UMLS:C0004153 - FACTA Search

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

Human plasma contains a factor capable of stimulating vascular prostacyclin generation even in atherosclerotic vessels with minimal in-vitro capacity for PGI2-synthesis. The activity of this prostacyclin stimulating plasma factor (PSPF) has been reported to be elevated in renal failure and hepatic coma. We are not aware of any data as to whether this PSPF plays a role in maintaining hemostatic balance in patients with peripheral vascular lesions. Therefore, we examined 62 patients with peripheral vascular disease (PVD). This study group was subdivided into normo- and hyperlipemic subjects, patients with and without maturity onset diabetes, and plasma beta-thromboglobulin levels higher and lower than 50 ng/ml. 10 healthy sex and age matched persons served as controls. Vascular prostacyclin formation was studied in vitro after incubation of the patients' plasma and a buffer control with various tissue samples (human femoral artery, rat abdominal and thoracic aorta of healthy and of streptozotocin induced diabetic animals, swine endothelial layer and remaining tissue (media and adventitia) and cultured endothelial (EC) and smooth muscle cells (SMC) of minipig arota. In addition, 6-oxo-PFG1 alpha formation by cultured EC and SMC (minipig aorta source) after incubation with tris HCl-buffer or plasma were estimated by means of specific radioimmunoassays. In general, tissue samples and cells incubated in plasma exhibit a marked increase of in-vitro PGI2-formation as compared to buffer. No difference could be found between PSPF of CHD-patients and healthy controls. Similar findings were obtained using incubated vascular tissue and cultured cells by means of the bioassay and specific RIA, respectively. These findings indicate that the PSPF does not seem to be of any clinical relevance in hemostatic regulation in patients with advanced atherosclerosis.
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PMID:Prostacyclin synthesis stimulating plasma factor in patients with peripheral vascular disease. 295 84

Epidemiologists studying the risk factors of coronary heart disease, as indicated by a heart attack, often presume that these risk factors combine in a susceptible host to increase the risk of the heart attack. The "biological" basis for the interaction of the key risk factors is often not considered in the analysis. A more rational model for the study of clinical heart disease, stroke, and peripheral vascular disease would be to separate the epidemiology of atherosclerosis from that of the clinical event. In the past, this has been extremely difficult because of the absence of techniques for the measurement of atherosclerosis in vivo, especially in well-defined populations. However, in recent years, greater emphasis on the quantification of atherosclerosis and its relationship to specific risk factors has improved our ability to study the underlying pathology that is atherosclerosis. Atherosclerosis is an example of a common-source epidemic. The environmental agent is the intake of cholesterol and saturated fat. The interaction of specific dietary factors and genetic determinants is the key to the evolution of atherosclerosis. There are marked variations in the evolution of the disease in different vascular beds as well as among individuals exposed to similar environmental factors. In the future, we will probably be able to study atherosclerosis as a continuous variable in populations and to relate the rate of progression, the extent of disease at any point in time, and topical distribution of atherosclerosis within individual vascular beds to specific genetic and environmental determinants.
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PMID:The epidemiology of atherosclerosis in 1987: unraveling a common-source epidemic. 304 99

Forty-eight patients (20 diabetic, 28 nondiabetic) with angiographically confirmed peripheral vascular disease (PVD) were examined to discover whether the measurement of pulse reappearance time (PRT) during reactive hyperemia is a more useful method than the measurement of peripheral systolic blood pressure (ankle pressure index; API) for making a specific diagnosis of PVD. Specific diagnosis refers to the degree and localization of occlusive atherosclerosis determined by Doppler ultrasound techniques for both measurements. We found that PRT and API both provided accurate qualitative proof of a peripheral blood flow deficit in diabetic and nondiabetic subjects. However, in relation to the angiographically defined degree and localization of sclerotic lesions, there were significant differences. The sclerotic degree of occlusive PVD in diabetic subjects was correlated with the results of the PRT (P less than .001), whereas the API was not (P greater than .05). The occlusion localization could only be distinguished by PRT measurements in both diabetic and nondiabetic subjects. Compared with control subjects (4.1 s) the half-maximum PRT of blood flow velocity was delayed in stenotic PVD to 5.7 s, in occlusive PVD of the upper leg to 14.3 s, in occlusive PVD of the lower leg to 29.6 s, and in multilevel disease to 45.0 s (P less than .0005 vs. control). The results show that Doppler sonographic measurement of the peripheral systolic blood pressure is only useful for an overall diagnosis of PVD in diabetic subjects, whereas PRT measurement, by quantifying the degree and localization of sclerotic lesions, can be used additionally either to confirm or to specify this diagnosis.
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PMID:Measurement of pulse reappearance time in diagnosis of peripheral vascular disease in diabetes. 304 11

Endothelial cells release a potent vasodilator which activates guanylate cyclase and thereby induces relaxation of vascular smooth muscle cells. The so-called endothelium-derived relaxing factor (EDRF) is released by acetylcholine, local and circulating hormones, and substances released from aggregating platelets or formed during activation of the coagulation cascade. Nitric oxide (NO) probably accounts for the factor's activity. Thus, endothelial cells produce endogenous nitrates causing vasodilatation and inhibition of platelet adhesion and aggregation. Under physiological conditions, EDRF may play a role in the prevention of vasospasm and thrombosis. On the other hand, the impairment of endothelial regulatory mechanisms in atherosclerosis and hypertension may be involved in the pathogenesis of vascular occlusion and thereby of myocardial infarction, stroke and peripheral vascular disease.
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PMID:[Endothelium-derived relaxing factor(s): endogenous nitrates in the circulation?]. 306 71

Ultrasonic investigations of the peripheral vessels (continuous Doppler with spectral analysis, echotomography) were performed to evaluate atherosclerosis of the main arteries (abdominal aorta, cervical arteries, lower limb arteries) in 50 coronary patients and 40 control subjects. In the main, our results support those of previously published series (epidemiological and autopsy studies): Atherosclerosis of the main arterial vessels is significantly more common (p less than 0.01) in coronary patients than in control subjects: carotid lesions: 70% (including 10% with severe stenosis) compared to 32% (no severe stenosis); aortic lesions: 50% (including 20% with severe stenosis) compared to 17.5% (7.5% severe stenosis); lower limb arteries: 58% (including 16% severe stenosis) compared to 12.5% (no severe stenosis). The difference of incidences of associations of atherosclerosed vessels between the two groups was significant (p less than 0.01): no peripheral vascular disease was detected in 57.5% of controls compared to only 12% of coronary patients; more than one territory diseased in 15% of controls compared to 58% of coronary patients. The severity of these lesions correlated with the presence of the three major cardiovascular risk factors which were studied (hypertension, smoking, hypercholesterolaemia) and was significantly higher (p less than 0.01) in coronary patients (38% had more than one major risk factor and only 10% had none) than in controls (47% had no risk factors and 6% had more than one). In addition, the preferential sites of atherosclerosis were also confirmed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Ultrasonic detection of arteriosclerosis of the main arterial trunks in the coronary patient]. 309 28

Platelets play an important role in the development of atherosclerosis. The arachidonic acid, whose oxygenated metabolites are potent regulators of the platelet-vessel wall interactions, is released from membrane phospholipids by the phospholipase (s) system (s). These membrane-linked phenomena are strongly modulated by the membrane physical properties. The present study was carried out to investigate the relationship between membrane fluidity and arachidonic acid metabolism in platelets from atherosclerotic patients. Twenty-one patients with peripheral vascular disease and twelve controls were studied. Platelets from patients showed an increase in membrane fluidity and enhanced thrombin-stimulated thromboxane synthesis. No alterations were found, however, in total phospholipid fatty acid composition. A significant decrease in the cholesterol/phospholipid ratio could account for the alterations in the membrane physical properties described in the platelets from patients.
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PMID:Membrane fluidity and thromboxane synthesis in platelets from patients with severe atherosclerosis. 309 71

Patients with insulin dependent diabetes mellitus who develop proteinuria may die prematurely, whereas those who do not develop this complication have a comparatively normal life span. The excess mortality in diabetics with proteinuria is from cardiovascular as well as renal disease, but the reason is unclear. Risk factors for vascular disease were therefore assessed in 22 insulin dependent diabetics with proteinuria, but not renal failure, who were matched for sex, age, duration of diabetes, and glycated haemoglobin (HbA1) values with a similar number who had normal urinary albumin excretion rates. Macrovascular disease (ischaemic heart disease and peripheral vascular disease) was present in 10 patients with proteinuria but in only three with normal albumin excretion rates, and proliferative retinopathy was detected in 11 and four patients in the two groups. There was no significant excess of smokers in the group with proteinuria. Blood pressure was, however, higher in the patients with proteinuria--mean systolic pressure 161 (SD 18) mm Hg compared with 135 (19) mm Hg (95% confidence interval of difference between means 15 to 38 mm Hg); mean diastolic pressure 90 (SD 12) mm Hg compared with 79 (15) mm Hg (confidence interval 3 to 19 mm Hg). The concentration of serum high density lipoprotein (HDL) cholesterol isolated by precipitation was lower in the patients with proteinuria (confidence interval 0.02 to 0.41 mmol/l). Their concentration of HDL2 cholesterol isolated by ultracentrifugation was also decreased (confidence interval 0.02 to 0.40 mmol/l), whereas HDL3 cholesterol tended to be increased (confidence interval -0.01 to 0.23 mmol/l). There was also a trend for serum cholesterol concentrations to be higher in the presence of proteinuria (confidence interval -0.39 to 1.20 mmol/l). The aggregation of risk factors for atherosclerosis in insulin dependent diabetes mellitus complicated by proteinuria helps to explain the increased prevalence of ischaemic heart disease and peripheral vascular disease reported in these patients. Early renal disease in insulin dependent diabetes may have an important role in hypertension and altered lipoprotein metabolism.
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PMID:Influence of proteinuria on vascular disease, blood pressure, and lipoproteins in insulin dependent diabetes mellitus. 311 68

Investigation of platelet function in a 55 year-old male suffering from peripheral vascular disease revealed platelet cyclooxygenase deficiency. Examination of femoral artery tissue at a later date likewise showed the presence of a cyclooxygenase defect. Investigated relatives were not affected. A 39 year-old male smoker admitted with an acute myocardial infarct without prodromal symptoms exhibited similar laboratory findings. In contrast to the cases reported in the literature so far, both our patients suffered from severe atherosclerosis, a relatively high platelet activity and an additional cyclooxygenase defect of cells other than the platelets. The patient with peripheral vascular disease died from sudden cardiac arrest.
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PMID:[Defects in the prostaglandin system. VII. (Generalized, inherited [?]) cyclooxygenase defect]. 314 31

The major antihypertensive mechanism of calcium antagonists is by decreasing the systemic vascular resistance, modified by the counter-regulatory responses of the baroreflexes and the renin-angiotensin-aldosterone system. In severe hypertension, the concept that calcium overload of the vascular myocyte could precipitate or aggravate peripheral vasoconstriction provides a logical basis for the use of these agents as first choice therapy; nifedipine, especially, has been well tested. As monotherapy for mild to moderate hypertension each of the three first-generation agents compares well with beta-blockers. Calcium antagonists may have a special role in the therapy of certain patient groups (elderly, black) or in those subjects whose life style involves intense physical or mental exertion (hemodynamics better maintained than with beta-blockade) or in patients with early end-organ damage such as left ventricular hypertrophy or renal insufficiency. However, the goal blood pressure may not be reached during monotherapy so that drug combinations may be required. Further indications for these compounds are as follows. Verapamil and diltiazem are frequently used in supraventricular tachycardias including acute and chronic atrial fibrillation. In the arrhythmias of the Wolff-Parkinson-White syndrome, there is the potential danger of provocation of anterograde conduction. Further indications for calcium antagonists, still under evaluation, include congestive heart failure (controversial), hypertrophic cardiomyopathy (verapamil), primary pulmonary hypertension (high doses required), Raynaud's phenomenon (nifedipine and diltiazem effective), peripheral vascular disease (proof not yet documented), cerebral insufficiency and subarachnoid hemorrhage (nimodipine promising), migraine, exertional bronchospasm, renal disease, atherosclerosis (experimental), and primary aldosteronism (nifedipine inhibits aldosterone release). Second-generation agents include dihydropyridines, such as nitrendipine, nicardipine, felodipine, amlodipine, nisoldipine, nimodipine, and isradipine. From these will be selected agents that are longer acting and provide higher vascular selectivity. New preparations of existing agents include slow-release formulations of nifedipine, verapamil, and diltiazem. Minor side effects include those caused by vasodilation (flushing and headaches), constipation (verapamil), and ankle edema. Serious side effects are rare and result from improper use of these agents, as when intravenous verapamil is given to patients with sinus or atrioventricular nodal depression from drugs or disease, or nifedipine to patients with aortic stenosis. The potential of a marked negative inotropic effect is usually offset by afterload reduction, especially in the case of nifedipine. Yet caution is required when calcium antagonists, especially verapamil, are given to patients with myocardial failure unless caused by hypertensive heart disease. Drug interactions of calcium antagonists occur with other cardiovascular agents such as alpha-adrenergic blockers, beta-adrenergic blockers, digoxin, quinidine, and disopyramide.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Calcium channel antagonists. Part III: Use and comparative efficacy in hypertension and supraventricular arrhythmias. Minor indications. 315 29

Results are presented of a retrospective analysis of 651 carotid endarterectomies in 605 patients with carotid territorial transient ischemic attacks (TIAs). All operations were performed by the same surgeon in a community hospital from 1963 to 1986. Arteriographic findings consisted of carotid stenosis of 50% or greater in 88.5% of patients and stenosis less than 50% and/or an ulcerated plaque in the remaining 11.5%. Medical risk factors were detected in 92% of patients; hypertension, peripheral vascular disease, and coronary atherosclerosis were most prevalent. All operative procedures were conducted with the patients under general anesthesia, routine shunting, and arterial closure without a patch. The perioperative stroke rate was 1.5% (10 patients); the morality rate was 0.8% (three deaths from myocardial infarction and two from stroke) for a combined stroke and mortality rate of 2.0% (13 of 605 patients). Follow-up (mean 61.8 months) was possible in 570 (96%) of the patients surviving operation without a perioperative stroke. The cumulative probability of late stroke (i.e., cerebral infarct ipsilateral to the operated artery) was 2.5% at 5 years and 8.1% at 10 years. When the perioperative stroke-mortality rate (2.0%) is combined with the data for late ipsilateral stroke, the 5- and 10-year probabilities of ipsilateral stroke were 4.5% and 9.9%, respectively (mean 1% per year for 10-year period). Coronary atherosclerosis accounted for 43% of late deaths and 16% of strokes. The perioperative stroke-mortality rate of 2.0% in this group of patients falls within the acceptable range for carotid endarterectomy in patients with TIA.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Carotid endarterectomy in patients with territorial transient ischemic attacks. 317 81

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