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)

We have reviewed the clinical records and histology of 135 patients who underwent temporal artery biopsy between 1973 and 1978. Biopsies were classified histologically as giant-cell arteritis (17%), atypical arteritis (6%), healed arteritis (2%), arteriosclerosis (67%), atherosclerosis (5%), or normal (3%). Most of the histological diagnoses made at the time of biopsy were confirmed but eight cases which had originally been reported as atypical or healed arteritis were classified as arteriosclerosis when reviewed. All 33 patients with histological evidence of arteritis were accepted as clinical cases of temporal arteritis (31) or polymyalgia rheumatica (2) and treated with steroids. A further 24 patients had negative biopsies (arteriosclerosis or atherosclerosis) but were considered on clinical grounds to have cranial arteritis. They too were treated and made a full recovery. In 43 cases, all of whom had negative biopsies, a final diagnosis was reached which was thought to account for the clinical symptoms (e.g., cerebrovascular accident, rheumatoid disease, migraine, etc.). As less than 60% of patients with clinical temporal arteritis had positive biopsies, we suggest that this procedure could be omitted and replaced by a trial of steroid therapy. Biopsy should be reserved for patients with a strong medical contraindication to steroid therapy, or who fail to respond to treatment promptly.
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PMID:Temporal artery biopsy in giant-cell arteritis. A reappraisal. 727 Jul 80

Dolichoectasia of intracranial arteries is an infrequent disease with an incidence less than 0.05% in general population. It represents 7% of all intracranial aneurysms. Commonly seen in middle age patients with severe atherosclerosis and hypertension, the affected arteries include the basilar artery, supraclinoid segment of the internal carotid artery, middle, anterior and posterior cerebral arteries; males are more frequently affected. The clinical features of these fusiform aneurysms are divided in three categories: ische-mic, cranial nerve compression and signs from mass effect. Hemorrhage may also occur. Nine patients with symptomatic cerebral blood vessel dolichoectasias are presented. Six of them were males with moderate or severe hypertension. Lesions were confined to the basilar artery in 3 cases, carotid arteries and the middle cerebral artery in 1 case, and both systems were affected in 4 patients. Middle cerebral arteries were affected in 5 cases and the anterior cerebral artery in one. An isolated fusiform aneurysm of the posterior cerebral artery is also presented (case 8) (Table 3). Motor or sensory deficits, ataxia, dementia, hemifacial spasm and parkinsonism were observed. One patient died from cerebro-meningeal hemorrhage (Table 2). All patients were studied with computerized axial tomography of the brain, 5 cases with four vessel cerebral angiography, 4 cases with magnetic resonance imaging (MRI) and case 5 with MRI angiography. Clinical symptoms depend on the affected vascular territory, size of the aneurysm and compression of adjacent structures. The histopathologic findings are atheromatous lesions, disruption of the internal elastic membrane and fibrosis of the muscular wall. The resultant is a diffuse deficiency of the muscular wall and the internal elastic membrane. Recent advances in neuroimaging such as better resolution of CT scan, magnetic resonance images (MRI) and MRI angiography increased the diagnosis of this pathology showing clearly the affected vessels. This avoids the use of conventional or digital subtraction angiography, reserved only for diagnosing suspected saccular aneurysm, evidence of subarachnoid hemorrhage or planning surgical treatment. The treatment of this entity may be medical or surgical. There is evidence suggesting a more favorable outcome with anticoagulation therapy, although antiaggregation is a reasonable alternative. In our experience no difference in clinical outcome was evident. Surgical treatment of this type of aneurysm includes intra- or extracranial occlusion of parent artery, clipping or aneurysm trapping, tourniquet occlusion, and circumferential wrapping with clip reinforcement. Endovascular occlusion has been accomplished with detachable balloon technique or coils. No surgical attempt was done in our cases. The prognosis is variable depending on the patients age, vessels involved and clinical complications.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Dolichoectatic intracranial arteries. Advances in images and therapeutics]. 756 39

Hospital administrative databases are used for studying resource use and medical outcomes. The ability to use administrative data to make comparisons among providers requires accurate adjustment of rates based on case mix. Adjustment for case mix often incorporates pre-existing patient conditions such as comorbidities. We tested the hypothesis that some circulatory comorbidities can appear positively or negatively associated with percutaneous transluminal coronary angioplasty (PTCA), not for clinical reasons, but because of the population used for modeling. When statistical models included all discharges with a principal or primary diagnosis of coronary atherosclerosis, or angina with coronary atherosclerosis, multivariate analysis revealed that discharges with dysrhythmias and the more severely ill were less likely to receive PTCA. However, when analysis excluded discharges treated with options (e.g. bypass) reserved for patients with more severe conditions, the presence of dysrhythmias and more severe illness increased the odds of receiving PTCA. Variability involving the direction of association between patient characteristics and a specific intervention illustrates that rates adjusted for patient characteristics cannot be properly interpreted without a clear understanding of the rationale underlying strategies for case-mix adjustment.
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PMID:Administrative databases, case-mix adjustments and hospital resource use: the appropriateness of controlling patient characteristics. 789 63

Low-density-lipoprotein (LDL) apheresis has the theoretical advantage over anion-exchange resins and hydroxymethylglutaryl coenzyme A inhibitors of decreasing lipoprotein(a) as well as LDL. To confirm this advantage, patients with heterozygous familial hypercholesterolaemia and coronary artery disease were randomised to receive LDL apheresis fortnightly (with disposable dextran sulphate/cellulose columns) plus simvastatin 40 mg daily, or colestipol 20 g plus simvastatin 40 mg daily. Quantitative coronary angiography was repeated after a mean of 2.1 years in 20 patients undergoing apheresis and in 19 on combination drug therapy. Changes in serum lipoproteins were similar in both groups apart from greater lowering by apheresis of LDL cholesterol (3.2 vs 3.4 mmol/L in drug group, p = 0.03) and lipoprotein(a) (geometric means 14 vs 21 mg/dL, p = 0.03). There were no significant differences in primary angiographic endpoints per patient but lesion-based and segment-based secondary endpoints were biased in favour of the drug group (change in minimum lumen diameter of lesions 0.07 vs -0.004 mm, p = 0.046; change in mean lumen diameter of segments 0.02 vs -0.06 mm, p = 0.01). None of the angiographic changes correlated with lipoprotein(a) concentrations. Per patient changes in % diameter stenosis and minimum lumen diameter in the two groups were as or more favourable than those observed in five published trials that assessed lipid-lowering drug therapy by quantitative coronary angiography. Although LDL apheresis combined with simvastatin was more effective than colestipol plus simvastatin in reducing LDL cholesterol and lipoprotein(a), it was less beneficial in influencing coronary atherosclerosis and should be reserved for patients unresponsive to drugs. Decreasing lipoprotein(a) seems to be unnecessary if LDL cholesterol is reduced to 3.4 mmol/L or less.
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PMID:Familial Hypercholesterolaemia Regression Study: a randomised trial of low-density-lipoprotein apheresis. 789 24

Today, multiple, thromboembolically generated cerebral infarcts are regarded as the main pathogenetic pathway of vascular dementia (VAD), with multi-infarct dementia (MID) as its clinical counterpart. However, taking into account other vascular mechanisms that may influence the brain, such as vessel-wall damage (atherosclerosis, hyalinosis, amyloid angiopathy, or blood-brain barrier dysfunction), cerebrovascular insufficiency (disturbance of systemic circulation, perfusion vulnerability related to the vascular anatomy of the brain, or disturbance of autoregulation), and hyperviscosity, it is evident that MID is not the only VAD category. The diagnosis of MID ought to be reserved for the combination of progressive dementia associated with cerebral ischemic events and evidence of infarction that is mainly associated with the large cerebral arteries. Subcortical white-matter dementia characterized by frontosubcortical symptomatology, white-matter lesions, and small-vessel involvement with or without lacunes/infarcts--a combination of lacunar dementia and Binswanger's disease--appears to be another important VAD disease.
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PMID:Heterogeneity of vascular dementia: mechanisms and subgroups. 839 62

Lipid apheresis has developed from a heroic treatment into a routine clinical therapy and currently is the major indication for performing extracorporeal plasma therapy. Whereas it was once reserved for patients with homozygous familial hypercholesterolemia, today it has a place in the secondary prevention of severe coronary heart disease when low-density lipoprotein (LDL)-cholesterol level exceeds 150 mg/dl, despite conservative treatment, in any type of primary hypercholesterolemia. Unselective plasma exchange has been replaced by a variety of selective procedures. The efficacy of the treatment can be maximized by combining LDL apheresis with the use of cholesterol synthesis enzyme inhibitors. Clinical studies have shown that drastic cholesterol reduction can result in regression of coronary atherosclerosis as well as in reduced cardiac morbidity and mortality. Technical progress comprises improved selectivity, online regeneration of adsorbers, and LDL adsorption from whole blood. Recently, a new LDL hemoperfusion procedure was successfully tested in a clinical pilot study; blood is passed directly over a lipid sorbent without prior plasma separation. If this system is demonstrated to be safe and effective in clinical Phase III trials, a further qualitative step in the rapid development of LDL apheresis will have made.
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PMID:Lipid apheresis: from a heroic treatment to routine clinical practice. 872 20

The purpose was 1) To assess the prevalence of abdominal aortic aneurysms (AAA) in elderly males with atherosclerosis and 2) to evaluate the value of physical exam (PE) by a vascular surgeon in detecting AAA. A total of ninety-six males older than 55 years referred to vascular surgery clinic with atherosclerotic disease were screened prospectively with PE by a vascular surgeon, followed by ultrasonography (US). Atherosclerosis was documented by ankle brachial index and duplex US. Patients who had recently undergone a vascular procedure, aortography, laparotomy, abdominal computed tomography, or US were excluded. Mean age was 67 years. Patients were 67 per cent Caucasian, 32 per cent black, and 1 per cent Hispanic. Presenting complaints were related to claudication (83%), carotid disease (19%), both (3%), and subclavian stenosis (1%). Patient characteristics included cigarette smoking (85%), hypertension (67%), cardiac disease (51%), diabetes (45%), stroke (18%), and chronic obstructive pulmonary disease (8%). One (1%) 3.7 cm AAA was detected by US. Sensitivity of PE was 100 per cent and specificity 92 per cent. Twenty-two (23%) patients were too obese for us to feel the aortic pulse. Screening cost was $14,250. The prevalence of AAA in this population is very low. AAA screening should be reserved for patients with a positive PE or who are too obese for the examiner to feel the aortic pulse.
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PMID:Abdominal aortic aneurysm screening in elderly males with atherosclerosis: the value of physical exam. 881 72

The demonstration of lipid loaded macrophages in atherosclerotic tissue has led to the development of in vitro systems to elucidate the mechanisms involved in lipid accumulation. Here we have characterised the changes which occur in human monocyte-derived macrophage (MDM) lipids during culture in either human serum (HS) or foetal calf serum (FCS). MDM cultured in HS were rapidly converted to lipid filled foam cells, as assessed using HPLC analysis and oil red-O staining and compared with the same cells grown in FCS. However, the lipids which accumulated were predominantly triglycerides with smaller amounts of unesterified cholesterol (UC) and only traces of cholesteryl esters (CE). alpha-Tocopherol (alpha-TocH) was present at higher levels in MDM cultured in HS compared to the same cells grown in FCS. MDM lipid accumulation was dependent on the triglyceride-rich lipoprotein (TGRL) fraction of human serum; accordingly, supplementation of FCS with human TGRL also induced MDM lipid accumulation. The relationships between cellular lipid accumulation and secretion of apolipoprotein E (apo E) and lipoprotein lipase (LPL) as well as expression of the low density lipoprotein receptor-related protein (LRP) were also examined. MDM lipid accumulation was associated with increased apo E secretion but did not alter extracellular LPL activity. The lipid accumulation which was induced by HS was potently inhibited (but not reserved) by the inflammatory cytokine interferon-gamma (IFN gamma), and this was associated with decreased apo E production, LPL secretion and expression of LRP. These studies reveal striking differences in the lipid composition of MDM cultured in either HS or FCS, and indicate that oil red-O staining is not necessarily associated with cholesteryl ester accumulation in human macrophages. Furthermore, the effect that serum-induced lipid accumulation has on the specific MDM functions studied should be appreciated when developing in vitro macrophage models.
Atherosclerosis 1997 Jan 03
PMID:Regulation of serum-induced lipid accumulation in human monocyte-derived macrophages by interferon-gamma. Correlations with apolipoprotein E production, lipoprotein lipase activity and LDL receptor-related protein expression. 905 Nov 97

3-Hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase is the key enzyme of cholesterol synthesis. HMG-CoA reductase inhibitors are potent reversible inhibitors of this enzyme, which act by competing for the substrate HMG-CoA. This review is mainly devoted to the 4 main HMG-CoA reductase inhibitors used today: lovastatin, simvastatin, pravastatin and fluvastatin. Depending upon the dosage, these drugs are able to reduce plasma cholesterol levels by more than 40%. After absorption, each undergoes extensive hepatic first-pass metabolism. Up to 5 primary metabolites are formed, some of which are active inhibitors. The elimination half-lives vary from 0.5 to 3.5 hours and excretion is mainly via the faeces. A limited number of drug interactions has been reported. Increases in liver enzymes and muscle creatine kinase activity are among the most severe adverse effects. These powerful drugs should be reserved for patients with high plasma cholesterol levels and/or those with cardiovascular disease. New therapeutic approaches to atherosclerosis are currently under investigation. HMG-CoA reductase inhibitors are the cornerstone of this research.
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PMID:Clinical pharmacokinetics of 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors. 911 84

Is Lp(a) culpable in atherosclerosis? This is a question for scientists. Lp(a) fulfills two of Koch's four criteria for causation for CHD. However, the actual mechanism by which Lp(a) promotes atherosclerosis remains unproven. Should we investigate Lp(a) as part of assessment of CHD risk? There are some reasons that favour measuring plasma Lp(a) in selected patients. First, a high Lp(a) can exist without physical or historical evidence. Second, the measurement of Lp(a) might affect diagnosis, treatment and/or prognosis. However, presently there is no standard assay for Lp(a) and there is no evidence for benefit of treatment elevated Lp(a). Furthermore, there is no current evidence that knowledge of a patient's Lp(a) status would affect management of other aspects of a patient's CHD risk. Lp(a) can be considered to be a non-modifiable potential CHD risk factor, as are family history and gender. If Lp(a) is to be measured, it must be done so using a validated, reliable and commonly used assay. Measuring Lp(a) could be reserved for subjects in whom there is equivocation over how aggressively to treat the traditional CHD risk factors, such as elevated plasma LDL cholesterol. If Lp(a) were found to be high in such a subject, the modifiable CHD risk factors should be addressed more aggressively. However, the medical community awaits the results of prospective studies addressing this particular issue.
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PMID:Is it time to measure Lp(a) as part of coronary heart disease risk assessment? 925 23


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