Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Coronary heart disease can be detected via echocardiography, if myocardial ischemia or infarction are present leading to segmental abnormalities of left ventricular function. The capability to demonstrate these regional changes is limited as far as TM echocardiography is concerned, whereas 2D echocardiography is more reliable. For this purpose, cross-sectional imaging of all segments in several planes is necessary. The complex mosaic of findings obtained in this way is best documented by means of a segmental scheme of representative sections. Infarct size then can be estimated by a segmental score. Depressed wall motion and systolic wall thickening are used as criteria for ischaemia and infarction. In the chronic phase, morphological changes can be identified additionally: Thinning, expansion and increased reflectivity of the infarcted areas. In acute myocardial infarction, echocardiography is mainly used if the course is complicated, in the chronic phase, if ECG-changes are questionable, or to evaluate residual ventricular function after large infarcts. Even the TM echocardiogram reliably estimates the ventricular damage caused by the infarct in the chronic phase.
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PMID:[Echocardiography in coronary heart disease]. 623 Jul 19

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

Quantitative regional wall motion analyses of 2-dimensional echocardiograms (2-D echo) have usually focused on large arcs (greater than 45 degrees) of the left ventricular (LV) perimeter rather than on small LV zones. Few studies have assessed changes in wall thickness. To determine normal ranges of regional LV function, the endocardial and epicardial contours of short-axis 2-D echoes obtained at the papillary muscle level of 10 normal subjects were manually traced. Then, 15 patients with acute myocardial infarction (MI) were studied, comparing their contours at admission with ranges determined from the normal subjects. In all patients with MI, 2-D echoes located abnormal wall motion involving at least the region identified as abnormal by the electrocardiogram and often extending into adjacent regions. All 9 patients with transmural MI had either decreased wall thickening or abnormal endocardial wall motion; all except 1 had focal thinning in the region of the MI. Of the 6 patients with nontransmural MI, 2 had abnormal endocardial wall motion, and all had decreased wall thickening. Evaluating regional wall motion at multiple points around the LV circumference should permit more precise delineation of LV function in health and disease than has been heretofore possible.
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PMID:Quantitative computer-assisted analysis of left ventricular wall thickening and motion by 2-dimensional echocardiography in acute myocardial infarction. 663 49

To determine whether piroxicam, a widely used, long-acting anti-inflammatory agent, causes scar thinning after acute myocardial infarction (MI), MI was produced in 16 anesthetized, open-chest dogs by ligation of the proximal left anterior descending coronary artery. The dogs were randomized into 2 groups and treated in a blinded fashion, 8 with piroxicam, 1 mg/kg i.v. at 15 minutes and at 3 hours after ligation (Group 1) and 8 with saline solution (Group 2). Two-dimensional echocardiograms were performed 7 days and 6 weeks after ligation. At 6 weeks, the dogs were killed and the hearts examined. Scar thickness was 7.1 +/- 0.3 mm in control dogs and 5.2 +/- 0.4 mm in piroxicam-treated dogs (p less than 0.01). The ratio of scar thickness to noninfarcted wall thickness was 0.87 +/- 0.03 (mean +/- standard error of the mean) in the control group, and was significantly lower (0.62 +/- 0.04) in the piroxicam-treated group (p less than 0.001). Regional function, expressed as the percent change in the area of the left ventricular cavity (% delta A) from short-axis 2-dimensional echocardiograms, was 42 +/- 3% 7 days after occlusion in the control group and was not significantly different in the treated group (34 +/- 5%). At the end of 6 weeks % delta A had improved in the piroxicam-treated group to 44 +/- 3% (p less than 0.05 compared with the value after 7 days), and was similar to % delta A of the control group at 6 weeks (43 +/- 3%). Thus, clinical doses of piroxicam administered early after MI caused moderate scar thinning, which was not associated with impairment of regional left ventricular function 6 weeks later.
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PMID:Morphologic and functional effects of piroxicam on myocardial scar formation after coronary occlusion in dogs. 669 91

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

Echocardiographic septal and posterior wall motion and thickness were measured in 55 subjects, of whom 20 patients with acute myocardial infarction, 20 with chronic coronary artery disease and 15 control subjects without evidence of cardiac disease. The results of the study that systolic thinning is indicative of an acute event. Abnormal changes in systolic wall thickening and wall motion occur commonly in patients with chronic coronary artery disease. Useful information about segmental wall motion abnormalities can be obtained from the echocardiogram when the areas involved can be visualized, but much of the ventricle is not routinely examined.
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PMID:Evaluation of segmental wall motion disturbances by echocardiography in ischemic heart disease. 726 82

Following prolonged ischemia, if not adequately reperfused, myocardium undergoes necrosis, scarring and thinning. The myocardium tends to dilate in the noninfarcted ventricular area, giving rise to ventricular remodelling. If the ischemic myocardium is adequately reperfused it can be saved and its temporarily depressed functions eventually be recuperated (viable myocardium). The extent of recovery of the postinfarction viable myocardium seems to affect ventricular remodelling. The integrity of the microcirculation of the non-contractile myocardium following prolonged ischemia is fundamental in maintaining a contractile reserve adequate enough for a functional recovery (myocardial viability). Protection of the microcirculation during ischemia-reperfusion is therefore of great importance for the role that the microcirculation plays in ensuring myocardial viability. Experimental studies and initial clinical observations showed that calcium-antagonists exert a beneficial effect in this respect. VAMI is a multicentre, randomized double-blind, placebo-controlled study whose aim is to ascertain the potentiality of verapamil in limiting regional functional damage in patients with acute myocardial infarction and undergoing early thrombolysis.
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PMID:[Myocardial viability in acute myocardial infarction and verapamil]. 763 65

Clinical and electrocardiographic features of 227 patients who died of an acute myocardial infarction (AMI) were compared with those of 150 survivors of a first AMI. Left ventricular (LV) free wall rupture was found in 93 patients aged > 50 years, but not in 134. The incidence of healed infarct (4 [4%] vs 50 [37%], p < 0.001), heart failure (11 [12%] vs 112 [84%], p < 0.001), and bundle branch block (11 [12%] vs 54 [40%], p < 0.001) was lower in patients with than without LV rupture. In patients with anterior AMI and early rupture (1 day), admission ST elevation was higher than in those with late LV rupture (> 1 day, 6.8 +/- 4.0 vs 4.0 +/- 2.7 mm, p < 0.01). However, lateral wall AMI had minimal ST elevation and accounted for 10% of ruptures. On day 2, the decrease in ST segment in patients with late LV rupture was less than in survivors (0.5 +/- 1.6 vs 3.2 +/- 2.9 mm, p < 0.001). Admission systolic blood pressure in patients who had early rupture was higher than in survivors (155 +/- 22 vs 137 +/- 22 mm Hg, p < 0.001) and in those with late rupture (135 +/- 23 mm Hg, p < 0.001). Late rupture was associated with infarct thinning and triggered by a physical strain in 18 of 45 patients (40%); infarct thinning, however, was present only in 4 of 48 patients (8%) with early rupture (p < 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relevance of electrocardiographic findings, heart failure, and infarct site in assessing risk and timing of left ventricular free wall rupture during acute myocardial infarction. 767 73

To investigate the clinical application of gadolinium diethylenetriaminepentaacetic acid (Gd-DTPA)-enhanced magnetic resonance imaging (MRI) in the management of acute myocardial infarction (AMI), we examined 44 patients with AMI within 1 month after onset. Enhanced images were classified into 4 types: nontransmural (type 1), transmural and homogeneous (type 2), transmural and marginal (type 3), and no enhancement (type 4). Each enhancement pattern was correlated with angiographic and thallium-201 imaging results. The redistribution images of thallium were graded on a 4-point scale from 0 (normal) to 3 (markedly reduced or absent activity). The percentage of the perimeter affected by asynergy was obtained from the left ventriculogram. Peak creatine kinase and the percentage of asynergic perimeter were significantly higher in type 3 than in other type patients. End-diastolic volume index was significantly higher in type 3 than in type 2 patients. Left ventricular ejection fraction was lowest, and end-systolic volume index, thallium-201 score, and incidence of wall thinning on MRI were highest in type 3 patients. Therefore, the transmural and marginal enhancement pattern (type 3) was compatible with extensive myocardial infarction with infarct expansion and less viable myocardium. In the other types, the infarction was small to moderate in size and left ventricular function was well preserved. Thus, Gd-DTPA-enhanced MRI may be useful in the evaluation of left ventricular function and myocardial viability of the infarct region after AMI.
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PMID:Gadolinium-enhanced magnetic resonance imaging in acute myocardial infarction. 788 81

The purpose of this study was to clarify whether the infarct expansion with cardiac rupture following acute myocardial infarction pathomorphologically differed from expansion without rupture. Eighteen autopsied patients with rupture were classified into acute phase (time between the onset of myocardial infarction and death < or = 36 h) and subacute phase (> 36 h). These patients were compared with 25 patients with no rupture using new parameters of expansion: radius index, cavity index, expansion area index and thinning-dilatation index of the left ventricle. In the acute phase, each parameter was significantly higher in the ruptured group than in the non-ruptured group (radius index: 0.49 +/- 0.28 vs 0.14 +/- 0.16, p < 0.005, cavity index: 0.21 +/- 0.09 vs 0.08 +/- 0.06, p < 0.005, expansion area index: 0.75 +/- 0.25 vs 0.34 +/- 0.23, p < 0.001, thinning-dilatation index: 2.89 +/- 1.31 vs 1.53 +/- 0.52, p < 0.001). However, in the subacute phase there were no differences in these parameters between the two groups. These data suggest that in the acute phase, but not the subacute phase, the degree of expansion and the proportion of expansion to infarcted area are associated with rupture.
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PMID:Clinico-pathological study of the role of infarct expansion in patients with cardiac rupture following acute myocardial infarction. 796 95


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