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

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

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

Seventy patients with hypertonic disease (HD) in the IInd stage were examined echocardiographically 30 days and 6 months after macrofocal myocardial infarction with the view to study contractility of myocardium of the left ventricle depending on its mass. Increase of the left ventricle mass (LVM) in patients with HD after infarction was established to be associated with rise of myocardial contractility. Fall of the LVM occurs at the account of thinning of ventricular wall without changes in volumic parameters of the left ventricle.
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PMID:[Left ventricular mass of the myocardium and its contractile capacity in hypertensive patients in the postinfarct period]. 806 12

Ventricular remodeling is a pathologic change in the size and shape of the heart after myocardial infarction. Human and animal studies have described the mechanisms responsible for the thinning and enlargement that progresses for years beyond the initial infarction. As a result of elevations in preload and afterload, ventricular pressures increase, and changes occur in both the infarcted and uninfarcted regions of the ventricle, increasing overall heart size. Recent investigation has demonstrated that the initiation of angiotensin-converting enzyme (ACE) inhibitor drugs after myocardial infarction reduces both systolic and diastolic wall stresses, thereby averting changes in heart size. These findings are significant, as increases in heart size and ventricular volumes have proved to be powerful predictors of early mortality after myocardial infarction.
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PMID:The role of angiotensin-converting enzyme inhibitors in reducing ventricular remodeling after myocardial infarction. 810 96

In contrast to the established nuclear imaging techniques magnetic resonance imaging (MRI) is only in the early phase of its application to detect viable myocardium after myocardial infarction. Although MRI techniques have only recently been employed to assess residual myocardial viability three approaches have been described to achieve this purpose: First, the use of signal intensity changes on spin-echo images with and without the application of contrast media to define irreversible injury to the myocardium in acute and subacute infarcts; second, measurement of metabolite concentrations within the infarct area using magnetic resonance spectroscopy, and third quantitation of myocardial thickness and systolic wall thickening in chronic infarcts with and without positive inotropic stimulation. When applying magnetic resonance techniques to detect viable myocardium by imaging techniques, it is useful to distinguish between acute infarcts and chronic infarcts that are more than 16 weeks old. After the time, practically all infarcts have healed and the necrotic myocardium has been transformed into scar tissue. MRI seems ideally suited to detect and characterize chronic myocardial scar and distinguish it from viable but hibernating myocardium because it clearly depicts the regional wall thinning which is a typical feature of transmural infarcts (Figure 1). In contrast, more recent infarcts, even if they are transmural and fail to show any contraction during systole, may not yet exhibit myocardial thinning. Therefore, simply depicting the acutely injured myocardium by MRI is not sufficient to differentiate between necrotic and stunned, but viable myocardium. On the other hand, an increase in signal intensity of acutely infarcted myocardium, which appears on T2 weighted spin-echo MR images only a few hours after occlusion of a coronary artery, can be used to determine the extent of irreversible myocardial damage (Figure 2). It is not clear, however, whether this area of increased myocardial signal intensity that is seen within the first week after the event only represents necrotic myocardium or incorporates some edematous viable myocardium in the infarct border zone. After three weeks, true infarct size may be more closely approximated by the area of increased signal intensity because the edema surrounding the infarct has presumably regressed and signal abnormalities are restricted to the pathologically determined infarct area. More recently, new pulse sequences and high field magnets permit separate observation of the endocardial and epicardial portion of the left ventricular wall. This may further improve the detection of residual viable cells which are preferentially located near the epicardium.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Magnetic resonance tomography imaging techniques for diagnosing myocardial vitality]. 815 Apr 14

Reperfusion that is too late to salvage ischemic myocardium reduces early infarct expansion, and captopril therapy favorably alters long-term left ventricular remodeling. To study whether the beneficial effects of these two therapies are additive, we examined the effects of captopril therapy after late reperfusion on left ventricular remodeling after acute myocardial infarction. Female Sprague-Dawley rats (n = 67) were randomly assigned to one of four groups: group 1, sham surgery and no treatment; group 2, left coronary artery ligation and no treatment (myocardial infarction [r MI]); group 3, left coronary artery ligation, reperfusion 2 hours later, and no treatment (late reperfusion [LR]); and group 4, left coronary artery ligation, reperfusion 2 hours later, and captopril treatment (LR-Cap). Captopril therapy (2 gm/L of drinking water) was begun in the LR-Cap group in the immediate post-operative period and continued for 20 days. Twenty-one days postoperatively, hemodynamic measurements were made before and after volume loading. The rats were killed, their hearts were removed, and passive pressure-volume curves were obtained. The hearts were then fixed at a constant pressure for morphometric analysis. Compared with the MI group, the LR group had a lower expansion index and a higher thinning ratio. There were no differences in hemodynamics, left ventricular volumes, or other morphometric indexes between the two groups. Compared with the MI and LR groups, the LR-Cap group had lower peak left ventricular end-diastolic pressure, lower left ventricular volume, lower left and right ventricular weights, and a leftward shift of pressure-volume curves.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of captopril therapy after late reperfusion on left ventricular remodeling after experimental myocardial infarction. 815 12

It is not yet clear whether 99mTc-methoxyisobutyl-isonitrile (MIBI)-uptake is a reliable indicator of myocardial viability, and a threshold value, differentiating viable from scarred myocardium, in comparison to a morphological and functional standard of reference has not been defined. MIBI-uptake was quantified in 800 segments from 55 patients with angiographically proven coronary artery disease with and without a history of myocardial infarction. Viable myocardium was defined from gradient-echo magnetic resonance images (MRI) as regions with systolic wall thickening or an end-diastolic wall thickness above the mean value -2.5 SD of a healthy control group (n = 21). Scar was defined as end-diastolic wall thickness > 2.5 SD below the normal mean value and absent systolic wall thickening or wall thinning. Mean MIBI-uptake of viable (n = 676; 79 +/- 14%) and scar segments by MRI (n = 124; 31 +/- 16%) was significantly different (P < 0.001). Segmental MIBI-uptake vs end-diastolic wall thickness (r = 0.7) and systolic wall thickening (r = 0.71) yielded a fair correlation. The highest values as regards sensitivity and specificity of MIBI-uptake in predicting the presence of scar were 89% and 96% respectively for MIBI-uptake < or = 50%. However, of the 136 segments with MIBI-uptake < or = 50%, 26 (19%) were viable by MRI, resulting in a positive predictive accuracy for scar tissue of 81%. Of the 26 segments diagnosed as scarred by MIBI-SPECT but viable by MRI, 25 (96%) were located in the inferoseptal region. MIBI-SPECT seems useful in the detection of viable myocardium after anterior myocardial infarcts, but over-estimates scar in the inferoseptal regions. Perfusion defects in these regions could be confirmed or denied by additional evaluation of myocardial morphology and function by MRI or tissue metabolism by positron emission tomography (PET).
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PMID:Regional 99mTc-methoxyisobutyl-isonitrile-uptake at rest in patients with myocardial infarcts: comparison with morphological and functional parameters obtained from gradient-echo magnetic resonance imaging. 817 90

The usefulness of cine magnetic resonance (MR) imaging was evaluated in 41 patients with acute (4 cases), subacute (21 cases) and chronic (16 cases) myocardial infarctions on the basis of the findings of thallium-201 myocardial SPECT. The overall rate of diagnostic accordance between cine MR imaging and SPECT was 85.0% (408/480). It was highest at the middle of the left ventricle (89.0%, 146/164) and lowest at the base (82.7%, 129/156). Measurement of wall thickness using the images printed on films was possible in 87.1% of segments (418/480). There was a significant difference in end-diastolic wall thickness and %-thickening between the infarcted and non-infarcted sites except for the base of the left ventricle. However, diastolic wall thinning was not remarkable in acute cases of less than one week after onset. In these cases %-thickening may be useful. Partial volume averaging on MR imaging and the inaccuracy of SPECT findings at the base also made meaningful comparison difficult. The most important diagnostic findings of myocardial infarction on cine MR imaging were end-diastolic wall thinning and abnormal motion such as akinesis and dyskinesis. It is concluded that cine MR imaging is a useful noninvasive examination method for evaluating the status of cardiac function in myocardial infarction.
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PMID:[Diagnosis of myocardial infarction by cine MR imaging--a comparative study with thallium-201 myocardial SPECT]. 844 96

Collagen which is present in the myocardium in relatively small amounts is the most abundant structural protein of the connective tissue network. Its structural organization consists of a complex weave of collagen fibers that surrounds and interconnects myocytes, groups of myocytes, muscle fibers and muscle bundles. The conformation of interstitial fibrillar collagen makes it highly resistant to degradation by all proteinases other than specific collagenases. In hearts with myocardial damage secondary to myocardial infarction, chronic ischemia, inflammation, or cardiomyopathy, a complex sequence of compensatory events occur that eventually result in an adverse left ventricular remodeling. This continual state of remodeling is characterized by persistent collagenase activity, fibrillar collagen degradation, and progressive myocyte loss. The net effect is a shift in the balance between collagen synthesis and degradation which leads to an inadequate fibrillar collagen matrix, progressive ventricular dilatation and sphericalization with wall thinning and eventual congestive heart failure.
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PMID:Ventricular remodeling in heart failure: the role of myocardial collagen. 854 Apr 1


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