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)

Rupture of plaque is an important factor in the initiation of acute myocardial infarction. Plaque rupture is related to stress distribution in atheroma, but morphological alteration in coronary atheroma plaque in vivo is little understood. Atheroma plaque was observed during the cardiac cycle using 3.5 or 2.8 F, 30 MHz intracoronary ultrasound (ICUS) in seven patients with coronary artery disease. Coronary ostial pressure (P) measurements were simultaneously performed. Seven of the eccentric stenotic sites were analyzed. Intima-medial thickness (Th) and regional radius of curvature (R) at the middle and lateral portions of the atheroma were measured. Delta Th and % delta Th were calculated from change in thickness from end-diastole to peak systole. These parameters of the middle portion were compared with those of the lateral portion. The lateral % delta Th was 20.1 +/- 13.6% (delta Th 0.13 +/- 0.08 mm; 0.69 to 0.56 mm), and was significantly greater than the middle % delta Th [5.8 +/- 6.6% (delta Th 0.06 +/- 0.08 mm; 1.24 to 1.18 mm), p < 0.05]. Regional radius of curvature did not significantly differ. Wall stress calculated as P x R/Th was greater at the lateral portion (peak systole 3.7 x 10(5) dynes/cm2, end-diastole 1.9 x 10(5) dynes/cm2) than at the middle portion (peak systole 1.4 x 10(5) dynes/cm2, end-diastole 0.9 x 10(5) dynes/cm2). The change in stress from end-diastole to peak systole at the lateral portion was significantly greater (1.8 x 10(5) dynes/cm2) than that at the middle portion (0.5 x 10(5) dynes/cm2). The change in stress during the cardiac cycle, caused by the increase in intracoronary pressure, was greater at the lateral than at the middle of the plaque. This imbalanced distribution of stress may result in greater thinning of plaque at the lateral portion. Therefore, the distortion of plaque may be a mechanism for atheroma rupture at the lateral portion.
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PMID:[Cyclic alteration in atheroma plaque morphology observed by intracoronary ultrasound: initiation mechanism of acute myocardial infarction]. 886 81

To investigate the mechanism of plaque rupture, we carried out morphologic and quantitative assessments of ruptured plaque with a 30-MHz intravascular ultrasound catheter before coronary intervention. Plaque rupture, defined as an echolucent intraplaque area communicating with arterial lumen, was noted in all of 22 patients with coronary artery disease examined in the study. The plaque was eccentric in 16 patients (73%) and in 10 of these 16 patients there was a tear at the margin of the plaque (63%). Calcification was noted in only 6 patients (22%). Plaque area ranged from 8.7 to 44.1 mm2. The ruptured area ranged widely, from 1.0 to 14.0 mm2, and the percent ruptured area also ranged widely, from 3.9% to 50.9%. Fibrous cap was recognized in 20 patients. The thickness of the fibrous cap ranged from 0.1 to 0.6 mm (mean, 0.36 mm) and thinning of the fibrous cap was noted in 16 patients (80%). From these results, we conclude that intravascular ultrasound can provide detailed observations of plaque rupture consistent with pathologic studies. Accordingly, it is a suitable method for evaluation of plaque rupture in vivo. Plaque weakness, due to the presence of atheromatous core, thin fibrous cap, and no calcification, seems to be the major determinant of plaque rupture. In addition, the great variation in cap thickness and ruptured area suggests the role of other triggers, such as mechanical and hemodynamic stress, in plaque rupture.
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PMID:Assessment of plaque rupture by intravascular ultrasound. 947 76

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

We searched the medical literature for articles containing markers of cardiac ischemia and echocardiography in the evaluation of patients presenting to the emergency department to determine their combined clinical use. Several published articles indicate two-dimensional echocardiography is a useful and cost-effective imaging technique for the evaluation of patients with chest pain in the emergency department. New studies are emerging that evaluate ischemic markers in combination with echocardiography to assess patients presenting to the emergency department with chest pain. We searched the MEDLINE Database for English-language articles published from December 1980 to August 1998 using the key words troponin, echocardiography, myocardial infarction, and emergency. These key words were crossed referenced to determine publications in this area. Pertinent trials and reviews were selected from the database. There were six articles evaluating biochemical markers of ischemia and echocardiography to assess patients presenting with acute coronary syndromes in the emergency department. Very few studies combined the information obtained from novel ischemic markers and echocardiogram analysis to help delineate potential cardiac etiologies of acute coronary syndromes. However, the limited studies available indicate that echocardiography is both sensitive and specific for detecting acute myocardial infarction. The presence of regional wall motion abnormalities increases the chance of in-hospital complications and likelihood of developing congestive heart failure after admission for unstable angina. The combined use of troponin T levels and echocardiographic imaging was a more powerful predictor of adverse events than were isolated results. Myocardial scarring with ventricular wall thinning or aneurysm may allow for rapid diagnosis of 'occult' coronary artery disease in a patient presenting with chest pain who does not have a previous history of a cardiovascular event. Echocardiography may also help identify other cardiovascular causes of chest pain, such as aortic dissection, aortic stenosis, cardiac tamponade, pericarditis, and hypertrophic cardiomyopathy. The clinical use of combining ischemic markers of disease with echocardiographic imaging seems justified given their unique clinical advantages. Future clinical trials are needed to determine whether the combination of novel ischemic markers and echocardiography can provide for a more expedient and accurate diagnosis, resulting in improved patient care and a safe reduction in unnecessary hospitalization.
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PMID:Clinical Use of Ischemic Markers and Echocardiography in the Emergency Department. 1117 40

A coronary artery aneurysm is defined as coronary dilatation that exceeds the diameter of normal adjacent artery segments, or is 1.5 times the diameter of the largest coronary artery. Coronary artery aneurysms are rare with an incidence of between 1.5% to 5%. The aneurysm is caused by destruction of the vessel media, thinning of the arterial wall, increased wall stress, and progressive dilatation of a segment of the coronary artery. The most common cause is atherosclerotic coronary artery disease. These aneurysms occasionally rupture but more commonly develop thrombus and hematoma leading to the appearance of the presence of an intramyocardial mass. We present the case of a 60-year-old man with hypertension who presented with a mass that was identified initially by transthoracic echocardiography in the setting of an inferior wall myocardial infarction, which was later recognized to be a thrombosed right coronary artery aneurysm.
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PMID:Thrombosed right coronary artery aneurysm presenting as a myocardial mass. 1556 76

We present the case of a 70-year-old man admitted in congestive heart failure. The patient was diagnosed 22 years ago of hypertrophic cardiomyopathy (HC). ECG showed a very peculiar and pathological form of left bundle branch block (LBBB). 2D-echocardiogram revealed a dilated left ventricle (LV) and ejection fraction of 25%. LV remodeling represents an important component of the pathophysiology of HC and, paradoxically, some patients develop LV wall thinning, systolic dysfunction, and congestive heart failure (in the absence of coronary artery disease). This evolution is designated as "end-stage" or "burned-out"phase. We present this rare LBBB and his pathological evolution along the time as unique manifestation of this "burned-out" phase. The mechanism of this wall thinning remains unclear but changes in ECG may alert us about it.
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PMID:Atypical left bundle branch block in dilative "burned-out" phase of hypertrophic cardiomyopathy. 1640 70

The purpose of this study is to demonstrate whether the signal intensity (SI) of myocardial infarction (MI) on contrast enhanced (CE)-cine MRI is useful for differentiating recently infarcted myocardium from chronic scar. This study included 24 patients with acute MI (36-84 years, mean age: 57) and 19 patients with chronic MI (44-80 years, mean age: 64). The diagnosis of acute MI was based on the presence of typical symptoms, i.e. elevation of the cardiac enzymes and the absence of any remote infarction history. The diagnosis of chronic MI was based on a history of MI or coronary artery disease of more than one month duration and on the absence of any recent MI within the previous six months. Retrospectively, the ECG-gated breath-hold cine imaging was performed in the short axis plane using a segmented, balanced, turbo-field, echo-pulse sequence two minutes after the administration of Gd-DTPA at a dose of 0.2 mmol/kg body weight. Delayed contrast-enhanced MRI (DCE MRI) in the same plane was performed 10 to 15 minutes after contrast administration, and this was served as the gold standard of reference. The SI of the infarcted myocardium on the CE-cine MRI was compared with that of the normal myocardium on the same image. The area of abnormal SI on the CE-cine MRI was compared with the area of hyperenhancement on the DCE MRI. The area of high SI on the CE-cine MRI was detected in 23 of 24 patients with acute MI (10 with homogenous high SI, 13 high SI with subendocardial low SI, and one with iso SI). The area of high SI on the CE-cine MRI was larger than that seen on the DCE MRI (p < 0.05). In contrast, the areas of chronic MI were seen as iso-SI with thin subendocardial low SI on the CE-cine MR in all the chronic MI patients. The presence of high SI on both the CE-cine MRI and the DCE MRI is more sensitive (95.8%) for determining the age of a MI than the presence of myocardial thinning (66.7%). This study showed the different SI patterns between recently infarcted myocardium and chronic scar on the CE-cine MRI. CE-cine MRI is thought to be quite useful for determining the age of myocardial infarction, in addition to its utility for assessing myocardial contractility.
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PMID:Differentiation of recently infarcted myocardium from chronic myocardial scar: the value of contrast-enhanced SSFP-based cine MR imaging. 1654 48

Hypertrophic cardiomyopathy patients rarely have left ventricular apical aneurysms without coronary artery disease and the pathophysiological processes responsible for apical wall thinning and aneurysm formation are not known exactly today. Here we present a rare nonobstructive hypertrophic cardiomyopathy case with an apical thrombotic aneurysm.
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PMID:Rare clinical presentation of nonobstructive hypertrophic cardiomyopathy: apical aneurysm with thrombus. 1708 37

The onset of coronary heart disease may be governed by distribution and magnitude of hemodynamic shear stress in the coronary arteries. This study numerically examines pulsatile blood flow through the left coronary artery system. A triphasic waveform is employed to simulate pulsating flow. Five non-Newtonian models, as well as the usual Newtonian model, are used to describe the viscous shear-thinning behavior of blood. It is concluded that when using computational fluid dynamics (CFD) to numerically investigate blood velocity profiles within small arteries, such the coronary artery system examined in this work, great care should be taken in choosing a blood viscosity model. It is suggested that the generalized power law model be the viscous shear thinning model of choice. When using CFD to investigate only patterns of wall shear stresses, the model selection is not as crucial and the simple Newtonian model will suffice but when the magnitude of WSS is of great importance, as in the case of the determining the development of coronary artery disease, the model selection is key.
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PMID:Calculation of wall shear stress in left coronary artery bifurcation for pulsatile flow using two-dimensional computational fluid dynamics. 1794 4


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