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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A study was made of events occurring in the arterial wall of the rat after administration of an atherogenic calcification-inducing diet and of vascular response in a model of combined metabolic aggression (atherogenic, calcification-inducing diet) and surgical aggression (adventitial resection). Female Sprague-Dawley rats were fed an atherogenic, calcification-inducing diet for 24 consecutive days, after which half the rats returned to standard diet (group I, n = 12) and the other half (group II) underwent resection of the adventitia on a segment of common iliac artery on day 25 before returning to standard diet. Normolipemic rats and rats that underwent adventitial resection without the atherogenic, calcification-inducing diet were used as the control groups. The rats were killed at 10 min, 1 and 24 h, 5, 14, 21, 30, 50, 70, 120 and 180 days. Morphologic studies were made with light microscopy and electron microscopy (scanning and transmission), as well as biochemical studies. Monocyte adherence and infiltration of the arterial intima, thickening of the subintimal space, the presence of monocyte-macrophages, calcification in the medial layer, intense adventitial fibrosis, and vacuolization of the endothelial cells of the adventitial microvessels were common findings in the two groups receiving the atherogenic, calcification-inducing diet. However, these groups differed in the intensity of calcification: the deep part of the medial layer did not become calcified when the adventitia was resected. Moreover, adventitial regeneration was delayed in group II with respect to the animals that underwent adventitial resection without atherogenic, calcification-inducing diet. We conclude that this diet induced atherosclerotic lesions in the vessel wall and inhibited adventitial regeneration in the rats that underwent resection.
Atherosclerosis 1996 May
PMID:Modifications induced by atherogenic diet in the capacity of the arterial wall in rats to respond to surgical insult. 876 78

The authors briefly report their experience regarding the opportunities offered by the use of current ultrasound methods in carotid surgery. They describe: a system for the quantification of athcromasic plaque used to monitor non-operated patients over time; ultrasound methods used to analyse the carotid wall to establish whether it can be utilised as an index of vascular aggression in hypertension, diabetes and atherosclerosis; the use of transcranial Doppler; criteria for the definition of high risk plaque; the applications of eco-color Doppler. The paper also illustrates a new pathology identified by the authors, defined as primary intimal fibrous hyperplasia, and the evolution of the carotid wall after endarterectomy. The structural characteristics of primary hyperplasia can only be shown using ultrasound given that arteriography cannot distinguish it from atheromatic stenosis. After endarterectomy the carotid wall is subject to hematic and hemodynamic stimuli which determine the type of evolution of the wall itself. The authors therefore examine the myointimal reaction, myointimal hyperplasia, early restenosis and late restenosis as different facets of the same phenomenon.
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PMID:[Ultrasonic quantification, value of color and contribution of transcranial Doppler sonography in carotid artery surgery]. 892 54

People with type II diabetes have a twofold to fourfold increased risk of dying from the complications of cardiovascular disease. Atherosclerosis and vascular thrombosis are major contributors. The increased risk is present before fasting hyperglycemia is seen. These individuals often have a sedentary life-style, poor physical conditioning, insulin resistance, centripetal obesity, hypertension, dyslipidemia, and a prothrombotic state. Chronic hyperglycemia is then added to these risk markers. Microalbuminuria may precede hyperglycemia in type II diabetes, occurs in 30% to 40% of these individuals after diabetes is established, and is a predictor of cardiovascular events. Early intervention in high-risk individuals may delay or prevent fasting hyperglycemia. An all-inclusive approach that focuses on early risk factor (or marker) identification and management to prevent or delay accelerated atherosclerosis and thrombosis in type II diabetes is an attractive strategy. However, the database to support this strategy is limited. In particular, large-scale prospective trial data are not available to support the concept of intensive glycemic regulation to prevent progression of macrovascular disease in type II diabetes. This is in contrast to the situation regarding microvascular disease of the eyes and kidneys. Recently, indirect data of a correlative nature have emerged, and short- and long-term prospective trials at early and late stages of type II diabetes are now being reported. These studies are analyzed and interpreted in this report. In contrast, the database to support an intensive antiplatelet regimen to prevent vascular thrombotic events in people with type II diabetes is large, and these studies are reviewed. They are of a type and magnitude to allow definite recommendations for aspirin therapy in type II diabetes. Aggressive therapy directed at hypertension, hyperlipidemia, and elevated urinary albumin in people with type II diabetes appears to be indicated. Increased attention to the multifactorial aspects of treatment of the type II diabetic patient is needed. Our present challenge is to translate these findings for patients and primary health care providers so that effective actions may be implemented.
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PMID:Multifactorial aspects of the treatment of the type II diabetic patient. 943 50

Atherosclerotic vascular disease is the major cause of death and disability in adult men and women living in the United States, where 13-14 million adults have a history of coronary artery disease (CAD). One-third of the 1.5 million individuals who experience a myocardial infarction (MI) each year will die and one half of these deaths will occur within 60 minutes of the event. The relation between elevated serum lipids and CAD has been corroborated by epidemiologic as well as pathologic evidence. Approximately 96 million people have total cholesterol levels > 200 mg/dL, with 38 million of these individuals having values > 240 mg/ dL. The National Cholesterol Education Program (NCEP) identified elevated low-density lipoprotein (LDL) cholesterol as a primary risk factor for CAD in 1988. This conclusion, along with recommendations for assessment and treatment, was reaffirmed in 1993. The NCEP also recommended that high-risk patients, with or without clinical manifestations of coronary atherosclerosis, should substantially lower their serum cholesterol levels. Specifically, the NCEP recommends that patients with CAD need to maintain serum LDL cholesterol levels of < or = 100 mg/dL; this means that the vast majority of patients need to decrease LDL cholesterol levels by > or = 30%. Aggressive dietary and/or drug therapy are recommended to achieve these reductions. In recent years, clinical trials have demonstrated the efficacy of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors ("statins") in lowering elevated levels of LDL cholesterol and decreasing the risk for clinical coronary events.
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PMID:Cholesterol lowering in the management of coronary artery disease: the clinical implications of recent trials. 1049 29

Hypercholesterolemia, particularly an elevated level of low-density lipoprotein (LDL) cholesterol, is an unarguably established risk factor for coronary artery disease (CAD). It is equally well established that lowering LDL cholesterol levels will decrease CAD-related morbidity and mortality in patients with established CAD. Although lipid-lowering therapy is known to retard the progression of atherosclerosis in patients with native coronary arteries, its effect in patients with coronary bypass grafts, which are particularly vulnerable to occlusion, is less well understood. Moreover, whereas several major clinical trials have documented the benefits of lowering LDL cholesterol in a variety of patient subpopulations, there has been far less clarity surrounding the question of whether aggressive lowering of LDL cholesterol is of greater benefit than moderate lowering of LDL cholesterol. The Post Coronary Artery Bypass Graft (Post-CABG) trial, a multicenter, randomized, double-blind clinical trial comprising 1,351 patients with elevated levels of LDL cholesterol and a history of bypass surgery was designed to determine whether aggressive lowering of LDL cholesterol levels with therapy based on 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors ("statins") is more effective than moderate lowering in delaying the progression of atherosclerosis in bypass grafts. Quantitative computer-assisted angiography was conducted at baseline and again at an average of 4.3 years. The primary angiographic outcome was the mean percentage per patient of grafts with a decrease of > or = 0.6 mm in lumen diameter. Patients who received aggressive therapy were significantly more likely than their moderate-treatment counterparts to achieve and maintain LDL cholesterol levels within the National Cholesterol Education Program's (NCEP's) recommended target of < or = 100 mg/dL (< or = 2.59 mmol/L). Moreover, the mean percentage of grafts with progression of atherosclerosis was 27% for aggressively treated patients, compared with 39% for those who were randomized to the moderate-treatment group (p < 0.001). This study demonstrates that aggressive lipid lowering is practical and worthwhile in at-risk patients. Aggressive treatment is far more effective than moderate treatment in lowering LDL cholesterol levels to the NCEP target level of < or = 100 mg/dL (< or = 2.59 mmol/L), and this intervention decreases the progression of atherosclerosis.
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PMID:Therapeutic efficacy of the lipid-lowering armamentarium: the clinical benefits of aggressive lipid-lowering therapy. 955 May 1

Atherosclerosis kills more patients with diabetes than all other causes combined. Aggressive reversal and treatment of dyslipidemias is the only proven prevention for coronary events in the patient with type 2 diabetes. Glycemic control with diet, oral hypoglycemic agents, and insulin, when necessary, is often only partially effective in normalizing lipid values in type 2 diabetes. Intensive treatment with lipid-regulating agents, particularly HMG-CoA reductase inhibitors, is often necessary to normalize diabetes-associated dyslipidemias. HMG-CoA reductase inhibitors are also the only agents thus far shown in prospective multicenter trials to reduce the risk of coronary events in diabetic patients.
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PMID:Vascular disease and lipids in diabetes. 970 27

Atherosclerosis presents many opportunities for the primary care provider (PCP) to positively affect the patient's outcome. The preventable nature of the disease should be a major focus of the PCP's relationship with the patient. Aggressive risk factor reduction clearly is beneficial in CAD and should be addressed at each visit with at-risk patients. Once the disease is established, the PCP's goal is prevention of complications by educating the patient about the disease and by appropriate diagnostic testing and referral when indicated.
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PMID:Atherosclerosis. 979 83

Atherosclerosis displays all the features of a chronic inflammatory process. Aggressions that ignite and fuel atherosclerotic inflammation warrant keen attention. Infection is a potential clue, implying microbes with certain discrete characteristics: a wide epidemiologic distribution, a tropism for the arterial wall, and an aptitude for persistence, latency and recurrence. The infectious theory has built up from the pioneering observations of Fabricant et al. (1978) on the arterial lesions provoked by Marek's disease herpesvirus in chicken. So far one virus (cytomegalovirus) and two bacteria (Chlamydia pneumoniae and Helicobacter pylori) have been implicated in human atherosclerosis, based upon experimental, sero-epidemiologic, or pathologic evidence. None of these potential contributions has yet been established beyond reasonable doubt. However, grounded on the suspicion about C. pneumoniae, provocative therapeutic evidence has added recently: according to two pilot studies, treatment with macrolide antibiotics appear to improve the prognosis of coronary artery disease in both its chronic and acute forms. If ongoing larger-scale studies confirm these preliminary results, a novel era will open in our capacity for explaining, treating and preventing atherosclerosis. An infectious aetiology of atherosclerosis is now to be considered earnestly, and is already being submitted to more intensive clinical and experimental investigation.
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PMID:[The infection theory in atherosclerosis]. 983 76

We report on the most recent data confirming the angiographic and pathological efficacy of LDL-apheresis for coronary atherosclerosis of a familial hypercholesterolemia (FH) patient using collected data of a large number of cases and especially of one autopsy case. Changes in coronary artery stenosis have been assessed angiographically in 37 FH patients in the LDL-Apheresis Regression Study (LARS) group of 13 institutions in Japan. Definite regression was observed in 21 segments by visual and computer analysis. Fourteen of 37 patients (37.8%) who had received LDL-apheresis treatment in combination with cholesterol-lowering drugs had at least one regressed segment without any progressed segment. We pathologically examined at autopsy the coronary arteries in one FH patient who had received long-term LDL-apheresis therapy before death. The results revealed the process of scarring of atheromatous plaque, suggesting pathological regression correlated with the angiographic regression shown in serial angiograms taken during LDL-apheresis treatment. It was further suggested that the formation of an eccentric thickened wall lesion rich in collagen fiber prevented atheromatous plaque from tearing off. Such tearing off might lead to an acute coronary event. Aggressive cholesterol-lowering therapy based on LDL-apheresis can induce both angiographic and pathological regression in coronary atherosclerosis of FH patients.
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PMID:Angiographic and pathological studies on regression of coronary atherosclerosis of FH patients who received LDL-apheresis treatment. 1007 40

Atherosclerosis of the carotid bifurcation is an observable sign of systemic disease driven by key risk factors and resulting in an epidemic of stroke, myocardial infarction, and vascular death worldwide. Aggressive integrative preventive interventions of controlling hypertension, hyperlipidemia, diabetes mellitus, smoking, systemic inflammation/infarction, depression, and hyperhomocyst(e)imia are needed in the medical management of these high-risk patients. Surgical indications for asymptomatic surgery may be recalled through the acronym CAROTID, which emphasizes knowledge of risk benefit to a particular patient, adequate disclosure, and physician--patient equipoise.
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PMID:Indications for treatment of asymptomatic carotid stenosis. 1073 43


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