF. Change in CBF was calculated as the product of cross-sectional area (CSA) and blood flow velocity in a large pial artery. Pial artery diameter was measured with the cranial window method and CSA was calculated (pi r2). Blood flow velocity was measured with a pulsed Doppler velocity meter. In 11 cats, CBF was measured duringg the control period and during electrical stimulation of sympathetic nerves. During stimulation, arterial diameter decreased 6 +/- 1%, but CBF did not change because velocity increased 19 +/- 5%. We also measured CBF with microspheres during control and after 60 s of sympathetic stimulation. Cerebral blood flow was 28 +/- 3 ml/min/100 g during control and 26 +/- 3 ml/min/100 g after 60 s of sympathetic stimulation (n = 5). It is likely that the increase in velocity durin sympathetic stimulation was due to compensatory dilatation of downstream arteries.

Animals↗
PubMed1982

Effect of volume-overload hypertrophy on the coronary circulation awake dogs.

Inadequate coronary reserve is present in left ventricular hypertrophy secondary to hypertension. Since this abnormality might be due in part to vascular hypertrophy of coronary resistance vessels in response to chronic hypertension, we studied a model of ventricular hypertrophy without hypertension. Volume-overload hypertrophy was produced by creating complete heart block in mongrel dogs; 6 to 7 weeks later the dogs were studied in the awake state. The thirteen dogs with chronic heart block had a 49% increase (P less than 0.05) in left ventricular mass compared with eight control dogs. The major findings in this study were: 1) at rest, coronary blood flow (microsphere technique) per unit weight of left ventricle was not increased in dogs with hypertrophy; and 2) the minimal coronary vascular resistance per unit weight of left ventricle calculated during iv adenosine infusion at a rate that produced maximal vasodilatation was not significantly higher in dogs with left ventricular hypertrophy than in controls (16.4 +/- 1.0 vs 14.7 +/- 1.5 kPa . litre-1 . min . 100 g, respectively). Minimal coronary vascular resistance of the entire left ventricle was significantly less in dogs with hypertrophy than controls (13.0 +/- 0.8 vs 17.3 +/- 1.7 kPa . litre-1 . min, respectively). This data suggests that vascular hypertrophy of coronary resistance vessels related to chronic hypertension may be the cause of the increased minimal coronary vascular resistance seen in dogs with pressure-overload left ventricular hypertrophy.

Adenosine↗
PubMed1982

Effect of hip position on blood flow to the femur in puppies.

Utilizing radioactive microspheres, blood flow to the femoral head of immature dogs was measured. Blood flow was measured with the leg in the control position, maximal abduction, submaximal abduction, and the human position of hip immobilization. Maximal abduction (to 90 degrees) significantly decreased flow to the capital femoral epiphysis. Submaximal abduction and the human position did not reduce blood flow. Measurement of flow in the control position immediately after forced abduction demonstrated marked reactive hyperemia. These data indicate that ischemia occurs during 90 degrees forced abduction of the hip. This finding supports the use of lesser degrees of abduction for hip immobilization in the treatment of congenital dislocation of the hip. The vascular anatomy of the head of the femur in puppies and children suggests that these data can be extrapolated to man.

Animals↗
PubMed1982

Transmural variation in the relationship between myocardial infarct size and risk area.

To test the hypothesis that the relationship between infarct area (IA) and area at risk (AR) varies in different layers of the left ventricle (LV), we occluded the circumflex coronary artery for 48 h in 20 conscious dogs. AR was determined by postmortem coronary stereoarteriography, and infarct area by pathological examination. Both AR and IA were divided into four layers: posterior papillary muscle (PPM), subendocardium (Endo), midwall, and subepicardium (Epi) and quantified with planimetry. Hemodynamics and regional myocardial flow with tracer microspheres (7-10 micrometers diam) were measured before and after coronary occlusion. IA was closely correlated with AR for PPM (r = 0.96), Endo (r = 0.97), and Epi (r = 0.92). However, the slope of IA/AR for Endo (1.30 +/- 0.08) was significantly steeper (P less than 0.05) than that for Epi (0.89 +/- 0.11); furthermore, the intercepts at zero infarction for PPM (0.5 +/- 0.1% of LV), Endo (4.2 +/- 0.4%), and Epi (0.1 +/- 0.7%) were significantly different from each other. Regional blood flow measurements indicate that the differences in IA/AR in various layers reflected earlier and greater total collateral flow to the noninfarcted AR in the epicardium. Thus IA/AR for the entire LV is a composite representing separate IA/AR specific to various transmural layers of the LV. In addition, this study demonstrates that the lateral border zone between the IA and the AR is minimal (less than 3-5 mm) in the subendocardium and midwall layers of the left ventricle.

Animals↗