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)

Under basal conditions the echocardiographic findings in anginal patients (pts.) without previous myocardial infarction appears usually normal. Consequently, the usefulness of the ultrasounds evaluation in angina pectoris has been commonly considered poor and the utilization of this technique in coronary artery disease has been restricted to the detection of myocardial infarction in its acute phase or to its chronic mechanical alterations. The purpose of this study was to assess the possibility offered by M-mode echocardiography to detect changes caused by transient myocardial ischemia at rest in man, in view of the possible diagnostic application of this technique. The reported results were obtained from 25 ischemic attacks (13 spontaneous and 12 ergonovine induced) with ST segment elevation or pseudonormalization of a basally negative T wave at rest. The semiautomatic computerized analysis of echocardiograms continuously recorded during these attacks showed a reduction of motion and of systolic thickening, accompanied by a diastolic thinning of the wall involved by the ischemia. These changes occur very early: they appear few seconds before ECG changes and are accompanied by a reduction of contraction and relaxation dP/dt and precede the onset of chest pain; moreover, they are followed by an increase in left ventricular internal diameters. In conclusion M-mode echocardiography is a sensitive technique capable to detect transient myocardial ischemia in the course of spontaneous or induced angina with ST segment elevation or positivity of negative T wave. This approach could be helpful in the diagnostic evaluation of patients with atypical chest pain and/or aspecific ECG changes and it can be complementary to other non invasive techniques such dynamic ECG and nuclear cardiology techniques.
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PMID:[Diagnosis of transient acute myocardial ischemia in man by M-mode echocardiography (author's transl)]. 732 34

Dynamic changes in left ventricular wall thickness represent a function of the myocardium which can be described, in normal subjects or in disease, without reference to behavior of other parts of the wall. Abnormalities of amplitude, rate and timing of wall thickness change interact in influencing overall ventricular performance, so that even this local function cannot be expressed as a single "index". Infarcted and acutely ischemic myocardium display reduced amplitude of thickness change. The degree to which they also show delayed wall dynamics in man is uncertain. Cross-sectional echocardiography has not been used to examine this aspect of regional thickness change, mainly because of the difficulties of processing "real-time" images. In the stable state of ischemic heart disease, such as exists in patients with angina, abnormalities of timing are common, even in the absence of significant reduction in overall thickness change, and lead to impaired energy transfer from the myocardium to the circulation. The degree of organization involved in normal myocardial function is better appreciated when one considers the complex phenomena which result from its disruption. In particular, rapid wall thinning in early diastole, normally associated with rapid filling, is revealed as an inherent property of the wall when it becomes dissociated from filling because relaxation is incoordinate. This demonstration of the active processes involved in ventricular relaxation provides an example of how the study of ischemic heart disease, in its differing local effects, may provide insight into the normal physiology of the myocardium.
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PMID:Wall thickness changes considered as regional myocardial function in ischemic heart disease. 745 Jun 62

In the past, hypertensive heart disease was the principal cause of congestive heart failure, but currently ischemic heart disease is the major etiologic factor. In the last 20 years, the role of myocardial infarction (MI) and the subsequent alteration in ventricular architecture of the infarcted and noninfarcted myocardium have become increasingly associated with a phenomenon known as ventricular remodelling. This process consists of left ventricular wall thinning in the infarction area, ventricular chamber dilatation, and compensatory hypertrophy of the noninfarcted portion of the myocardium. This article describes the pathophysiologic transformation that begins with MI and ventricular remodeling and ends in congestive heart failure.
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PMID:The pathophysiologic process of ventricular remodeling: from infarct to failure. 771 50

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

Extracellular structural remodeling is the compensatory response of the tissue following pathological stage. Myocardial infarction, which leads to adverse remodeling, thinning of the ventricle wall, dilatation and heart failure, is one of the leading causes of death. Remodeling implies an alteration in the extracellular matrix and in the spatial orientation of cells and intracellular components. The extracellular matrix is responsible for cardiac cell alignment and myocardial structural integrity. Substances that break down the extracellular matrix, specialized proteinases as well as inhibitors of proteinases, appear to be normally balanced in maintaining the integrity of the myocardium. Myocardial infarction leads to an imbalance in proteinase/antiproteinase activities causing alterations in the stability and integrity of the extracellular matrix and adverse tissue remodeling. To explore mechanisms involved in this process and, in particular, to focus on matrix metalloproteinases, their inhibitors, and activators, an understanding of proteinase and antiproteinase is needed. This review represents new and significant information regarding the role of activated matrix proteinases antiproteinases in remodeling. Such information will have a significant impact both on the understanding of the basic cell biology of extracellular matrix turnover, as well as on potential avenues for pharmacological approaches to the treatment of ischemic heart disease and failure.
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PMID:Proteinases and myocardial extracellular matrix turnover. 906 88

Coronary aneurysm in Kawasaki's disease (Acute febril infantile mucocutaneous lymph node syndrome, MCLS) may cause sudden death in childhood and ischemic heart disease in adults. We encountered two adult autopsy cases of Kawasaki's disease with multiple coronary aneurysms. The first case was a 56-year-old man who hospitalized due to recurrent syncope since 51 years of age. At age 55 coronary angiography (CAG) had shown multiple aneurysms in the left and right coronary artery. In September 1991, he developed chest pain and was brought to the hospital, almost dead on arrival (DOA). The patient died later the same day despite cardiopulmonary resuscitation. Autopsy findings showed cardiomegaly (470 g) with multiple coronary aneurysms of three coronary arteries. Microscopically, intimal thickening and medial thinning were found in the aneurysmal wall with calcification and disruption of the internal elastic lamina. The second case, a 28-year-old man had been diagnosed with rheumatic fever and mitral regurgitation at 4 years of age. Coronary aneurysms were noted on CAG at 26 years of age. In April 1992, he developed fever and was admitted to a local hospital where he was diagnosed with infectious endocarditis. After his being transferred to our hospital, disturbance of consciousness suddenly developed and he died in September 1992. Autopsy findings showed cardiomegaly (430 g) with left ventricular hypertrophy and multiple coronary aneurysms in left anterior descending coronary artery and left circumflex coronary artery. The aneurysmal wall showed intimal thickening and medial thinning with multiple recanalizations of occlusive lumina and fibrous intimal thickening. The mitral valve showed mild fibrosis and calcification without valvular deformity. There was no evidence of bacterial endocarditis. Both cases were finally diagnosed as Kawasaki's disease. Ischemic heart disease or lesions related to coronary aneurysm in Kawasaki's disease may show an increased incidence in the near future. Kawasaki's disease should have been followed even in adulthood after treatment in childhood.
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PMID:[Adult multiple coronary aneurysms of Kawasaki's disease's sequelae; two autopsy cases]. 952 43

Coronary atherosclerosis is by far the most frequent cause of ischemic heart disease and plaque disruption with superimposed thrombosis is the main cause of the acute coronary syndromes of unstable angina, myocardial infarction, and sudden coronary death. Therefore, for event-free survival, the vital question is not why atherosclerosis develops but rather why, after years of indolent growth, it suddenly becomes complicated by life-threatening thrombosis. Therefore, we have to focus on plaque composition and vulnerability to rupture and plaque thrombogenicity rather than on plaque size and stenosis severity. The risk for plaque disruption depends more on plaque vulnerability (plaque type) than on degree of stenosis (plaque size). Lipid-rich and soft plaques are more vulnerable and prone to rupture than collagen-rich and hard plaques. They are also highly thrombogenic after disruption because of high content of tissue factor. There seems to be three major determinants of a plaque's vulnerability to rupture: 1) the size and consistency of the lipid-rich atheromatous core, 2) the thickness of the fibrous cap covering the core, and 3) ongoing inflammation and repair processes within the fibrous cap. Lipid accumulation, cap thinning, lack of smooth muscle cells (smc), and macrophage-related inflammation destabilize plaques, making them vulnerable to rupture. In contrast, smc-related healing and repair processes stabilize plaques, protecting them against disruption. Plaque size or stenosis severity tell nothing about a plaque's vulnerability. Many vulnerable plaques are invisible angiographically due to their small size and compensatory vascular remodeling.
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PMID:Plaque pathology and coronary thrombosis in the pathogenesis of acute coronary syndromes. 1038 96

Transmyocardial laser revascularization (TMLR) is an alternative surgical procedure for the patients with intractable coronary artery disease. Efficacy of the treatment has been established, however, the mechanism of TMLR is still controversial. In this study, we investigated the effect of TMLR on acute myocardial ischemia with pathological analysis. Under general anesthesia, the hearts of mongrel dogs were exposed. Then, the anterior descending branch of the left coronary artery was ligated to make the ischemic area on the left ventricle. Laser punctures were made 30 minutes after coronary ligation in the TMLR group (n = 5), and no further procedure was performed after coronary ligation in the AMI group (n = 5). One month after these operations, the hearts were extirpated for pathological studies. The avascular area and the viable area in the infarcted area were macroscopically separated by Evans blue dye and triphenyltetrazolium chloride (TTC) staining. Thickness of the left ventricular wall in the infarcted area was also measured and compared. Furthermore, all of the infarcted area and the lased area were microscopically examined with Masson's trichrome stain. The size of the infarcted area in the TMLR group was smaller than that in the AMI group. It was significantly different (p < 0.05) in the basal and apical regions. As a result, the ratio of the viable area by the avascular area was larger in the TMLR group than in the AMI group. It was significantly different (p < 0.05) in the apical region. In the basal region, the thickness of the left ventricle in the AMI group was thinner than that of untreated dogs (normal group: n = 5), and there was no difference between the normal group and the TMLR group. Whereas in the apical region, significant difference of the thickness was found among AMI, TMLR, and normal groups (p < 0.05). In conclusion, our study supported; 1) TMLR reduced overall infarcted size, and increased the viable area in the infarcted area, 2) TMLR prevented the thinning of the left ventricular wall.
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PMID:Pathological analysis of transmyocardial laser revascularization for acute myocardial ischemia. 1057 92

Myocardial ischemia, an uncommon cause of sudden death in dogs, usually results in infarction and fibrosis of the myocardium. Necropsy examination of a 13-year-old German Shepherd dog that died suddenly demonstrated multifocal myocardial thinning and loss in the left and right ventricular free wall and right atrium. Histopathologic examination confirmed the myocardial thinning to be sites of myocyte atrophy and loss, with loose reticulin-positive fibrovascular tissue and adipocytes and little fibrosis. Many intramural coronary arteries were irregularly thickened and partially occluded by segmental intimal and medial deposits of periodic acid-Schiff-positive, Congo red-negative amorphous extracellular material. This finding is consistent with hyaline arteriosclerosis. These vascular lesions likely lead to insufficient perfusion of the affected myocardium and gradual loss of myofibers without the acute necrosis and fibrosis characteristic of infarction.
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PMID:Coronary arteriosclerosis with myocardial atrophy in a 13-year-old dog. 1460 24


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