Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Physical inactivity is a risk factor for the development of atherosclerosis. Members of a state chapter of the American Academy of Pediatrics were assessed about their practice behaviors and knowledge related to physical activity and fitness assessments. During health supervision evaluations 19% obtained a physical activity history and 7% measured a heart rate response to exercise. When assessing physical fitness 24% obtained an activity history which included kind, intensity, duration and frequency. 64% limited their physical fitness evaluation to an inspection of general appearance and weight, while 1% used a bicycle ergometer or treadmill, 4% used a step-test and 10% ran a child in place. Only 42% used the information to make recommendations about physical activity. 75% were not familiar with ACSM or AHA recommendations about exercise. Barriers cited to increasing physical activity and fitness assessments included lack of physician time, office space, staff time, and physician training. This survey demonstrates the need for increasing the awareness level of pediatricians about the role of exercise in preventing CHD and the need to incorporate such evaluations into their routine practice.
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PMID:Physical activity and fitness assessment. 195 Sep 43

Altogether 160 free living subjects (aged 30-60 years) most of whom had moderate hypercholesterolemia were randomised into the following diet groups to find out long-term effects of different fat-modified diets: (1) control diet 35/14:10:4 (energy percents from fat/saturated:monounsaturated:polyunsaturated fatty acids in actual diets); (2) AHA type diet 32/10:8:8; (3) monoene-enriched diet 34/11:11:5; (4) reduced-fat diet 30/12:8:3. LDL cholesterol fell equally with the AHA type diet (4.54 +/- 0.97 vs. 4.21 +/- 0.89 mmol/l (mean +/- S.D., 0 vs. 6 months), P = 0.001) and with the monoene-enriched diet (4.55 +/- 0.95 vs. 4.25 +/- 0.95 mmol/l, P = 0.004) during the 6-month study. Moderate amounts of polyenes or monoenes as part of natural diets did not decrease HDL cholesterol level in the long term. Serum lipid values remained unchanged with the reduced-fat diet. Analysis by apolipoprotein E phenotypes showed a decrease in LDL cholesterol only in subjects with phenotype 3/3 in the monoene-enriched group (-8.6 +/- 8.7 vs. +1.3 +/- 15.4, percent change in LDL cholesterol E 3/3 vs. E 4/3 + 4/4), but in the AHA type group LDL cholesterol decreased similarly in phenotypes E 3/3 and E 4/3 + 4/4 (-6.9 +/- 10.1 vs -6.9 +/- 16.5).
Atherosclerosis 1994 Jan
PMID:Long-term effects of three fat-modified diets in hypercholesterolemic subjects. 815 91

The primary objective of the Diabetes Atherosclerosis Intervention Study (DAIS) is to determine by quantitative coronary angiography whether long-term correction of the dyslipoproteinemia of diabetes with micronized fenofibrate results in evidence of decreased progression or regression of angiographically measured obstructive coronary atherosclerosis. The purpose of this communication is to describe the angiographic methodology for the DAIS project, and to present data documenting the reproducibility of measurements that will determine the primary outcome of DAIS. Four hundred eighteen subjects between the ages of 40 and 65 were entered from 11 centers in Canada, France, Finland, and Sweden, with 305 males and 113 females. Thirty-two percent of subjects had undergone a previous coronary artery intervention, either PTCA or bypass grafting. Subjects underwent coronary arteriography at baseline according to a strictly defined protocol. The coronary tree was divided into AHA segments and quantitative analysis of segments was performed using the cardiovascular measurement system described by Reiber. Geometric parameters including mean lumen diameter, minimum lumen diameter, maximum lumen diameter, and segment length were determined. In 15 studies, measurements were carried out on the same frame by two observers, and at least 1 week apart by the same observer. In 13 studies, measurements were performed by the same observer on two separate injections of the same coronary artery. The mean of the standard deviation of the differences of measurements of all segments for the primary study analyst was 0.029 mm, with a mean of correlation coefficients of 1.00. Between two observers, the mean of the standard deviations of segmental mean lumen diameters was 0.347 mm with a mean of coefficients of variation of 0.78. The mean of standard deviations for measurements of segmental mean lumen diameter from two separate coronary injections was 0.122, with a mean of correlation coefficients of 0.94. The mean of correlation coefficients for minimum lumen diameter were 0.98 for intraobserver variability, 0.77 for inter-observer variability, and 0.96 for inter-angiogram variability. For segment length the corresponding values were 0.99, 0.79, and 0.94. These data demonstrate that a high level of reproducibility and precision may be achieved in a multicenter study in assessment of the coronary tree in carefully performed studies using this methodology. We anticipate the results will provide a statistically powerful conclusion with new and unique data to answer the question of the effect of long-term correction of dyslipoproteinemia on coronary atherosclerosis in type II diabetic patients with dyslipoproteinemia.
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PMID:Diabetes Atherosclerosis Intervention Study (DAIS): quantitative coronary angiographic analysis of coronary artery atherosclerosis. 967 91

The expression of CD143 (angiotensin-I-converting enzyme, ACE) in cardiovascular diseases may be an important determinant of local angiotensin and kinin concentrations. Much of the experimental and clinical evidence suggests a crucial role for Ang II in fibrogenesis and the development of atherosclerosis. Therefore, we have studied the distribution of CD143 in atherosclerotic and non-atherosclerotic segments isolated from different parts of the human vascular tree, including aorta and coronary, carotid, brachial, renal, iliac and femoral arteries, and staged according to the AHA. Two hundred and thirty native and formalin-fixed specimens of 80 patients were analysed by sensitive APAAP-technique using ten different monoclonal and polyclonal antibodies to human CD143 and several controls. In non-atherosclerotic segments or intimal thickening, CD143 was found almost restricted to the endothelial cells of adventitial arterioles and small muscular arteries. In contrast, a striking accumulation of CD143 was detected in all early and advanced atherosclerotic lesions. This de-novo occurrence of CD143 within the intimal vascular wall was caused by spindle-shaped subendothelial cells with macrophagic/histocytic features, activated macrophages and foam cells. In addition, advanced lesions of atherosclerosis showed a marked neo-expression of CD143 in newly formed intimal microvessels. Hypocellular fibrotic plaques depleted in microvessels and macrophages showed only little CD143. The de-novo occurrence of CD143 was dependent on the stage of atherosclerosis but not on its particular localisation within the vascular system. This early and obligatory CD143 expression at an unusual vascular site may contribute to unusual tissue levels of angiotensins as indicated by co-localisation of immunoreactive Ang II. Thus, it may be an important pathogenetic step in the development of atherosclerosis and an established target for pharmacological prevention.
Atherosclerosis 2000 May
PMID:CD143 in the development of atherosclerosis. 1078 32

Atherosclerotic mouse models develop little ischemic organ damage and no infarctions, despite the presence of large atherosclerotic lesions. Therefore, we hypothesize that luminal changes do not follow atherosclerotic lesion development. Because a phenomenon that may explain the discrepancy between luminal changes and lesion size is vascular remodeling, we measured parameters of vascular remodeling in the carotid arteries (CAs), thoracic aorta (TA), and abdominal aorta (AA) of apolipoprotein E (apoE)-deficient (apoE(-/-)) and apoE*3-Leiden mice, 2 well-known mouse models of atherosclerosis. Atherosclerotic lesions were classified (American Heart Association [AHA] types II through V), and plaque thickness, compensatory enlargement versus constrictive remodeling, lumen diameter, stenosis, and media thickness were measured relative to the nondiseased arterial wall. In CAs, plaque thickness increased during atherogenesis. CAs showed compensatory enlargement (apoE(-/-) 55%, apoE*3-Leiden 38%). Regression analysis revealed a positive correlation between plaque and lumen area (for apoE(-/-), R=0.95; for apoE*3-Leiden, R=0.90). Medial thinning and elastolysis were also observed. During atherogenesis, lumen diameter decreased (apoE(-/-) -69%, apoE*3-Leiden -40%), and stenosis >70% developed. TA and AA showed similar features, but neither developed a progressive decrease in lumen diameter or stenosis >70%. In CAs, TA, and AA of apoE(-/-) and apoE*3-Leiden mice, atherogenesis is associated with compensatory enlargement, medial thinning, and elastolysis. A progressive decrease in lumen diameter and stenoses >70% occur only in CAs. Vascular remodeling is more prominent in apoE(-/-) mice.
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PMID:Compensatory enlargement and stenosis develop in apoE(-/-) and apoE*3-Leiden transgenic mice. 1149 66

According to the Third Report of the Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III), patients with low-density lipoprotein (LDL) cholesterol > or = 130 mg/dL should be discharged on lipid-lowering therapy. When LDL cholesterol levels are between 100 and 129 mg/dL, evaluation of ratios of LDL cholesterol/high-density lipoprotein (HDL) cholesterol or total cholesterol/HDL cholesterol may provide additional insight into a patient's risk status. Patients who were using statin therapy before admission for an acute coronary syndrome should be continued on lipid-lowering therapy. The American College of Cardiology/American Heart Association (ACC/AHA) 2002 guideline update for management of patients with unstable angina and non-ST-segment elevation myocardial infarction recommends statin therapy at discharge as a class I indication, level of evidence A. Furthermore, studies confirm that statin therapy begun early during hospitalization can prevent ischemic events in patients who are treated by an invasive strategy and those who are treated only by a medical strategy. However, studies suggest that patient compliance with a statin regimen after discharge is far from optimal. There are 2 programs available to help ensure that appropriate patients receive and continue taking lipid-lowering therapy. These programs are the Cardiac Hospitalization Atherosclerosis Management Program (CHAMP) and the Guidelines Applied in Practice (GAP).
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PMID:Optimizing lipid management in patients with acute coronary syndromes. 1261 96

This paper intends to make an update of recent publications and guidelines for evaluation in coronary symptom-free patients undergoing vascular surgery. It emphasizes the role of preoperative clinical evaluation that should identify the most appropriate testing, and treatment strategies to optimize care of the patient and avoid unnecessary testing in this era of cost containment. Selective preoperative coronary artery disease screening and revascularization achieve excellent perioperative and late results after high-risk vascular surgery. Supplemental preoperative evaluation is discussed (exercise ECG, stress echocardiography and stress tomoscintigraphy). Asymptomatic patients with good functional capacity can undergo intermediate-risk surgery without further non-invasive testing. Conversely, further noninvasive testing is often considered for patients with poor functional capacity or moderate functional capacity but higher-risk surgery especially for patients with 2 or more intermediate risk predictors. Additional testing may be considered on an individual basis for patients without clinical markers but with poor functional capacity prior to vascular surgery, particularly those with several minor clinical risk predictors. Because of a higher prevalence of silent myocardial ischaemia in diabetes mellitus, these patients require specific care. Until further data are available, indications for myocardial revascularization in the perioperative setting are similar to those in the ACC/AHA guidelines for use of myocardial revascularization in general. General practitioners, cardiologists, angiologists, vascular surgeons and anaesthesiologists should collaborate and aim to slow down the progression of atherosclerosis by giving their patients an optimum secondary cardiovascular prevention.
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PMID:Evaluation, severity and prognostic significance of silent myocardial ischaemia in vascular patients. 1291 58

Non-invasive quantitative indices of atherosclerosis are promising new parameters for an improved prognostic stratification of patients with risk factors that aim at individualized risk factor assessment and modification. In a recently published ACC/AHA consensus document, further data on the diagnostic and prognostic value of coronary calcified plaque quantification were strongly encouraged prior to its use in the general population. In this present work we summarize data published since, which contribute significantly to the prognostic value of fast CT-based noninvasive coronary calcified plaque quantification. It is a measure of atherosclerostic disease activity and is hence an index for the likelihood of future cardiovascular events. Current data indicate that noninvasive quantification of coronary atherosclerosis has incremental prognostic value beyond conventional single risk factor assessment. However, it is not clear yet whether it has a significant value beyond quantitative combined risk assessment using complex risk prediction models such as Framingham charts. Results from ongoing prospective trials such as the MESA study in the US and the Heinz Nixdorf Recall study in Germany will clarify some of the pending issues. In addition, it is still unclear, at what stage of the disease process, which of the available imaging tools will provide optimal diagnostic and prognostic value for the individual patient.
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PMID:[Prognostic value of noninvasive coronary plaque burden quantification in patients with risk factors]. 1296 26

Recent developments into antherothrombosis, the leading cause of morbidity and mortality in Western Society, may help to change our treatment strategy to a more casual approach. The composition of the atherosclerotic plaque, rather than the percent stenosis, appears to be a critical predictor for both risk of plaque rupture and subsequent thrombogenicity. A large lipid core, rich in tissue factor (TF) and inflammatory cells including macrophages, and a thin fibrous cap with compromise of its structural integrity by matrix degrading enzymes, such as metalloproteinases (MMPs), render a lesion susceptible to rupture and subsequent acute thrombosis. Thrombosis may lead to a complete occlusion or, in the case of mural thrombus or intraplaque hemorrhage, to plaque progression. Disruption of a vulnerable or unstable plaque (type IV and Va lesions of the AHA classification) with a subsequent change in plaque geometry and thrombosis may result in an acute coronary syndrome. The high-risk plaque tend to be relatively small, but soft or vulnerable to "passive" disruption because of high lipid content. Inflammatory processes are important components of all stages of atherosclerotic development, including plaque initiation and disruption. As such the early steps in atherosclerotic lesion formation are the over expression of endothelial adhesive protein (i.e. selectins, VCAM and ICAM), chemotactic factors (MCP-1), growth factors (M-CSF), and cytokines (IL-2) that will facilitate the recruitment, internalization and survival of blood-borne inflammatory cells into the vascular wall. Macrophages, following what appears to be a defense mission by protecting the vessel wall from excess lipid accumulation, may eventually undergo apoptosis with release of MMPs and TF. Specific cell recruitment in the vessel wall and build-up of the extracellular matrix are coordinated by a wide variety of stimulators and inhibitors. Active interaction of immune competent cells within the atherosclerotic lesions appears to play a pivotal role in the control of atherosclerotic plaque evolution and, therefore, deserves particular attention from the research community with the ultimate goal of improving preventive and therapeutic medical approaches. Inflammation, thrombosis and atherosclerosis are interdependent and define a triad within the complex pathogenic process of atherothrombosis.
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PMID:Evolving concepts in the triad of atherosclerosis, inflammation and thrombosis. 1527 86

For clinicians plasma C-reactive protein (CRP) levels are the only widely available tests that provide a tangible link between inflammation and atherosclerosis. New AHA/CDC joint guidelines from 2002-03 now include the measurement of CRP as a class IIa recommendation for stratifying patients with known cardiovascular disease (CVD) at a moderate (10-20%) 10-year event risk and a class IIb recommendation for patients without known CVD [1]. While the association of CRP and atherosclerosis is by now accepted, the molecular biology behind the association is evolving rapidly into a fascinating story. While some of the story remains obscure, this review aims to bridge the clinical and basic science and identify what is known about the role of this ancient molecule in atherosclerosis. The review covers CRP's interaction with atherosclerosis' major ingredients and cell types including the endothelium, monocytes and neutrophils, lipoproteins and the complement system. Taken together, the clinical and basic science leave the tantalizing impression that CRP has a fundamental role in atherogenesis, and hint at a more complex immunomodulatory effect which transforms the acute inflammatory response to vascular injury into the chronic inflammation seen in atherosclerosis.
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PMID:Evidence for C-reactive protein's role in (CRP) vascular disease: atherothrombosis, immuno-regulation and CRP. 1530 44


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