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Biomedical subjects

M M LeWinter

Publications and source records attributed to M M LeWinter.

At least 73 records · Page 4Linked to original sources
PubMed1985

Biaxial mechanical properties of the pericardium in normal and volume overload dogs.

The two-dimensional mechanical properties of the pericardium from dogs with a normal or chronically enlarged heart were studied in vitro. A 3.0-cm-square piece of the pericardium overlying the right and/or left ventricle was excised. An approximately 1.0-cm-square target was marked at the center, and its dimension was measured electrooptically. When immersed in physiological saline at 37 degrees C, the specimen was stretched and unloaded sinusoidally in one direction while force in the transverse direction was held constant. The tension-stretch relationship was highly reproducible and was insensitive to strain rate in the range of 0.002-0.1 Hz. Hysteresis was present. The pericardium was mostly anisotropic; however, the direction of maximal compliance varied among dogs. The elastic properties of the pericardium overlying the left and right ventricles were the same in most cases. Substantial stress relaxation was observed; in contrast, insignificant creep developed over 30 min. In five dogs with chronic cardiac dilatation due to an infrarenal aortocaval shunt, the tension-stretch curves were shifted significantly to the right (i.e., greater deformation at the same tension level). However, the pericardial viscoelastic properties and thickness were unchanged. In other words, chronic cardiac dilatation resulted in a more compliant pericardium.

Animals↗
PubMed1985

Relationship between myocardial fiber direction and segment shortening in the midwall of the canine left ventricle.

Myocardial fiber orientation undergoes an orderly transition from the epicardium to the endocardium in the left ventricle, with circumferential fibers predominating in the middle one-third of the heart wall. How fibers lying at different depths in the myocardium, running in different directions, interact to produce local deformation is not known. To define the relationship between the orientation of uniaxial myocardial fibers and local wall motion, we placed three sets of ultrasonic dimension gauges in the middle one-third of the apex-to-base distance of the left ventricle of nine dogs. One pair was placed in line and two intentionally out of line with the presumed local fiber direction. The relative angle between the gauge and the local myofibers was determined by the use of postmortem radiography and histological techniques. Our results show that in the midwall of the left ventricle, myocardial segment shortening is maximal in the direction of local fibers; the shortening measured by gauges placed out of line with the local fiber axis by more than 30 degrees was significantly less than the actual in-line fiber shortening which occurred. This suggests that functional tethering between midwall fibers and endocardial or epicardial fibers does not play a major role in the pattern of midwall deformation. We also documented that an external reference line can be used to predict midwall myofiber direction. Using this line as a guide, ultrasonic dimension gauges could be placed within an average of 12 degrees (range: 0.5 to 18.5 degrees) from the local fiber axis.

Animals↗
PubMed1984

Role of parietal pericardium in acute, severe mitral regurgitation in dogs.

Mitral regurgitation (MR) resulting from acute disruption of the mitral valve apparatus leads to serious hemodynamic sequelae. The lesion produces major elevation of left atrial (LA) and pulmonary artery pressures and decreases forward cardiac output. Clinical studies have shown hemodynamic patterns in acute MR similar to those seen in constrictive pericardial disease, suggesting that the pericardium serves to importantly limit cardiac filling in this condition. This hypothesis has not been tested in an animal model in which the intrapericardial pressure can be directly measured. In the present study intrapericardial and intracardiac pressures were measured in 8 dogs before and after the production of acute MR. After production of MR, mean LA pressure increased from 8 +/- 3 to 20 +/- 7 mm Hg (p = 0.004) and the peak LA V wave averaged 31 +/- 13 mm Hg. Mean right atrial pressure increased slightly, from 4 +/- 2 to 5 +/- 1 mm Hg (p less than 0.008). Intrapericardial pressure increased in each dog, but the increment was invariably small (1 +/- 2 to 3 +/- 2 mm Hg, p = 0.001) and there was no tendency to equalization of pressure between right- and left-sided cardiac chambers. Thus, the role of the pericardium in the immediate hemodynamic response to acute, severe MR is minor.

Animals↗
PubMed1984

Acute effects of doxorubicin (adriamycin) on left ventricular function in dogs.

Although chronic doxorubicin (adriamycin) cardiotoxicity often is attributed to repeated episodes of acute myocardial injury, the acute effects of doxorubicin on in vivo left ventricular performance have not been studied in a carefully controlled setting. Accordingly, we recorded high-fidelity left ventricular pressures and segmental dimensions before and after either intravenous or intracoronary doxorubicin in twelve open-chest dogs. Propranolol was administered to prevent reflex sympathetic stimulation, and heart rate was held constant by atrial pacing. Intravenous doxorubicin (1.5 mg/kg) (n = 6) caused significant decreases in all measured indices of myocardial contractility, in association with a large decrease in left ventricular systolic pressure (125 +/- 28 and 81 +/- 23 mm Hg before and 5 min after doxorubicin, respectively, P less than 0.01). Intracoronary doxorubicin (0.075 to 0.3 mg/kg) (n = 6) caused similar decreases in percent segment shortening (from 19 +/- 7 to 16 +/- 8, P less than 0.05), mean normalized shortening rate (from 0.87 +/- 0.34 to 0.71 +/- 0.37 segment lengths/sec, P less than 0.05), and peak positive left ventricular dP/dt (by 10 +/- 11%, P less than 0.07), although left ventricular systolic pressure was only modestly decreased (126 +/- 20 and 113 +/- 17 mm Hg before and after doxorubicin, respectively, P less than 0.01). Intracoronary doxorubicin also slowed the rate of left ventricular relaxation, as evidenced by an increase in the time constant for isovolumic pressure fall from 32.0 +/- 9.0 to 36.9 +/- 7.5 msec, and significantly altered the relationship between left ventricular pressure and dimension at end-diastole.

Animals↗
PubMed1984

Sonomicrometry: its application as a routine monitoring technique in cardiac surgery.

We utilized ultrasonic-dimension crystals in approximately 50 patients during a three-year period to evaluate clinical sonomicrometry as a routine monitoring tool in patients undergoing cardiac operations. Standard research piezoelectric pulse transit ultrasonic transducers were modified with a hooked attachment in a tethered configuration to facilitate accurate alignment and quick insertion for the measurement of myocardial segment length changes. These segment crystals were used both intraoperatively and postoperatively to evaluate the left ventricular pressure-geometry relationships and to serve as a continuous monitor of myocardial function. The left ventricular pressure-volume relationship was varied by temporarily reapproximating the pericardium (pericardial closure resulted in a 12% reduction in fractional shortening, a 5% decrease in end-diastolic segment length, and an 8% increase in pulmonary artery diastolic pressure). During both the intraoperative and postoperative periods, we found good correlation between thermodilution, stroke volume, and myocardial dimensions; no correlation was noted between pulmonary artery diastolic pressure and stroke volume. No bleeding or major complications resulted from the use of these sonomicrometry transducers. Our initial clinical experience with sonomicrometry seems to support its use as a potentially valuable monitoring tool.

Blood Pressure↗
PubMed1984

Effect of sodium nitroprusside on ventilation-perfusion mismatching in heart failure.

Sodium nitroprusside has been shown to lower arterial partial pressure of oxygen (PaO2) in patients with congestive heart failure and respiratory failure. The multiple inert gas elimination technique was used to evaluate the effect of sodium nitroprusside infusion on pulmonary gas exchange in five patients with congestive heart failure. During sodium nitroprusside infusion, mean values of cardiac output increased and mean values of arterial pressure, pulmonary artery pressure, pulmonary artery wedge pressure and pulmonary vascular resistance decreased. Cardiac output increased in each patient and PaO2 decreased in all but one patient (mean 75.6 +/- 15.1 to 68 +/- 17.5 mm Hg, p = 0.032). Distributions of ventilation and perfusion showed increased perfusion of lung units with low (less than or equal to 0.1) ventilation-perfusion ratios in all subjects during sodium nitroprusside infusion (mean 3.89 +/- 1.52 to 11.33 +/- 7.42% of cardiac output, p = 0.027, paired t test). The amount of shunt (fractional perfusion of lung units with ventilation-perfusion ratio = 0) increased in the two patients with some shunt present in the baseline measurements. The mean total low ventilation-perfusion perfusion (shunt plus ventilation-perfusion less than or equal to 0.1) was significantly increased from 4.38 +/- 1.54 to 14.7 +/- 9.37% (p = 0.023) during sodium nitroprusside infusion. Total low ventilation-perfusion perfusion was negatively correlated with mean pulmonary artery pressure and pulmonary artery wedge pressure (r = -0.949 and -0.946, respectively). Although sodium nitroprusside infusion increased cardiac output and overall oxygen transport in all patients, it worsened ventilation-perfusion mismatching. The mechanism is probably pulmonary vasodilation or increased cardiac output, or both.

Aged↗
PubMed1984

Pericardial adaptations during chronic cardiac dilation in dogs.

The manner in which the pericardium adapts to chronic cardiac dilation is not known. Recent work from our laboratory indirectly suggested that the size of the pericardium and/or its pressure-volume relation was altered by chronic cardiac enlargement. To examine this question further, we compared pericardial pressure-volume and stress-strain relations, surface area, mass, and average thickness in seven normal dogs and seven with chronic volume overload hypertrophy due to a systemic arteriovenous fistula. Dogs with significant cardiac hypertrophy had an increased pericardial volume at any pressure and a proportionality constant for the slope of the entire curve as determined by nonlinear regression analysis. This was associated with parallel increases in pericardial surface area and mass such that average thickness was unchanged. Stress-strain analysis of the data revealed that the mechanical properties of the pericardium were not significantly different in dogs with chronic cardiac dilation. These results indicate that during chronic cardiac dilation the pericardium enlarges in size and mass. The pericardial chamber is more compliant, although the intrinsic stiffness of the pericardium appears to be unchanged. Further, since pericardial mass is increased, the response to chronic dilation appears to also involve the addition of new pericardial tissue.

Animals↗
PubMed1983

Protective effects of aspirin against acute myocardial infarction and death in men with unstable angina. Results of a Veterans Administration Cooperative Study.

We conducted a multicenter, double-blind, placebo-controlled randomized trial of aspirin treatment (324 mg in buffered solution daily) for 12 weeks in 1266 men with unstable angina (625 taking aspirin and 641 placebo). The principal end points were death and acute myocardial infarction diagnosed by the presence of creatine kinase MB or pathologic Q-wave changes on electrocardiograms. The incidence of death or acute myocardial infarction was 51 per cent lower in the aspirin group than in the placebo group: 31 patients (5.0 per cent) as compared with 65 (10.1 per cent); P = 0.0005. Nonfatal acute myocardial infarction was 51 per cent lower in the aspirin group: 21 patients (3.4 per cent) as compared with 44 (6.9 per cent); P = 0.005. The reduction in mortality in the aspirin group was also 51 per cent--10 patients (1.6 per cent) as compared with 21 (3.3 per cent)--although it was not statistically significant; P = 0.054. There was no difference in gastrointestinal symptoms or evidence of blood loss between the treatment and control groups. Our data show that aspirin has a protective effect against acute myocardial infarction in men with unstable angina, and they suggest a similar effect on mortality.

Adrenergic beta-Antagonists↗
PubMed1983

Effects of direct-current electrical shocks on systolic and diastolic left ventricular function in dogs.

Although direct-current (DC) electrical shocks do not significantly alter left ventricular systolic performance, their effects on ventricular diastolic properties and the role of sympathetic stimulation in maintaining postshock contractility are unknown. Accordingly, we studied both diastolic and systolic left ventricular performance in seven open-chest dogs before and after three consecutive 50 joule DC shocks applied directly to the heart. High-fidelity left ventricular pressure and segmental dimensions were recorded as pressure was varied systematically under conditions of beta-adrenergic blockade. The exponential left ventricular end-diastolic pressure-segment length relationship was not significantly altered by electrical shocks. Likewise, pre- and postshock beats matched for loading conditions did not differ in peak positive dP/dt, end-systolic segment length, or percentage of segment shortening, although mean normalized shortening rate decreased by approximately 11% (p less than 0.05). However, the time constant (T) for isovolumic pressure fall, an index of the rate of left ventricular relaxation, increased after shocks in all animals (T = 42.2 +/- 5.3 and 51.1 +/- 7.0 msec before and after shock, respectively; (p less than 0.01). We conclude that high-energy electrical shocks applied directly to the heart cause modest slowing of left ventricular relaxation but do not have important effects on left ventricular compliance or on systolic myocardial performance. These data suggest that DC shocks have only minor functional consequences when applied to normal hearts, even when sympathetic compensation is prevented.

Animals↗
PubMed1983

Mechanism of increase in left ventricular end-diastolic pressure after contrast ventriculography in patients with coronary artery disease.

Elevation in left ventricular (LV) end-diastolic pressure (EDP) after contrast ventriculography (CV) has been proposed as a form of stress intervention in patients with coronary artery disease (CAD). The mechanism of this change has not been delineated. Accordingly, we performed two studies in CAD patients. In study 1 (n = 10), CV was repeated 3 minutes after an initial study. LVEDP rose from 14.9 +/- 6.6 mm Hg prior to the first ventriculogram to 26.9 +/- 10.8 mm Hg 3 minutes after the first ventriculogram (p less than 0.05) and immediately prior to the repeat CV (performed to evaluate the changes in volume produced by the first ventriculogram). In four patients with LV micromanometer pressures, the entire diastolic pressure-volume relation was shifted upward. LV ejection fraction (EF) and end-diastolic volume (EDV), peak LV pressure, and peripheral vascular resistance were unchanged at the time of repeat CV, and there was no correlation between the change in EDP and any of these variables. In study 2 (n = 6), gated radionuclide angiography was performed prior to and at minutes 2 to 7 after CV as were measurements of LV and right ventricular (RV) pressures. While both LV and RV EDP rose following contrast ventriculography, LV and RV EDV and EF were unchanged. We conclude that alterations in LVEDP after CV are unrelated to changes in LV or RV EDV and are most likely mediated by a decrease in myocardial compliance.

Adult↗
PubMed1983

Radionuclide analysis of pulmonary blood volume: the response to spontaneous angina pectoris and sublingual nitroglycerin in patients with coronary artery disease.

By manually assigning pulmonary regions of interest and deriving pulmonary time-activity (volume) curves, we were able to make count estimates of pulmonary blood volume (PBV) from gated cardiac blood pool scans. Five patients with coronary heart disease developed angina spontaneously while under a gamma camera. This produced an increase in cardiac volumes (p less than 0.05), a reduction in left ventricular ejection fraction (p less than 0.01), along with a marked increase in PBV (0.010 +/- 0.003 to 0.015 +/- 0.002 units, p less than 0.05). Nitroglycerin was then administered and reduced PBV in association with a return to normal in cardiac systolic function and size. In patients with stable chronic ischemic heart disease, sublingual nitroglycerin also reduced PBV (p less than 0.05), although not as much as when administered during an anginal episode. We conclude that gated imaging of the chest can be utilized to follow changes in PBV serially. These changes can be utilized to evaluate clinically important changes in hemodynamic status and the response to pharmacologic interventions.

Adult↗
PubMed1983

Regional circumferential lengthening patterns in canine left ventricle.

We employed sonomicrometers in open-chest dogs to study lengthening of short segments of circumferentially oriented myocardium located at the base, midportion, and apex of the anterior left ventricular free wall. Left ventricular pressure was varied by inferior vena caval occlusion and volume expansion. Diastole was divided into rapid and slow lengthening phases. Rapid lengthening was completed first at the basal site at each of three successive levels of left ventricular diastolic pressure (LVDP). At the base, significant further lengthening occurred during the slow lengthening phase while at the apex virtually all lengthening was completed during the rapid phase. At low LVDPs, peak lengthening rates (dl/dt) were greatest at the apex. As LVDP was increased, regional differences in dl/dt diminished. These results indicate that there is regional variation in the timing of the phases of diastole and in lengthening patterns of the left ventricle. The volume-dependent variation in lengthening rates that we observed is consistent with the concept of regional differences in elastic recoil, which may contribute to active ventricular filling.

Animals↗
PubMed1980

Enhanced left ventricular shortening during chronic volume overload in conscious dogs.

Prior work with the arteriovenous fistula model indicates that left ventricular performance is at least normal and may be enhanced during chronic volume overload. The present study was undertaken in conscious dogs to determine whether ejection-phase indices of ventricular function are enhanced after 1 mo of volume overload, using an experimental design in which loading conditions could be accounted for and animals were used as their own controls before and after volume overload. We also examined the response of the volume-overloaded left ventricle to an afterload stress and the role of adrenergic stimulation in maintenance of function. Both at rest and during hemodynamically matched conditions, percent shortening (ultrasonic dimension gauges) and mean shortening rates were increased during volume overload. This difference was maintained during phenylephrine-induced blood pressure elevation, although diastolic dimensions increased more in control studies during phenylephrine. Propranolol produced significantly larger reductions in these indices during volume overload than in the control state. Thus, ejection-phase function is enhanced during volume overload, at least in part due to increased adrenergic stimulation.

Animals↗