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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of early short-term exercise on late scar formation of myocardial infarction is unknown. Therefore, rats anesthetized with ether underwent proximal left coronary artery occlusion. Infarct extent was assessed 24 hours later by electrocardiographic criteria (QRS morphology). Immediately after electrocardiography, the rats were divided into two groups. Group 1 rats (n = 8) were subjected to daily graded swimming (up to 45 minutes a day) starting 24 hours after coronary occlusion for a total of 7 days followed by 2 weeks of nonswimming. Group 2 rats (n = 7) served as a control group and were not subjected to swimming. Twenty-one days after coronary occlusion, the rats were anesthetized, their heart excised and wall thickness determined histologically. Noninfarcted septal wall thickness was similar in both Groups 1 and 2. A ratio for transmural infarcts was obtained from multiple measurements by dividing scar thickness by noninfarcted septal wall thickness. Ratio of scar thickness divided by noninfarcted wall thickness for the control (nonswimming) group was 0.48 +/- 0.05 (mean +/- standard error of the mean); however, in the exercise (swimming) group, there was marked scar thinning with a ratio of 0.25 +/- 0.02 (mean +/- standard error of the mean, p less than 0.001). Infarct extent assessed by planimetry as percent of left ventricular slices was similar in both groups. Thus, early short-term swimming exercise during the first week after experimental myocardial infarction even when followed by 2 weeks without swimming, has long-lasting effects on scar formation.
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PMID:Short-term exercise has a prolonged effect on scar formation after experimental acute myocardial infarction. 663 Jul 75

Two-dimensional echocardiographic measurements of regional left ventricular end-diastolic wall thickness and systolic wall thickening were studied during coronary artery occlusion and early after reperfusion and compared with measurements of regional myocardial infarct size. In 25 closed chest anesthetized dogs with left anterior descending coronary artery occlusion followed by reperfusion, the occlusion period was 3 minutes in group I (n = 4), 20 minutes in group II (n = 4), 60 minutes in group III (n = 5) and 180 minutes in group IV (n = 12). Infarct size in groups III and IV was quantitated using the triphenyltetrazolium chloride technique. After coronary occlusion, wall thickening was replaced by thinning in the center of the ischemic region at the midpapillary echographic short-axis section, and no improvement in function occurred up to 60 minutes after reperfusion, except in group I. Ischemic zone end-diastolic wall thickness did not change significantly from control to the end of the coronary occlusion period, except Group IV. At 60 minutes after reperfusion, end-diastolic wall thickness increased only slightly in groups I and II (by 7.2 and 0.24%, respectively), but a marked increase was observed in groups III and IV (by 41 and 50%, respectively). The percent change in ischemic zone end-diastolic wall thickness from before reperfusion to 60 minutes after reperfusion correlated well with the amount of myocardial necrosis in corresponding segments (r = 0.936, standard error of estimate = 11.4%); an increase in segmental end-diastolic wall thickness of more than 25% was generally associated with 20% or more segmental necrosis. It is concluded that significantly increased regional end-diastolic wall thickness early after reperfusion is associated with irreversibly damaged myocardium, and this might be used as an index of myocardial salvage.
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PMID:Increased regional end-diastolic wall thickness early after reperfusion: a sign of irreversibly damaged myocardium. 671 5

Hypertension and atherosclerotic coronary arterial obstruction frequently coexist in patients. However, the effect of increased aortic pressure on ischemic segmental dysfunction is not well understood. We studied the effects of aortic pressure increases on segmental left ventricular function during myocardial ischemia. Eighty-two dogs instrumented with three to six pairs of pulse-transit piezoelectric crystals were studied in an awake, unsedated state to measure segmental wall thickness. A pneumatic balloon occluder was positioned around the proximal left anterior descending artery (LAD). Thirty-three dogs underwent LAD occlusion and served as normotensive controls (group A). Group B dogs (n = 23) received a 6-hour infusion of phenylephrine (PE) beginning 5 minutes after LAD occlusion to increase aortic diastolic arterial pressure to 120-130 mm Hg; aortic pressure was then allowed to return to normal for the subsequent 18 hours. The eight dogs in group C received a 6-hour infusion of PE, but no coronary arterial occlusion was produced. In group D (n = 12), distal constriction of the thoracic aorta was maintained for 24 hours after LAD occlusion. Regional myocardial blood flow (RMBF) was measured with radioactive microspheres in six conscious dogs and both RMBF and intramyocardial PCO2 were measured in seven open-chest dogs to assess alterations in regional myocardial oxygen supply and demand. Segments of myocardium were arbitrarily grouped according to the amount of net systolic thickening (NET) present 5 minutes after LAD occlusion and before increasing aortic pressure: group 1 retained 67-100+% of control NET, group 2 0-67%, and group 3 less than 0% (paradoxic motion). In dogs receiving PE plus LAD occlusion and in dogs with aortic constriction and LAD occlusion, NET was transiently depressed in groups 1 and 2 compared with the normotensive cohort; 24 hours after occlusion, NET in groups 1, 2 and 3 did not differ significantly from that in the normotensive dogs. Systemic hypertension resulted in a significant increase in endocardial and midwall RMBF and, in seven open-chest dogs, decreased the intramyocardial accumulation of carbon dioxide after LAD occlusion. Increased aortic pressure in dogs without coronary occlusion produced reversible decreases in end-diastolic wall thickness, NET and LV dP/dt. Thus, the production of systemic hypertension with diastolic pressures of 110-120 mm Hg acutely or for 6 hours during evolving canine myocardial infarction does not appear to exert an important deleterious effect on myocardial oxygen supply and demand. However, 24 hours of mildly increased aortic pressure accentuates end-diastolic wall thinning in segments with paradoxic systolic motion and results in a failure of their return to control values at this period.
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PMID:Effects of systemic hypertension on ischemic and nonischemic regional left ventricular function in awake, unsedated dogs after experimental coronary occlusion. 679 86

A technique for epicardial mapping of segmental myocardial function at multiple sites over both right and left ventricles was developed using a high-resolution, 7.5-MHz, short-focus, miniaturized, M-mode echocardiographic transducer worn on the fingertip. Myocardial function was determined from the extent and time course of systolic thickening and diastolic thinning at each site mapped. The technique was characterized in an open-chest canine model of myocardial ischemia. Ischemia was induced by transient or permanent coronary occlusion in 17 dogs. Acute occlusions produced reduced segmental thickening within 10-15 seconds and, often, overt systolic thinning of ischemic myocardium. Rhodamine fluorescence perfusion maps were compared with echocardiographic maps in nine dogs. Segmental thickening was reduced in perfused segments adjacent to, but not involved by, ischemia, as well as ischemic segments. Reproducibility appeared satisfactory for quantitative analysis of grouped data on multiple segments, and qualitative analysis in individual segments. Initial human studies performed during coronary bypass surgery in 11 subjects showed echocardiographic abnormalities in the six patients with ventriculographic abnormalities and in four with normal ventriculograms. Transmural infarctions were akinetic, showing no change in thickness throughout the cardiac cycle. Hypokinetic segments distal to high-grade coronary stenosis were common, although most segments distal to stenosis contracted normally. Reversal of segmental contraction abnormalities by coronary bypass grafting was shown in three subjects, while worsening of function was seen in previously abnormal segments in two and in a previously normal segment in one subject. Epicardial echocardiographic mapping is a practical method for intraoperative assessment of myocardial function during coronary surgery in man that may enhance our understanding of the pathophysiology of coronary disease and the effects of coronary surgery.
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PMID:Epicardial mapping of segmental myocardial function: an echocardiographic method applicable in man. 698 15

Regional left ventricular function was studied serially by quantitative two-dimensional echocardiography (2-D echo) in 20 dogs after left anterior descending coronary artery ligation. Normal values for regional myocardial thickening were established in 20 healthy dogs and used as a standard to recognize abnormally contracting segments (ACS). In normal hearts, the mean percent thickening tended to increase from base (25.8%) to apex (34.0%), but showed considerable diversity from segment to segment (range 20.0-40.0%); nevertheless, at least some degree of thickening was seen in every segment. After coronary occlusion, myocardial segments either thinned or failed to thicken. At the papillary muscle level, there was an improvement in function between 2 and 48 hours, with thinning at 2 hours and thickening at 48 hours. Tissue infarct size (IS) determined at 48 hours was related to IS derived from a weighted summation of ACS at 2, 24 and 48 hours. At 2 hours, ACS considerably overpredicted and correlated poorly with tissue IS (25.3% vs 13.4%; r = 0.60); by 48 hours, IS predicted by ACS had decreased to 15.3% (p less than 0.05) and had an improved, but only fair correlation with tissue IS (r = 0.73, SEE = 4.9%). We conclude that there is considerable heterogeneity to myocardial thickening by 2-D-echo, but failure to thicken is not seen in the normal dog heart. In many dogs, the extent of myocardial dysfunction 2 hours after coronary ligation exceeds that seen later. Tissue IS is difficult to predict accurately from ACS. Since the amount of muscle dysfunction is not necessarily equivalent to the amount of tissue necrosis in acute myocardial infarction, ACS may be more appropriate used to tract the course of infarction rather than to predict IS.
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PMID:Serial evaluation of myocardial thickening and thinning in acute experimental infarction: identification and quantification using two-dimensional echocardiography. 708 4

Seven dogs were instrumented with a left ventricular micromanometer and pairs of ultrasonic crystals to measure left ventricular wall thicknesses (control and ischemic regions) and short and long left ventricular axes; cuff occluders were placed around the left circumflex coronary artery and the inferior vena cava. Measurements were performed at rest, after 2 min of partial and complete coronary occlusion, and 1 and 10 min after release of partial and complete coronary occlusion. Left ventricular wall thickness in the ischemic region showed reduced systolic thickening during partial coronary occlusion and systolic thinning during complete coronary occlusion. During diastole, at zero pressure (inferior vena cava obstruction) the left ventricular short axis was unchanged during partial coronary occlusion but significantly increased (creep) during complete coronary occlusion (P less than 0.05), whereas after release of both partial and complete coronary occlusion the short axis at zero pressure decreased significantly (P less than 0.025). Left ventricular wall thickness at zero diastolic pressure in the ischemic region was significantly thinner during complete coronary occlusion than during control and significantly thicker (reactive hyperemia) 1 min after release of both partial and complete coronary occlusion. The long left ventricular axis remained unchanged during the entire experiment. At end-diastole, the long/short axis ratio was normal during partial (1.72; control 1.68; NS) and complete coronary occlusion (1.69; NS), but it decreased significantly from control of 2.10 to 1.99 with partial coronary occlusion and 1.85 with complete coronary occlusion (P less than 0.01). The changes in the L/S ratio during partial and complete coronary occlusion were proportional to changes in left ventricular chamber volume (correlation coefficient 0.94). Our data show that left ventricular shape remains normal at end-diastole during partial and complete coronary occlusion but becomes significantly more spherical at end-systole, with reduction of the normal tendency for the ventricle to become more elliptical during systole. These elliptical and spherical shape changes of the left ventricle during partial and complete coronary occlusion appear to be closely related to the chamber volume.
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PMID:Left ventricular geometry during partial and complete coronary occlusion in the conscious dog. 711 5

The significance and usefulness of two-dimensional echocardiography (2DE) in the evaluation of superacute phase of myocardial infarction were studied in 13 dogs with coronary occlusion, and 2DE findings were compared with the hemodynamic indices. Myocardial infarction was produced by the occlusion of anterior descending branch of the left coronary artery in 13 anesthetized adult mongrel dogs. In 6 dogs, the end-diastolic area and percent fractional shortening (%FS) in each short-axis view of the left ventricle at the level of the mitral valve, chordae tendineae, papillary muscles, low papillary muscles and apex were measured during 60 minutes, and end-diastolic wall thickness of infarct area situated in the transitional zone between the septum and the anterior wall were compared with that of non-infarct area immediately and subsequent 60 minutes after occlusion. Positive dP/dt/P, time constant T and cardiac output were measured simultaneously with an echocardiographic study. Severe enlargement and expansion of the left ventricular cavity (ballooning) and a decrease of %FS and thinning of the left ventricular wall perfused by the occluded artery occurred immediately after occlusion and persisted during subsequent 60 minutes. Time constant T was significantly prolonged, while positive dP/dt/P and cardiac output were decreased immediately and continued up to 60 minutes after occlusion. 2DE findings corresponded well with the changes of cardiac function and hemodynamics determined simultaneously. We concluded that the detection of the left ventricular ballooning is important in the diagnosis of superacute phase of myocardial infarction in dogs.
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PMID:[Echocardiography in superacute phase of myocardial infarction: an experimental study]. 718 11

Nonlethal myocardial ischemia produces profound and long-lasting effects on regional ventricular function and metabolism (myocardial stunning) and protects against myocardial infarction from subsequent prolonged ischemia (ischemic preconditioning). Two-dimensional echocardiography (2DE) is an essential tool for quantitative analysis of regional and global left ventricular (LV) function during myocardial ischemia and reperfusion and the study of these phenomena. However, the inability to perform 2DE in the open-chest rat heart has seriously limited the use of this model. To investigate the effect of transient coronary occlusion on segmental wall motion and LV geometry, we employed a 20 MHz intravascular ultrasound catheter placed on the epicardial surface of the rat heart (n = 15) to yield 2DE images suitable for quantitative analysis. Three 2-minute left coronary occlusions were made, separated by 5 minutes of reperfusion, with imaging during occlusion and at 5 and 60 minutes of reperfusion. Ischemic and nonischemic wall thicknesses, LV cross-sectional area, estimated LV volume, and the fractional changes of these parameters were measured. In eight animals these values were also compared with necropsy measurements of wall thickness, LV cross-sectional area, and volume. LV and right ventricular structures were well visualized in short-axis cross-sectional images in all animals, and images suitable for quantitative analysis were obtained in 92% of the periods. Coronary occlusion caused immediate, marked LV cavitary expansion, which rapidly returned to normal by 5 minutes of reperfusion. Active systolic thickening of the anterior wall at baseline (47% +/- 3%) became passive thinning during occlusion (-6% +/- 2%) and recovered partially, to 30% +/- 3% at 5 minutes of reperfusion and 42% +/- 4% at 60 minutes (p < 0.0005 at 5 minutes of reperfusion vs baseline; p not significant at 60 minutes). Recovery of thickening after 5 minutes of reperfusion was not different after the first versus third occlusion (23% +/- 4% vs 30% +/- 3%; p = 0.19). Measurements made by 2DE correlated well with those made by necropsy, although wall thickness was slightly thicker by 2DE. We conclude that epicardial echocardiography with an intravascular ultrasound catheter provides quantifiable 2DE images in this model and yields accurate information on segmental wall thickening and ventricular geometry not available by other techniques. Left coronary occlusion in the rat is associated with marked global and segmental LV expansion, which rapidly reverses with reperfusion. Postischemic regional wall motion abnormalities are present after coronary occlusion as brief as 2 minutes and can be measured accurately. The effect of multiple brief occlusions is not cumulative.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Quantitative two-dimensional echocardiographic assessment of regional wall motion during transient ischemia and reperfusion in the rat. 775 1

Previous studies have demonstrated that transforming growth factor-beta (TGF-beta) can accelerate wound healing, inhibit free radical formation and limit myocardial ischemia/reperfusion injury in a variety of experimental models. However, it is unknown whether exogenous TGF-beta 1 can attenuate the prolonged contractile dysfunction that is observed after a brief, reversible ischemic insult (myocardial stunning). Thus, open-chest dogs undergoing a 15-min left anterior descending coronary artery occlusion and 4 h of reperfusion were given TGF-beta 1 as an intravenous bolus (250 micrograms) at 24 h and again at 1 h before coronary occlusion (n = 5). Control dogs (n = 7) received equivalent amounts of vehicle. The two groups were similar with respect to occluded bed size, collateral blood flow and rate-pressure product. Fundamental physiological parameters, such as body temperature, arterial pH, PO2 and hematocrit, were within normal limits throughout the experiment. In control dogs, regional myocardial function (assessed as systolic thickening fraction) remained depressed throughout the 4 h reperfusion period, indicating severe myocardial stunning. TGF-beta 1 did not produce any significant improvement in the recovery of regional function; 4 h after reperfusion, paradoxical systolic thinning was still present in both treated and control groups, with thickening fraction being -22.5 +/- 6.1% and -31.0 +/- 5.3% of baseline, respectively (P = N.S.). These results demonstrate that a large dose of TGF-beta 1 given before ischemia fails to attenuate myocardial stunning in the open-chest dog, suggesting that this growth factor does not exert protective effects in the setting of reversible myocardial ischemia/reperfusion injury.
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PMID:Effect of transforming growth factor-beta 1 on myocardial stunning in the intact dog. 834 Sep 31

Left ventricular hypertrophy is an adaptive response to long standing hypertension. However, the influence of left ventricular hypertrophy with hypertension on extent of infarct expansion has not been studied. We compared the effects of left ventricular hypertrophy with hypertension on infarct expansion in spontaneously hypertensive rats (SHR, n = 76), Wistar-Kyoto rats (WKY; n = 46) and spontaneously hypertensive rats treated with delapril, an angiotensin converting enzyme (ACE) inhibitor (SHRD; n = 39). The survival rates at 7 days after myocardial infarction were 41%, 24%, and 46% for WKY, SHR, and SHRD. The survival rate of SHR was significantly lower than those of both SHRD and WKY (P < .05). In the surviving rats (18 SHR, 19 WKY, 18 SHRD), both left ventricular cavity area (LCVA) and the infarct segment length per the noninfarct segment length (FW/IVS), measured as indices of left ventricular dilation, were significantly less in SHR and SHRD than in WKY, and the thickness of the left ventricular free wall (Wth), used as an index of left ventricular thinning, was significantly higher in both SHR and SHRD than in WKY (P < .01). However, there was no significant difference in FW/IVS, LCVA, and Wth between SHR and SHRD. Hemodynamic findings 1 week after coronary occlusion demonstrated that all rats were in heart failure, and there were no significant differences in hemodynamics among the three groups. In conclusion, our findings showed that hypertrophy with hypertension reduced infarct expansion, but that reduction of blood pressure by ACE inhibitor did not reduce infarct expansion more than hypertrophy did. However, this finding suggest that an ACE inhibitor may improve the rate of survival of patients with left ventricular hypertrophy with hypertension.
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PMID:Effects of chronic hypertension and left ventricular hypertrophy on the extent of infarct expansion in rats. 886 21


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