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

With the onset of ischemia, the length of myocardial segments increases rapidly, distorting ventricular geometry. Permanent stretching and thinning of infarcted zones have been termed infarct expansion. Although these changes are noted within minutes in vivo, infarct expansion may not be seen for days in postmortem preparations. The apparent postmortem reversal of early infarct expansion suggests that early expansion may be a functional phenomenon, reversible in the early hours of infarction. Alternatively, reversal of expansion may be a postmortem artifact, concealing the importance of underlying structural abnormalities. Myocardial infarction was produced in five dogs by occluding the left anterior descending coronary artery. Ultrasound sonomicrometers were used to measure myocardial segment end-diastolic length in the infarct and normal zones. After 3 hours of ischemia, the heart was arrested in diastole and biopsy specimens were taken from the normal and infarct zones. Sarcomere length was measured from electron photomicrographs, and myofiber width was measured from light photomicrographs. After 3 hours of ischemia, infarct zone segment length had increased significantly more than normal zone length (116 +/- 11 [SD] versus 103 +/- 4% of control length, p less than 0.05), whereas 2 minutes after cardiac arrest, both the infarct and normal zones returned to preischemic segment length, demonstrating apparent reversibility of early infarct expansion. However, histologic study revealed that the infarct zone myofibers were significantly thinner than normal zone myofibers (7.9 +/- 0.3 versus 9.4 +/- 0.3 micron, p less than 0.001) and sarcomere length in the infarct zone was significantly longer than that in the normal zone (1.9 +/- 0.2 versus 1.5 +/- 0.2 micron, p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Early infarct expansion: structural or functional? 403 Dec 98

The validity of X-ray CT in the functional diagnosis of several cardiovascular diseases was evaluated. CT was useful for assessing the amount and the characteristics of intrapericardial fluid, and it was also useful for the diagnosis of cardiac tamponade and constrictive pericarditis. A dynamic scan was found to be useful for determining the location, direction and the magnitude of intracardiac shunts, and for differentiating the true lumen from the false lumen in dissecting aortic aneurysms. As direct evidence of myocardial infarction, a filling defect in the infarcted area and late enhancement of the same area on delayed scan were noted. Regional wall motion abnormalities could be demonstrated by ECG gated CT, and other findings such as myocardial thinning, ventricular aneurysm and mural thrombi in the infarcted area were documented.
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PMID:Advance of cardiac computed tomography--functional evaluation of the cardiovascular system. 405 36

The significance of a combined echocardiographic study of patients who survived myocardial infarction for evaluation of ventricular hemodynamic disturbances was shown. According to the ultrasonic B-scanning data the left ventricular end-diastolic and endsystolic volumes in such patients were increased, and ejection fraction values, delta S and VCF were markedly decreased. The most pronounced left ventricular pump and contractility dysfunctions occurred in transmural and anterior myocardial infarctions. During M-mode echocardiography in patients with posterior wall hypokinesia, the prolongation of isovolumic relaxation and contraction followed by the shortening of rapid filling was observed. A significance correlation between the prolongation of isovolumic relaxation and polygraphic T interval was found. The thinning of the left ventricular hypokinetic posterior wall was observed during the ejection period, and that of hypokinetic ventricular septum was seen within the cardiac cycle. The signs of more marked left ventricular dilatation with its decreased contractility were found in patients with systolic murmur recorded soon after myocardial infarction development. Such a murmur phonocardiographically recorded was a sign of mitral valve insufficiency.
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PMID:[Left ventricular function in patients who have had a myocardial infarct, based on echocardiographic study data]. 650 23

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

The purpose of this study was to determine if exercise undertaken during the phase of incomplete healing after myocardial infarction influences scar formation. Eighteen ether-anesthetized rats underwent coronary artery occlusion (CAO) and were paired by matching ECG infarct size as assessed by QRS morphology. One member of each pair was randomized to a nonswimming group (NoS) or a graded swimming (S) protocol group (up to 40 minutes of swimming per day) beginning 7 days after CAO. Twenty-one days after CAO, rats were reanesthetized, hearts were excised and examined under magnification, and were then sectioned for histology. Transmural scar thickness (mm) measured on gross pathologic specimens was thinner in the S rats (1.0 +/- 0.2, p less than 0.05) than in the NoS rats 1.4 +/- 0.3, p less than 0.05), while noninfarcted septal wall thickness (mm) was similar in the two groups (2.2 +/- 0.1 versus 2.1 +/- 0.1, respectively). The thinnest portion of the scar in S rats measured only 0.6 +/- 0.2 mm compared to that of NoS rats (1.1 +/- 0.3 mm, p less than 0.05). In this experiment exercise during the healing phase of acute myocardial infarction (AMI) caused thinning of the transmural scar.
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PMID:The effect of early exercise on myocardial infarct scar formation. 663 61

We have developed an ECG-gated NMR-CT, and used it with 16 patients. The saturation recovery images are not able to separate heart muscle from the blood pool, but in inversion recovery images, heart muscle can be differentiated from the ventricles. The region of myocardial infarction is revealed as wall thinning and/or wall motion abnormality. From the two-gated inversion recovery images (the end-diastole and end-systole images) we obtained, we evaluated a wall motion abnormality in the left ventricle, and calculated the ejection fraction of the left ventricle. This information was then compared with the findings of a nuclear medicine study carried out one week interval and which included 10 of the 16 patients tested with the ECG-gated NMR-CT. The wall motions in both methods are well correlated, with the exception of the inferior wall. The values of the ejection fraction in the NMR image were moderately low, but two modalities showed a satisfactory correlation (r = 0.85).
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PMID:ECG-gated NMR-CT for cardiovascular disease. 668 Feb 4

Cardiac anatomy was defined by gated nuclear magnetic resonance (NMR) imaging at a magnetic field strength of 3.5 kGauss in eight normal subjects and 10 patients with chronic myocardial infarctions. Multisectional imaging was performed with the spin-echo technique and encompassed most of the left ventricle in an imaging time of 5 to 12 min. In all subjects internal cardiac structure was well delineated without the use of any type of contrast medium. The myocardial wall-blood interface was sharply defined, resulting in visualization of trabeculations, papillary muscle, and chordal structures in both ventricles. In patients with ischemic heart disease, the extent of postinfarctional wall thinning, aneurysms, and mural thrombi were depicted on NMR images. Images obtained with the second spin-echo (delay time = 56 msec) demonstrated high signal intensity in regions of the left ventricular chamber adjacent to the site of aneurysms or infarctions; this finding suggested stasis of blood in a region of akinesis or dyskinesis. The results of this study show that gated NMR is feasible as a technique for imaging the human heart and is capable of demonstrating a variety of left ventricular abnormalities associated with chronic myocardial infarction. NMR is a completely noninvasive technique for clinical imaging of the cardiovascular system.
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PMID:Imaging by nuclear magnetic resonance in patients with chronic ischemic heart disease. 669 14

Conventional and enhanced computed tomographic (CT) examinations were performed in 103 patients with myocardial infarction for evaluation of the diagnostic usefulness of CT. After intravenous bolus injection of contrast material, an initial filling defect and late enhancement of the infarcted myocardium appeared on the cardiac CT images. These two findings were direct evidence of myocardial infarction; the former was found mostly in the patient with recent myocardial infarctions, and the latter was recognized both in those with recent and those with "remote" infarctions. Wall thinning at the site of infarction was found by enhanced CT mostly in patients with anteroseptal or extensive anterior infarctions, and was rarely found in patients with inferoposterior infarctions. Left ventricular aneurysms and ventricular thrombi were found by enhanced CT in 39 and 23 of the 103 subjects, respectively, and the sensitivity of CT in detecting intracardiac thrombi was higher than that of two-dimensional echocardiography. Calcification of the myocardium and pericardial effusion associated with myocardial infarction were also detected by conventional nonenhanced CT. Thus, cardiac CT was found to be a useful test in evaluating patients with myocardial infarction.
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PMID:The usefulness of x-ray computed tomography for the diagnosis of myocardial infarction. 673 78

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

Although much attention has been directed toward interventions which reduce myocardial infarct size, the effect of such agents on the healing phase of myocardial infarction is not well understood. The present study examines the effect of the nonsteroidal anti-inflammatory agent ibuprofen, previously demonstrated to be able to reduce infarct size, and of aspirin on the healing of experimentally produced myocardial infarcts. Thirty-nine anesthetized, open-chest dogs were subjected to proximal left anterior descending coronary artery occlusions for 6 weeks. Four groups of dogs were studied: (1) a control (untreated) group: (2) ibuprofen, 12.5 mg/kg intravenously 15 minutes and 6, 12, 18, and 24 hours after occlusion (high dose); (3) ibuprofen, 12.5 mg/kg intravenously 15 minutes and 3 hours after occlusion (low dose); (4) aspirin, 30 mg/kg intravenously 15 minutes and 3 hours after occlusion. The average thickness of the transmural scar and of the noninfarcted left ventricular wall was determined from multiple measurements of formalin-fixed left ventricular slices. The ratio of transmural scar to noninfarcted wall thickness was determined. In control animals the ratio was 0.87 with only 1 of 15 animals having a ratio less than 0.60. High-dose ibuprofen-treated animals had an average ratio of 0.59 (difference not significant [NS] compared with control values), with 6 of 9 animals having a ratio less than 0.60 (p less than 0.02 compared with control values). Low-dose ibuprofen-treated animals had an average ratio of 0.66 (p less than 0.05 compared with control values), with 4 of 8 animals having a ratio less than 0.60 (p = NS compared with control values). In the aspirin-treated animals, the ratio was 0.88 (p = NS compared with control values), with 0 of 7 animals having a ratio less than 0.60 (p = NS compared with control values). Although 1 of 22 animals had ratios less than 0.60 in the control and aspirin groups, 10 of 17 had ratios less than 0.60 in the ibuprofen-treated groups (p less than 0.001). Scars in treated animals did not differ from those in control animals histologically or by analysis of hydroxyproline content per unit weight. Thus, ibuprofen, a nonsteroidal anti-inflammatory agent which reduces infarct size, is shown to increase the incidence of scar thinning after myocardial infarction.
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PMID:Scar thinning due to ibuprofen administration after experimental myocardial infarction. 682 46


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