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

The potential of magnetic resonance imaging (MRI) to detect and localize acute myocardial infarction (AMI) in 27 patients a mean interval of 15 days after AMI was evaluated. Eighteen asymptomatic volunteers were also studied to determine the specificity of the observations. The diagnosis of AMI was established by conventional criteria; the infarct was localized by electrocardiography in all patients, technetium pyrophosphate scintigraphy in 19 and necropsy in 1 patient. MRI detected increased myocardial signal intensity in 88%, cavitary signal in 74% and regional wall thinning in 67% of the patients. At least 1 of these 3 features was seen in the area of the infarct in each patient. The sensitivity of these MRI observations was not influenced by location of the infarct or presence of Q waves. Asymptomatic volunteers also had increased myocardial signal in 83%, cavitary signal in 94% and wall thinning in 11% of cases. Some patients had these findings in myocardial segments not suspected of being involved by recent or remote AMI. It is concluded that AMI can be detected by MRI performed an average of 15 days after infarction. However, the hearts of normal volunteers and apparently normal myocardial segments of patients with AMI may have the MRI findings previously associated with AMI. Of these findings, wall thinning was the most predictive of and specific for AMI.
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PMID:Detection and localization of recent myocardial infarction by magnetic resonance imaging. 301 85

To determine 1) whether the effect of intravenous nitroglycerin (NG) therapy during acute myocardial infarction on creatine kinase infarct size is influenced by infarct location (anterior vs. inferior), timing (therapy less than 4 hours vs. greater than or equal to 4 hours after onset of pain), and dose response (mean blood pressure greater than or equal to 80 mm Hg vs. less than 80 mm Hg during the first 12 hours) and 2) whether NG therapy modifies infarct expansion, 310 patients were randomly allocated to NG (n = 154) and control (n = 156) groups. NG infusion was titrated to lower mean blood pressure by 10% in normotensive and 30% in hypertensive patients, but not below 80 mm Hg, and was maintained for 39 hours. Measurements included clinical variables, creatine kinase infarct size (geq) as well as left ventricular (LV) asynergy, LV ejection fraction, expansion index, and thinning ratio on serial two-dimensional echocardiography. Compared with controls, creatine kinase infarct size was less in the NG group (41 vs. 55 geq, p less than 0.001), in anterior (44 vs. 58 geq, p less than 0.05), and inferior (39 vs. 53 geq, p less than 0.025) NG subgroups, and in early than late NG subgroups (43% vs. 22% decrease). Other indexes of infarct size also improved (p less than or equal to 0.05) with NG compared with controls. Thus, by 10 days, LV asynergy was 40% less, LV ejection fraction was 22% more, and Killip class score was 41% less. A negative effect of mean blood pressure less than 80 mm Hg with NG was reflected in these indexes. In addition, expansion index increased (p less than 0.001) by 31% and thinning ratio decreased (p less than 0.001) by 17% in controls by 10 days but remained unchanged with NG. Infarct-related major complications were less frequent in the NG than the control groups: infarct expansion syndrome (2% vs. 15%, p less than 0.0005), LV thrombus (5% vs. 22%, p less than 0.0005), cardiogenic shock (5% vs. 15%, p less than 0.005), and infarct extension (11% vs. 22%, p less than 0.025). Mortality was less in NG than in control groups in-hospital (14% vs. 26%, p less than 0.01), at 3 months (16% vs. 28%, p less than 0.025) and 12 months (21% vs. 31%, p less than 0.05), but this advantage was only found in the anterior subgroups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intravenous nitroglycerin therapy to limit myocardial infarct size, expansion, and complications. Effect of timing, dosage, and infarct location. 313 26

To assess the usefulness of X-ray computed tomography (CT) and magnetic resonance imaging (MRI) in detecting and evaluating ischemic heart disease, conventional and enhanced CT were performed for 180 patients (150 with transmural infarction, 12 with subendocardial infarction, and 18 with angina pectoris). MRI examinations were performed for 38 patients (31 with transmural infarction, three with subendocardial infarction, and four with angina pectoris). With enhanced CT, two findings in the myocardium were direct evidence of myocardial infarction: 1. filling defects on the early scans, and 2. late enhancement of the myocardium on the delayed scans. The former were observed mainly at the sites of recent anterior myocardial infarction and the latter were seen in about half of the patients with recent and remote anterior myocardial infarctions. However, these findings were inadequately imaged in patients with inferoposterior infarction and subendocardial infarction. Among 137 patients with transmural infarction, enhanced CT revealed left ventricular aneurysms in 51 (37%) and ventricular thrombi in 26 (19%). ECG-gated MRI apparatus having a superconducting magnetic operating at 0.25 Tesla was used, and data for this study were collected using the single-slice spin echo technique. In eight of nine patients with acute myocardial infarction, gated MRI demonstrated the infarcted myocardium as regions of high signal intensity relative to that of the adjacent normal myocardium. Such a difference in MRI signal intensity was scarcely recognized in the chronic stage of myocardial infarction, but the indirect findings of infarction, such as regional wall thinning, wall motion disturbances, left ventricular aneurysms, and ventricular thrombi were easily detected using MRI. No characteristic finding was obtained by CT or MRI in patients with angina pectoris.
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PMID:[Diagnostic evaluation of ischemic heart disease by X-ray computed tomography and magnetic resonance imaging]. 342 26

The prognosis of patients with acute myocardial infarction is related to the infarction size. We evaluated the ability of a clinical technique, two-dimensional echocardiography, to assess infarct size based on the extent of regional contraction abnormalities. Conscious closed-chest dogs with preplaced coronary snares underwent permanent coronary occlusion. The animals were studied by two-dimensional echo 20 min and 2 days after occlusion. The extent of myocardial contraction abnormalities (systolic wall thinning instead of normal systolic thickening) was correlated with the infarct size determined pathologically. Some dogs had pressure-induced left ventricular hypertrophy. Extent of regional contraction abnormalities demonstrated by two-dimensional echo correlated well with infarct size both early (20 min) (r = 0.92) and late (2 days) (r = 0.94) after permanent coronary occlusion. Dyskinesis extent modestly overestimated the infarct size. The relationship between dyskinesis and infarct size were similar in both normal and left ventricular hypertrophied hearts. We then undertook a study to assess the effects of coronary reperfusion on dyskinesis-infarct size relationships. Conscious, closed-chest dogs underwent 1-2 h of coronary occlusion followed by 2-10 days of coronary reperfusion. Significant regional dyskinesis was present after 1-2 h of occlusion and decreased by 50-60% of the occlusion value after 2 days of reperfusion without further change in extent of dyskinesis between 2 and 10 days of reperfusion. Of importance, however, was that there was no significant correlation between infarct size and extent of regional dyskinesis by two-dimensional echo after reperfusion, either after 2 days (r = 0.09) or 10 days (r = 0.29) of reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Late effects of coronary reperfusion on regional left ventricular function. Can infarct size be estimated noninvasively? 353 3

Thirty of 32 cases with cardiac rupture (CR) complications in the myocardial infarction were found out of a total of 91 cases of acute myocardial infarction (AMI). The mean age of the ruptured group in females was significantly younger than that of the non-ruptured group. Twenty-one cases showed free wall rupture of the left ventricle, six perforation of ventricular septum and three double rupture. All cardiac ruptures occurred in cases of transmural infarction. The age of AMI was histologically estimated. Nine cases complicated within the first 24 hours of AMI showed rupture of the left anterior wall. CR in the periphery within the infarct occurred at any time during the first week after onset, and cases of the central rupture were increased in number after the 3rd day of AMI. Pathologic findings indicated that elevated wall tension was considered to be most closely related to the cause of CR. Thirty two cases of CR were classified into three types: (1) blowout type, (2) hemorrhagic dissecting type, and (3) thinning-with-rupture type. Hemorrhagic dissecting type was characterized by multiple endocardial ulcers and fissure canals extending from the ulcer with hemorrhage in the surrounding myocardium. Complex fissure was seen in two cases of this type.
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PMID:Classification of cardiac rupture complicated in myocardial infarction. Pathological study of 32 cases. 363 Jul 5

To verify the role of infarct expansion (IE) in ventricular septal rupture (VSR) after transmural acute myocardial infarction (TAMI), topographic parameters were measured using tomographic imaging with two-dimensional echocardiography (2-D echo) and computer-aided analysis in four groups of patients: 8 patients with VSR (Group 1); 24 patients with TAMI but no mechanical complications (Group 2); 11 normal athletes (Group 3); 5 adults with congenital ventricular septal defect (Group 4). Measurements made on end-diastolic outlines of mid-left ventricular (LV) short-axis images included: LV asynergy (akinesis and/or dyskinesis), expansion index (asynergy/nonasynergy-containing endocardial segment length), thinning ratio (asynergic/nonasynergic wall thickness), and new indexes of regional shape distortion (RSD) by quantifying the deviation of the actual asynergic segment from the ideal asynergic arc constructed using the nearly circular nonasynergic contour. In Group 1, clinical IE (hypotension, congestive heart failure, no signs of new infarction) preceded detection of the VSR and portable 2-D echo showed the VSR associated with LV asynergy, marked IE, and RSD. Although Groups 1 and 2 had similar LV asynergy (28.7 vs. 26.9% LV) and ejection fraction (38.9 vs. 41.8%), Group 1 had higher expansion index (1.50 vs. 1.17, p less than 0.05), lower thinning ratio (0.54 vs. 0.67, p less than 0.005), and higher RSD parameters (e.g., peak distortion, Pk or maximum radial distance from the ideal arc, 19.3 vs. 3.9 mm, p less than 0.01; area of distortion, Ad, 7.4 vs. 1.1 cm2, p less than 0.05) than Group 2. Groups 3 and 4 had normal regional and global function and no evidence of expansion, thinning, or RSD. Thus, IE with marked diastolic RSD on an early 2-D echo after TAMI might identify patients at risk for VSR.
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PMID:Role of infarct expansion in rupture of the ventricular septum after acute myocardial infarction: a two-dimensional echocardiographic study. 367 96

Alterations in afterload may occur during acute myocardial infarction (AMI), but it is unknown whether such alterations cause long-term changes in the left ventricular topography or alter healing of the AMI. AMI was produced by ligation of the left anterior descending coronary artery in open-chest dogs. Eight dogs were randomized to a methoxamine group with an infusion dose of 30 micrograms/kg/min starting 1 hour after ligation for 4 hours to increase systemic systolic pressure by 40 to 50 mm Hg, and 8 were randomized to a saline control group (n = 8). Seven days later the dogs were killed and the hearts examined. The ratio of infarct wall thickness to noninfarct wall thickness was 1.13 +/- 0.03 (mean +/- standard error of the mean) in control dogs and was 0.98 +/- 0.03 in the dogs treated with methoxamine (p less than 0.005). An expansion index was determined as previously reported and expansion was considered to have occurred if this index exceeded 1.09. The expansion index was 0.98 +/- 0.06 in the control group and 1.18 +/- 0.07 in the methoxamine group (p less than 0.05). Histologic analysis suggested a lag in the healing rate in the methoxamine-treated dogs. Thus, early, brief increases in afterload cause infarct expansion and thinning and appears to slow the early healing phase of AMI in dogs.
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PMID:Effects of transient increased afterload during experimentally induced acute myocardial infarction in dogs. 396

The healing phase of acute myocardial infarction (AMI) is initiated by proteolysis of necrotic myocardium, followed by infiltration of fibroblasts and deposition of collagen. To assess whether ibuprofen, a potent antiinflammatory agent, preserves existing collagen and enhances deposition of new collagen during infarct healing, biochemical and morphologic studies were made of experimentally induced myocardial infarcts in untreated rats and in rats treated with ibuprofen. All treated rats received 12.5 mg/kg of ibuprofen at 1, 6 and 18 hours after AMI. Group 1 rats underwent measurement of myocardial hydroxyproline (HP) content at 24 hours after AMI. Group 2 rats received ibuprofen, 12.5 mg/kg, twice a day for 2 additional days, with measurement of myocardial HP at 3 days (group 2a) or 21 days (group 2b) after AMI. Group 3 rats received ibuprofen, 12.5 mg/kg, twice a day for 6 additional days with measurement of HP content, or infarct size and degree of thinning at 21 days after AMI. Compared with untreated rats, ibuprofen-treated rats had significantly greater amounts of HP in the infarct at 24 hours (group 1, 8.9 +/- 2.2 nmol/mg dry weight vs untreated, 7.1 +/- 2.8 nmol/mg dry weight, p less than 0.04) and at 21 days (group 2b, 112 +/- 37 nmol/mg dry weight vs untreated, 91 +/- 39 nmol/mg dry weight, p less than 0.05, and group 3, 125 +/- 51 nmol/mg dry weight vs untreated, 91 +/- 39 nmol/mg dry weight, p less than 0.003). Substantial scar thinning was noted in all rats; no difference in scar thinning was noted between treated and untreated rats at 21 days after AMI.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of ibuprofen on the healing phase of experimental myocardial infarction in the rat. 400 5

In view of clinical interest in the efficacy of beta-adrenergic blockade during acute myocardial infarction (AMI), we have determined the long-term effect of therapy on scar formation after experimental myocardial ischemia. Intact anesthetized dogs underwent acute occlusion of the left anterior descending coronary artery, by means of a balloon catheter, which permitted monitoring of the aortic-peripheral coronary artery pressure gradient during the 4-hour period of balloon inflation. Practolol administration was begun 15 minutes after the onset of ischemia in group A. Control animals (group B) received procainamide to approximate the antiarrhythmic action of beta blockade. Only group A exhibited significant reduction in the ST segments during acute ischemia. Chronic therapy was maintained for 1 month and the mature scar formed in the myocardium was assessed after 4 months. The extent of subendocardial scar was similar in both groups but subepicardial scar formation was significantly less in group A. There was also a significant decrease in the percentage of total myocardium involved with scar in this treatment group. Although thinning of the left ventricular wall was similar for both groups in the central scar region, this process was significantly reduced at the lateral margin in group A. Thus, specific beta-receptor blockade during acute myocardial ischemia and sustained during the repair process can result in a reduced quantity and altered distribution of mature scar.
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PMID:Effects of beta-adrenergic inhibition on scar formation after myocardial infarction. 614 52

Systolic wall thickening abnormalities are sensitive indicators of ischemia and infarction. One purpose of this investigation was to assess the relation between coronary risk area, infarct size and wall thickening abnormalities (dyskinesia) using 2-dimensional echocardiography (2-D echo) in a closed-chest conscious dog model of acute myocardial infarction. The second purpose was to study the effects of systemic hypertension (SH) and left ventricular (LV) hypertrophy on these relations. Our hypothesis was that the infarct size and the extent of 2D echocardiographic dyskinesia would be quantitatively different in SH-LV hypertrophy, a condition in which coronary vascular reserve is diminished. Permanent circumflex coronary occlusion was performed in 15 conscious normal dogs and in 14 dogs with LV hypertrophy secondary to renal hypertension. Two-dimensional echocardiograms were obtained before, 20 minutes after and 2 days after coronary occlusion. The systolic wall thickening along 12 equidistant radii was analyzed in short-axis images. Percent dyskinesia on 2-D echo was defined as the percentage of radii showing systolic thinning. Infarct size was determined pathologically and risk area was determined angiographically. For a given risk area, coronary occlusion resulted in a larger infarction in dogs with SH-LV hypertrophy than in normal dogs (p less than 0.05). Two-dimensional echocardiographic dyskinesia correlated well with infarct size both at 20 minutes (r = 0.92) and 2 days (r = 0.94); dyskinesia modestly overestimated the infarct size and underestimated the risk area. The relations were similar in both normal and SH-LV hypertrophy groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relations between 2-dimensional echocardiographic wall thickening abnormalities, myocardial infarct size and coronary risk area in normal and hypertrophied myocardium in dogs. 622 35


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