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W Y Lew

Publications and source records attributed to W Y Lew.

At least 37 records · Page 2Linked to original sources
PubMed1993

Mechanisms of volume-induced increase in left ventricular contractility.

Volume-induced increases in left ventricular (LV) contractility were studied in 18 anesthetized dogs. Denervation eliminated cardiac reflexes, and hearts were paced at 100 +/- 9 (SD) beats/min. Acute volume loading increased LV end-diastolic pressure from approximately 4 to 14 mmHg within 1 min. Contractility increased over 10 min as measured by a decrease in end-systolic length (ESL) (sonomicrometer) at matched LV end-systolic pressure (ESP) or increase in LVESP measured at matched ESL. Volume-dependent increase in contractility was not attenuated by verapamil (0.3 +/- 0.2 microgram/kg i.v., n = 6) or myocardial stunning (15 min ischemia, 30 min reperfusion, n = 6) but was attenuated by ryanodine (1-16 micrograms/kg i.v., n = 6), which alters calcium release from the sarcoplasmic reticulum. From 1 to 10 min after volume loading, LV anterior ESL (measured at LVESP 132 +/- 12 mmHg) decreased by 6.7 +/- 0.5% before, but only by 4.0 +/- 1.7% after 1 microgram/kg ryanodine (P < 0.05). The LVESP (measured at anterior ESL 11.6 mm) increased 32 +/- 4 mmHg before, but only by 17 +/- 12 mmHg after 1 microgram/kg ryanodine. In conclusion, acute volume loading produces a time-dependent increase in LV contractility, which is mediated in part by an increase in calcium release from the sarcoplasmic reticulum.

Animals↗
PubMed1993

Cellular mechanisms of endotoxin-induced myocardial depression in rabbits.

We investigated the mechanisms by which endotoxic shock induces intrinsic myocardial depression by studying cardiac myocytes isolated from 10 anesthetized instrumented rabbits given 172 +/- 42 (mean +/- SD) micrograms/kg IV endotoxin. Left ventricular (LV) depression developed 4 +/- 1 hours after endotoxin administration, with a 15 +/- 4% increase in LV internal end-systolic diameter, measured with sonomicrometers at a matched LV end-systolic pressure of 65 +/- 10 mm Hg. Normal LV pressure, arterial PO2, and pH were maintained to minimize confounding effects of ischemia, hypoxia, and acidosis. Cardiac myocytes from endotoxin-exposed rabbits had less unloaded cell shortening and lower peak rates of cell shortening (-dL/dt) and lengthening (+dL/dt) at [Ca2+] levels ranging from 0.5 to 16 mM when compared with myocytes isolated from normal rabbits or rabbits undergoing an identical protocol but without exposure to endotoxin. At 2 mM [Ca2+], cell shortening was depressed by approximately 25% because of a decrease in action potential duration (207 +/- 70 versus 375 +/- 64 milliseconds). In contrast, there was only mild impairment of sarcoplasmic reticulum (SR) function. When myocytes were restimulated after rest periods of 4 to 480 seconds, the decrement in cell shortening (rest decay), peak -dL/dt and peak +dL/dt, and the recovery from rest decay were similar in myocytes from endotoxin-treated and normal rabbits. There was a greater decrement in cell shortening in the second beat of postrest recovery in myocytes from endotoxin-treated rabbits than in normal myocytes. This was partly due to a 12% decrement in action potential duration with rest decay, which did not occur in normal myocytes. The SR Ca2+ content assessed by contractures in 10 mM caffeine was similar in the two groups. We conclude that endotoxic shock produces a LV depression in vivo that persists in isolated myocytes studied in vitro. This intrinsic myocardial depression is largely related to endotoxin-mediated sarcolemmal alterations, which shorten action potential duration, and is not due to alterations in SR function.

Acidosis↗
PubMed1991

Influence of systolic pressure profile on rate of left ventricular pressure fall.

We examined the influence of the systolic left ventricular pressure (LVP) waveform on the rate of isovolumetric LVP fall, as assessed by the time constant tau. Seven open-chest dogs were instrumented with a micromanometer in the left ventricle, with segment length gauges in the anterior and posterior midwall of the left ventricle, and with a balloon-tipped catheter in the proximal aorta. The intra-aortic balloon was inflated before the onset of ejection (early) or during midejection (late) to produce timed and graded increases in peak LVP of 2-20 mmHg. The rate of LVP fall slowed significantly more with late than with early increases in LVP (tau increased 1.5 +/- 0.5 vs. 0.5 +/- 0.3%/mmHg increase in peak LVP, respectively, P less than 0.001). For a similar increase in peak LVP, there was a progressively greater increase in tau when the timing of balloon inflation was progressively delayed from early to late ejection (in 10-ms increments). The differential effect of early vs. late pressure increases on tau was not related to regional differences in segment length behavior nor to an increase in regional nonuniformity between anterior and posterior sites. We conclude that under the experimental conditions of an intact, ejecting left ventricle, the systolic pressure profile is an important determinant of the rate of pressure fall. The rate of LVP fall slows in direct proportion to the magnitude of increase in systolic pressure. The sensitivity to systolic load increases progressively throughout the ejection period, so that the rate of LVP fall slows significantly more with late than with early pressure increases.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1991

Transmural myocardial deformation in the ischemic canine left ventricle.

The myocardium is a complex three-dimensional structure consisting of myocytes interconnected by a dense collagen weave that courses in different directions. Regional ischemia can be expected to produce complex changes in ventricular deformation. In the present study, we examined the effects of ischemia on two- and three-dimensional finite strains during acute transmural myocardial ischemia in 13 open-chest anesthetized dogs. In contrast to systolic deformation observed during the control period in which circumferential shortening exceeded longitudinal shortening, our results indicate that after 5 minutes of acute ischemia, end-systolic in-plane lengthening across the left ventricular wall occurs in approximately equal amounts in the circumferential and longitudinal directions. Along with these changes in extensional strains, there were significant negative transverse shearing deformations during ischemia. Myocardial ischemia also resulted in a loss of the normal end-systolic transmural gradients of shortening and thickening. Three-dimensional end-diastolic strains indicate that the left ventricular wall undergoes a significant passive reconfiguration that varies transmurally with lengthening in the epicardial tangent plane and wall thinning increasing from the epicardium toward the endocardium. The large systolic changes in shearing deformations with ischemia could potentially influence collateral blood flow and certainly indicate that uniaxial measurements of deformation in the ischemic myocardium, which do not account for shearing deformation, are incomplete and must be interpreted with caution. Moreover, normal transmural systolic gradients in deformation, which would be anticipated on geometric grounds, are lost during ischemia, implying that the material properties of ischemic tissue or the loading conditions imposed on the ischemic region by partially impaired adjacent myocardium vary transmurally.

Animals↗
PubMed1991

Dihydropyridine receptors are primarily functional L-type calcium channels in rabbit ventricular myocytes.

We measured [3H]PN200-110 binding and patch-clamp currents in rabbit ventricular myocytes to determine if there is a disparity between the density of dihydropyridine-specific receptors and functional L-type calcium channels, as has been reported for skeletal muscle. The dihydropyridine receptor density was 74.7 +/- 4.2 fmol/mg protein (mean +/- SEM, Kd = 1.73 +/- 0.29 nM, n = 6) in ventricular homogenates and 147 +/- 6 fmol/mg protein (Kd = 1.15 +/- 0.16 nM, n = 4) in myocytes. Ventricular homogenates contained 121 +/- 9 mg protein/g wet wt (n = 7). These values were used to calculate a dihydropyridine receptor density of 12.9 dihydropyridine sites/micron2 for ventricular homogenates and 14.8 dihydropyridine sites/micron2 for myocytes. The number of functional L-type calcium channels (N) was calculated from measurements of whole-cell current (I), single-channel current (i), and open probability (po), where N = I/(i x po). We measured sodium current through calcium channels (I(ns)) to avoid calcium-induced inactivation. Whole-cell (I(ns)) and single-channel (i(ns) and po) measurements were obtained under similar ionic conditions at a test potential of -20 mV. In six cells, the peak I(ns) was approximately 105 pA/pF. The single-channel conductance was 40.8 +/- 2.6 pS (n = 12), and i(ns) at -20 mV was 1.96 pA. The mean po at -20 mV was 0.030 +/- 0.002 in 16 patches in which only a single channel was evident. The calculated density of functional L-type calcium channels was approximately 18 channels/micron2.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Independent influence of left atrial pressure on regional peak lengthening rates.

We examined the influence of left atrial pressure on regional peak lengthening rates in six open-chest dogs. Sonomicrometers were implanted in the midwall of the anterior apex, the midanterior wall, and the posterior wall of the left ventricle. A bolus of blood was injected into the left atrium during ventricular systole by a computer-driven power injector to produce an isolated increase in left atrial pressure without altering the peak rate of left ventricular pressure fall, regional systolic shortening, or end-systolic length. Several left atrial injections of different volumes were performed over a wide range of left ventricular end-diastolic pressure (LVEDP) (from 7 to 22 mmHg). The peak lengthening rate increased in direct proportion to the increase of left atrial pressure. This effect was significantly greater in the apical than midanterior or posterior sites and decreased at all sites at higher LVEDP. Similar size left atrial injections produced greater increases in atrioventricular pressure gradient but smaller increases in left atrial pressure at low compared with high LVEDP. We conclude that left atrial pressure is an independent determinant of regional peak lengthening rates in the intact left ventricle. The influence of left atrial pressure is attenuated at higher LVEDP because of a smaller change in the diastolic pressure gradient, although viscoelastic effects may play a role.

Animals↗
PubMed1990

Finite strains in anterior and posterior wall of canine left ventricle.

Piezoelectric crystals were implanted in the anterior and posterior midwall of the left ventricle in six anesthetized dogs to compare regional two-dimensional finite deformations. Increasing left ventricular end-diastolic pressure (LVEDP) from 3 to 18 mmHg caused a similar expansion in the end-diastolic configuration (similar end-diastolic principal strains), but maximal lengthening was more circumferential in the anterior wall (-18 +/- 13 degrees) and more longitudinal in the posterior wall (-54 +/- 19 degrees). End-diastolic in-plane shears were negative in both regions, consistent with a left-handed diastolic torsion. As LVEDP increased, maximal shortening strains increased similarly (similar end-systolic principal strains), but there was a preferential increase in end-systolic circumferential strain in the anterior wall and preferential increase in longitudinal strain in the posterior wall. End-systolic in-plane shears were small and positive in both regions. The circumferential strain accurately reflected maximal end-diastolic and end-systolic principal strains in the anterior wall at mid and high LVEDP but underestimated the maximal end-diastolic principal strain by 50% and the maximal end-systolic principal strain by 30% in the posterior wall at all LVEDPs. We conclude that the magnitude of end-diastolic and end-systolic strains is similar for anterior and posterior walls over a wide range of LVEDP. However, there are regional differences in the directions of maximal deformation that should be considered when evaluating regional ventricular function.

Animals↗
PubMed1989

Influence of nonuniformity on rate of left ventricular pressure fall in the dog.

We examined the influence of nonuniformity in regional ventricular function on the rate of left ventricular pressure fall in 10 anesthetized dogs. Ultrasonic segment gauges were implanted in the midwall of the anterior, lateral, and posterior left ventricle. In seven dogs, nonuniformity was produced by infusing isoproterenol (0.4 microgram/ml) into the mid-left anterior descending coronary artery at low flow (0.5 +/- 0.7 ml/min) and high flow (1.5 +/- 1.2 ml/min) rates, for total doses of 0.1 +/- 0.1 and 0.3 +/- 0.2 micrograms, respectively. This produced a dose-dependent increase in anterior segment shortening so that shortening was completed earlier and marked segment lengthening occurred during isovolumic relaxation. Lateral and posterior segments were not directly stimulated. The heart rate, left ventricular end-diastolic pressure, and peak systolic pressure remained constant. However, tau, the time constant of left ventricular pressure fall, increased from 32 +/- 8 to 37 +/- 10 ms with the low dose, and from 35 +/- 6 to 49 +/- 12 ms with the high dose of isoproterenol. Similar results occurred in two dogs when isoproterenol was infused into the proximal, mid, or distal left anterior descending and in three dogs with infusions in the left circumflex coronary artery. We conclude that nonuniformity of regional left ventricular function is an important and independent factor regulating the rate of pressure fall in the intact ejecting left ventricle.

Animals↗
PubMed1989

Nonuniformity and volume loading independently influence isovolumic relaxation rates.

We examined the influence of loading conditions and nonuniformity of left ventricular (LV) function on the rate of LV pressure fall in seven anesthetized dogs. Loading conditions were altered with vena cavae occlusions and/or intravenous infusions of dextran. Nonuniformity was produced by injecting 8-20 ng of isoproterenol into the mild left anterior descending coronary artery to produce an asynchronous and early onset of segment lengthening in the anterior wall. Temporal and regional nonuniformity were quantified with indexes derived by comparing segment lengths in the anterior and posterior walls, measured with midwall sonomicrometers. The rate of LV pressure fall was assessed with peak -dP/dt, the time constant, tau, and the duration of isovolumic relaxation. Volume loading decreased the rate of LV pressure fall without altering the nonuniformity indexes. Intracoronary isoproterenol produced nonuniformity and decreased the rate of LV pressure fall without altering global loading conditions. The effects of isoproterenol (in a constant dose) were similar irrespective of the LV volume. We conclude that in the intact, ejecting left ventricle, loading conditions and nonuniformity are important determinants of the rate of LV pressure fall, but these two factors exert their influence by mechanisms that are largely independent.

Animals↗
PubMed1988

Fine needle aspiration cytology: its role in the management of breast tumours.

Fine needle aspiration (FNA) cytology is a cost-effective and clinically reliable tool in the management of breast tumours. This report summarizes the experience with 364 patients who had FNA of the breast. There was a total of 115 cancers of which 108 (93.9%) were diagnosed on FNA. There were no false positives amongst aspirates diagnosed as 'malignant'. Thirty-one patients had mastectomy with prior frozen section and nine had advanced or recurrent disease with no biopsy confirmation. FNA was 'suspicious of malignancy' in 12 patients of which 10 were malignant and two were benign on histology. There were 216 patients with 'benign' FNA and 28 FNA were 'unsatisfactory'. Biopsy confirmation was recommended in all clinically malignant or doubtful cases. Forty-one (19%) of the patients with 'benign' FNA and 13 (46%) of the 'unsatisfactory' group had excision biopsies which revealed six cancers, giving a false negative rate of 5.2%. FNA cytology gives rapid and reliable results which contribute towards planning of further management of the patient. It can replace the more painful tru-cut biopsy and reduce the need for excision biopsy and frozen section in the initial diagnosis of breast tumours. It is also an effective modality to monitor and confirm suspected recurrences. Although a negative FNA does not completely exclude malignancy, it can be used to reassure the surgeon and the patient and to support their decision not to operate.

Aged↗
PubMed1988

Functional consequences of acute anterior vs. posterior wall ischemia in canine left ventricles.

We compared the consequences of acute anterior and posterior wall ischemia on regional left ventricular function in seven open-chest dogs. Circumferentially oriented sonomicrometers were implanted in the midwall of the anterior and posterior left ventricle. The left anterior descending (LAD) and left circumflex (LCX) coronary arteries were each occluded for 3 min, with 45 min of reperfusion between the two occlusions. The ischemic areas at risk, as assessed by postmortem perfusion techniques, were similar for anterior (34.5 +/- 12.5 g) and posterior (32.3 +/- 9.4 g) wall ischemia. Both occlusions produced a similar increase in end-diastolic pressure. After LAD occlusion, total segment shortening (end diastole to aortic valve closure) in the nonischemic posterior wall increased from 8.0 +/- 3.9 to 10.8 +/- 4.4%, solely caused by increased isovolumic shortening. In contrast, with LCX occlusion, total segment shortening in the nonischemic anterior wall increased significantly more, from 10.5 +/- 3.8 to 14.6 +/- 4.2% caused by nearly equal increases in isovolumic and ejection phase shortening. Thus, with both LAD and LCX occlusions, there was increased shortening in nonischemic areas during isovolumic systole, which was "wasted" in paradoxically stretching the ischemic zone. However, a compensatory increase in nonischemic area ejection phase shortening occurred only with LCX occlusions. These findings may explain the greater functional impairment that occurs with LAD than LCX occlusions.

Acute Disease↗
PubMed1988

Regional variation in pericardial contact pressure in the canine ventricle.

We studied eight open-chest dogs to determine whether there is regional variation in pericardial contact pressure (PCP). Flat, air-filled balloons were used to measure PCP simultaneously over the lateral walls of the right and left ventricles while cardiac volume was varied by dextran infusion. End-diastolic and mean PCP were significantly higher over the left than right ventricle at high (20.3 +/- 1.0 mmHg) and middle levels (13.7 +/- 0.9 mmHg) of left atrial pressure. At high left atrial pressures, the end-diastolic PCP over the lateral left ventricle was 9.1 +/- 2.4 mmHg compared with 4.3 +/- 2.3 mmHg over the lateral right ventricle (P less than 0.05). At middle levels of left atrial pressures, end-diastolic PCP was 6.2 +/- 3.5 mmHg over the left ventricle and 1.5 +/- 2.4 mmHg over the right ventricle (P less than 0.05). These variations in PCP persisted after severing the pericardial diaphragmatic attachments and after turning the dogs such that one or the other balloon was dependent. Regional distribution of PCP was studied by positioning a single balloon sequentially at multiple ventricular sites. PCP was consistently higher over the lateral wall of the left ventricle than either the anterior or posterior walls of the right or left ventricle. After aortic occlusion, end-diastolic PCP increased more over the left than right ventricle. In contrast, with pulmonary artery occlusion, end-diastolic PCP increased more over the right than left ventricle. Pericardial pressure varies regionally, and a single pericardial pressure may be an oversimplification when used to describe pericardial restraint on the cardiac volume.

Animals↗
PubMed1988

Technique for measuring regional two-dimensional finite strains in canine left ventricle.

We developed a technique to measure regional two-dimensional deformations in the myocardium. Three piezoelectric crystals were implanted in a triangular array in the left ventricular anterior midwall in six anesthetized dogs. Each crystal was used in a dual function, to both transmit and receive ultrasonic signals from the other two crystals. In this manner, the three segment lengths of the crystal triangle throughout the cardiac cycle were simultaneously recorded. The orientation of the crystal triangle with reference to the left ventricular long and minor axes was determined. The orientation and three segment lengths of the crystal triangle were used to calculate the circumferential strain E11, the longitudinal strain E22, the in-plane shear strain E12, and the mutually perpendicular principal strains E1 and E2. Also, the orientation of the first principal direction or the in-plane angle was determined, which was defined as the angle between the first principal direction (E1) and the circumferential direction (0 degree). This information fully describes the regional two-dimensional myocardial deformations. This technique was applied to measure regional myocardial deformations at three different left ventricular end-diastolic pressures (LVEDP) of 2 +/- 1 (mean +/- SD), 8 +/- 1, and 17 +/- 2 mm Hg. The first principal direction at end-systole was oriented away from the circumferential direction at low LVEDP (-43 +/- 21 degrees) but became progressively closer in each animal to the circumferential direction as LVEDP increased to mid (-26 +/- 18 degrees) and high (-14 +/- 13 degrees) levels. The end-systolic ratio E11/E1 was 0.6 +/- 0.2 at low LVEDP, but increased toward unity in each animal to 0.9 +/- 0.1 at mid and high LVEDP. Thus, at low LVEDP, the greatest systolic deformation occurred in a direction different from the circumferential orientation. Therefore, circumferential strain measurements (E11) significantly underestimated the greatest systolic deformation (E1). However, as LVEDP increased, the first principal direction rotated closer toward the circumferential orientation, and circumferential strain measurements adequately estimated the greatest systolic deformation. Nevertheless, the presence of significant amounts of shortening along either the longitudinal (E22) or the second principal direction (E2) in the midwall necessitated the use of the two-dimensional method. The change in end-diastolic configuration as LVEDP increased from 1 +/- 1 to 16 +/- 1 mm Hg was also examined. Unlike the end-systolic data, the end-diastolic first principal direction did not deviate significantly from the circumferential direction at any LVEDP.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1988

Time-dependent increase in left ventricular contractility following acute volume loading in the dog.

Acute volume alterations were produced in eight anesthetized dogs to determine if the contractility of the left ventricle is partially volume-dependent. Pressures were measured in the left ventricle with a micromanometer and regional ventricular function was measured with sonomicrometers implanted in the midwall of the anterior, lateral, and posterior left ventricle. Regional end-systolic pressure-length relations (ESPLR) were determined with transient venae cavae occlusions. The ESPLR data were fitted to a quadratic equation, then end-systolic lengths were compared at matched end-systolic pressures at multiple time periods after the acute load alterations. Bilateral vagotomy, carotid sinus denervation, and stellate ganglion denervation were performed to prevent reflex alterations in contractility. The heart was paced at a constant rate. In seven animals, dextran was infused intravenously over 77 +/- 23 seconds (+/- SD) to increase left ventricular end-diastolic pressure from 5 +/- 2 to 13 +/- 3 mm Hg and peak pressures from 113 +/- 11 to 147 +/- 18 mm Hg. The end-diastolic lengths increased 14 +/- 6% in the anterior, 9 +/- 2% in the lateral, and 12 +/- 4% in the posterior segments. The ESPLR was measured immediately (77 +/- 23 seconds), early (3 +/- 1 minutes), and late (10 +/- 2 minutes) after initiation of the volume load. In all three regions, there was a significant time-dependent leftward shift in the ESPLR. From 1 to 10 minutes after the volume load, the regional end-systolic lengths decreased by a mean of 4-6% when compared at a matched end-systolic pressure of 96 +/- 10 mm Hg, and decreased by 7-9% when compared at a matched pressure of 139 +/- 20 mm Hg. The end-systolic lengths immediately after the volume load were not significantly different from the control value (compared at a matched end-systolic pressure) but were significantly shorter 10 minutes after the volume load. The leftward shift of the ESPLR represented a true increase in contractility and not merely a recovery from a transient myocardial depression. A similar leftward shift in the ESPLR occurred in four animals after release of a partial venae cavae occlusion, producing an acute volume load without acute hemodilution. Acute volume loads in four animals treated with propranolol also produced a leftward shift in the ESPLR, ruling out the possibility that a time-dependent increase in circulating catecholamines was responsible for the alterations in contractility. In five animals, the ESPLR shifted to the right after a transient (1-2 minutes) decrease in venous return.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenergic beta-Antagonists↗
PubMed1988

Early gastric cancer: 52 cases of combined experience of two south Australian teaching hospitals.

Fifty-two patients with early gastric cancer are described. At presentation, the average age was 60 years and the male:female ratio was 3:2. The patients had presenting symptoms indistinguishable from those due to benign peptic ulcer disease. Endoscopic examination with multiple biopsies was the most accurate means of diagnosis, with an overall 93% detection rate. The tumours were located predominantly along the lesser curve (75%) and in the antrum (64%), with ulcerated or depressed lesions most common and flat lesions least common. Approximately 58% of lesions were of intestinal type, submucosal invasion was seen in 45% and lymph node metastases had occurred in 7% of cases. Lesser curve and antral lesions were more likely to be ulcerated. Ulcerated lesions were on average, the same size as non-ulcerated lesions. Body lesions were larger than antral lesions and lesions which had spread to the submucosa were larger than mucosal lesions. Diffuse-type lesions were more likely to be ulcerated than intestinal-type lesions and dysplasia was more commonly associated with intestinal-type lesions than with diffuse or mixed-type lesions. The crude 5-year survival rate was 80%, but only one death was associated with a recurrence of gastric cancer.

Adenocarcinoma↗
PubMed1987

Influence of ischemic zone size on nonischemic area function in the canine left ventricle.

The relationship between ischemic zone size and nonischemic area function was examined in seven anesthetized dogs. Regional ventricular function was measured with sonomicrometers implanted in the midwall of the anterior apex, posterior base, and posterior apex of the left ventricle. Ventricular volume was varied to three levels, corresponding to left ventricular end-diastolic pressures of 7, 12, and 19 mmHg. A small, moderate, and large area of anterior wall ischemia was produced with sequential occlusions of the distal, mid, and proximal left anterior descending coronary artery, respectively. Each occlusion was maintained for 15-30 min; then ventricular volume was varied to three levels, chosen so that end-diastolic segment lengths in the nonischemic areas were matched to their control (preischemia) values. With acute ischemia, paradoxical lengthening developed in the ischemic zone during isovolumic systole. This was accompanied by an increase in isovolumic shortening in the nonischemic areas. The amount of nonischemic area isovolumic shortening increased with increasing ischemic zone size, suggesting that more nonischemic area shortening was expended in paradoxically stretching the ischemic zone. With moderate and large areas of ischemia, the amount of "wasted" isovolumic shortening by nonischemic areas was greater at low than at high ventricular volumes. It is concluded that the ischemic zone imposes a mechanical disadvantage on nonischemic areas in direct relation to ischemic zone size and is inversely related to the ventricular volume.

Animals↗