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

Tests of platelet behaviour in vitro, particularly aggregation and retention and in vivo tests such as measurement of platelet survival and plasma levels of beta-thromboglobulin are frequently abnormal in diabetic patients, particularly in those with vascular disease. The concept has therefore arisen that platelet hyper-reactivity is one factor responsible for diabetic microangiopathy. Whereas there is experimental and histological evidence for the mediation of platelets in the pathogenesis of atherosclerosis, direct evidence of platelet involvement in microangiopathy is scanty. Similar alterations in platelet behaviour have been observed in a variety of other conditions with vessel wall damage in common and evidence is presented which suggests that these platelet abnormalities may be secondary to vessel wall injury. In diabetic subjects, some changes in platelet behaviour are reversed by improved glycaemic control. Evidence that platelets are involved in the pathogenesis of diabetic microangiopathy therefore remains circumstantial, though current trials of anti-platelet agents may enable a more precise evaluation of their role.
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PMID:Platelets and diabetic vascular disease. 623 Feb 70

Platelet activation may participate in the pathophysiology of myocardial infarction occurring in patients with normal coronary arteriogram. We investigated this possibility in a series of 9 such patients (group A) during a standardized bicycle exercise test as myocardial infarction had occurred in all of them during or soon after strong physical exercise. Twelve patients with effort-induced angina and coronary atherosclerosis (group B) and eleven healthy subjects (group C) served as test groups. Peripheral venous blood was collected by separate venipuncture before, at peak exercise and during recovery. As a sensitive index of activation, the shape of the circulating platelets was examined with a phase contrast microscope after instantaneous fixation of the whole blood. The percentage of non strictly disc-shaped platelets with one or more thin pseudopods was determined. Simultaneously, the plasma levels of platelet factor 4 (PF4) and of beta-thromboglobulin (beta-TG) were measured. At rest, there was no significant difference in the platelet morphology nor in the plasma levels of platelet specific proteins between the three groups. During exercise, a significant change in platelet shape occurred in group A and B patients and not in the healthy subjects. This platelet activation was not related to myocardial ischemia since it occurred to a similar extent in group B patients who developed electrocardiographic changes and in group A patients who did not. There was no detectable release of platelet proteins during exercise in any group.
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PMID:Exercise-induced platelet activation in myocardial infarction survivors with normal coronary arteriogram. 624 54

Plasma level of beta-thromboglobulin (beta TG), a useful marker of in vivo platelet "release reaction,"was determined by radioimmunoassay in 69 patients, with three types of primary hyperlipidemia (IIa, IIb, IV) and compared with the findings in age- and sex-matched healthy controls and 57 patients with established atherosclerosis and peripheral vascular disease. Malondialdehyde (MDA) formation, used for assessment of prostaglandin synthesis, was determined in 51 and plasma platelet factor 4 (PF4), measured by radioimmunoassay, in 48 of the patients with hyperlipidemia. Results were correlated to five serum lipids and lipoprotein levels in the patients with hyperlipidemia. beta TG was significantly increased in the patients with hyperlipidemia and peripheral vascular disease, compared to those in the controls (p < 0.001); it was significantly higher in the patients with hyperlipidemia than in those with peripheral vascular disease. PF4 and MDA formation were also increased in the patients with hyperlipidemia, and significantly higher levels of MDA were obtained in patients with type IIb and type IV hyperlipidemia than in those with type IIa hyperlipidemia (p < 0.02). beta TG and MDA correlated weakly with total serum cholesterol triglycerides and very low density lipoprotein-triglyceride. There was also a significant correlation between beta TG and PF4, and MDA production. These results indicate that in vivo platelet "release reaction" and MDA formation are increased in hyperlipidemic patients. The release reaction is more enhanced in those with hyperlipidemia than in the patients with peripheral vascular disease. They suggest that the abnormal platelet function is related to the elevated levels of serum lipids and lipoproteins in the hyperlipidemic patients and not only to the atherosclerotic changes associated with hyperlipidemia.
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PMID:Enhanced in vivo platelet release reaction and malondialdehyde formation in patients with hyperlipidemia. 645 May 32

Of the various biological roles assigned to growth factors at the beginning of this article, the factors described here are largely associated with the response to injury. These represent a special type of factor since two of them, PDGF and MDGF, are carried in the circulation by the platelet and the monocyte respectively, and can therefore be delivered to sites where a proliferative response would be an important event in the restitution of tissue continuity. The role of the endothelial-derived growth factor in these phenomena is not clear at present. Atherosclerosis has been suggested to represent a protective proliferative response that has gone awry and become disease. In this instance both PDGF and MDGF could play important roles, since platelets have been associated with the early injury phenomenon and macrophages appear to be present in virtually all phases of the development of the lesions of atherosclerosis from the fatty streak to the fibrous plaque and the complicated lesion. In each of these circumstances the macrophage may be important in lesion progression and possibly in lesion initiation. PDGF may also be important in initiation of some lesions, and in some instances would undoubtedly participate in the fibroproliferative response that occurs during organization of a thrombus.
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PMID:Growth factors from platelets, monocytes, and endothelium: their role in cell proliferation. 681 81

We studied 27 non-insulin-dependent diabetics without apparent atherosclerosis (AS) to investigate whether abnormal platelet function is related to asymptomatic atherosclerosis in diabetes mellitus. The degree of AS was quantitatively evaluated by determining the intimal plus medial thickness (IMT) of the carotid artery wall with ultrasound high-resolution B-mode imaging. Based on our previous finding that the upper threshold of the IMT was 1.1 mm in healthy subjects, the patients were divided into the AS-positive group with the IMT > 1.1 mm, (n = 17) and the AS-negative group with the IMT < 1.1 mm (n = 10). Among five variables measured as the factors concerned with thrombogenesis, only plasma levels of beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4) were significantly higher in the AS-positive group than in the AS-negative group. Chronic administration of pentoxifylline (300 mg/day) significantly reduced the abnormally high plasma levels of beta-TG and PF4 in 7 patients of the AS-positive group to normal levels, without lowering the normal plasma beta-TG and PF4 levels in the remaining 10 patients. Pentoxifylline treatment did not affect the plasma levels of the 3 other variables, von Willebrand factor, 6-keto prostaglandin F1 alpha and thromboxane B2. This study suggests that the progress of atherosclerosis in diabetes mellitus is associated with in vivo platelet activation and platelet activation does not occur in diabetics without carotid atherosclerosis. Pentoxifylline may impede the vicious cycle in which atherosclerosis is accelerated by platelet activation.
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PMID:Platelet activation in diabetic patients with asymptomatic atherosclerosis. 795 14

Sixteen patients with lower limb atherosclerosis (LLAS) stage II-III received autotransfusions of blood irradiated by ultraviolet light. Vascular wall antithrombogenic properties assessed before the treatment in the patients and controls were found deteriorated in LLAS subjects. The cuff test did not affect the antithrombogenic characteristics. The course of autotransfusions produced a clinical improvement and strengthening of the antithrombogenic properties. The cuff test demonstrated a significant decline in platelet aggregation in response to ADP, thrombin, collagen, ristomycin, arachidonic acid; of platelet factor 4, thromboxane B2, beta-thromboglobulin. Concentrations of antithrombin III, plasminogen, prostacyclin rose. The autotransfusions were made on "Izolda" device MD-73 (1 ml of blood per 1 kg b. mass). Irradiation dose 750 J/m2, wave length 254 nm. Platelet aggregation was studied according to Born technique in O'Brien modification. Thromboxane B2, 6-keto-PGF1 alpha, beta-thromboglobulin and TF 4 were measured by radioimmunoassay, antithrombin III and plasminogen by chromogenic substrates.
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PMID:[The antithrombogenic properties of the vascular wall and platelet aggregation in patients with atherosclerosis of the arteries of the lower extremities following a course of treatment with UV-irradiated autologous blood transfusion]. 802 Jul 15

Platelet catecholamine content may reflect integrated plasma catecholamine concentrations over time. The present study aimed at examining sympathetic nervous system (SNS) involvement in essential hypertension by assessing platelet noradrenaline (NA) and typically beta-adrenoreceptor mediated responses to adrenaline (A) infusion as indices of sympathetic tone. Healthy white men were recruited by public advertising and screening (mean +/- SD): Hypertensives (n = 13, sitting blood pressure [BP] 153 +/- 13/106 +/- 7 mmHg, age 34 +/- 5 years, weight 83 +/- 10 kg) were compared to normotensives (n = 13, sitting BP 114 +/- 9/75 +/- 9 mmHg, age 30 +/- 6 years [n.s.], weight 82 +/- 9 kg [n.s.]). Loss of platelet granular contents (including NA) prior to analysis was minimized by studying young subjects (age range 20-40 years, minimal atherosclerosis), using arterial blood sampling, and processing blood immediately. These procedures resulted in plasma beta-thromboglobulin and platelet factor 4 levels which were not significantly different between groups. Sympathetic activation resulting from stress was minimized by not labelling subjects as either hypertensive or normotensive. Mean arterial platelet NA content was significantly higher in hypertensives (64 +/- 31 pg/mg of platelet weight) compared to normotensives (43 +/- 20 pg/mg, p < 0.05) both at baseline and following 35% expansion of the circulating platelet pool by A infusion (p < 0.05) and correlated with arterial NA in the hypertensives (r = 0.79, p < 0.002) but not in the normotensives (r = 0.04, n.s.). Similar increases in platelet and plasma A during infusion in both groups suggest unchanged platelet uptake capacity and plasma clearance in the hypertensive group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sympathetic nervous system involvement in essential hypertension: increased platelet noradrenaline coincides with decreased beta-adrenoreceptor responsiveness. 806 4

The platelet-aggregatory response, platelet-release factors and markers of thrombin generation in vivo were studied prospectively in 53 patients participating in a randomized clinical trial evaluating the influence of nicardipine on the progression of coronary atherosclerosis. Coronary lesions were measured quantitatively and progression was defined as a decrease in minimum diameter by > or = 0.4 mm. At repeat angiography 24 months after study entry, 20 of the 53 patients had progression of 28 coronary narrowings. Only thrombin-induced enhanced platelet aggregation differentiated patients with from those without coronary disease progression, with an estimated odds ratio of 2.49 (95% confidence interval 1.10 to 5.66). The aggregatory response to adenosine diphosphate, collagen, epinephrine and platelet-activating factor were not different in the 2 groups of patients, nor were measurements of platelet factor 4, beta-thromboglobulin, thromboxane B2, 6-keto-prostaglandin F1 alpha and fibrinopeptide A. During 46.8 months of follow-up after repeat angiography, coronary events occurred in 11 of the 20 with and 6 of the 33 without progression (difference 37%, p = 0.013, confidence interval 11 to 63%). Those with coronary disease progression and an enhanced thrombin-induced platelet aggregation had a worse prognosis than those with no disease progression and a low thrombin-induced platelet aggregation. Thus, patients with coronary disease progression and future coronary events have an enhanced thrombin-induced platelet aggregation. This platelet abnormality may be a marker of increased risk and may play a causative role in the development of coronary events.
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PMID:Platelet aggregation, coronary artery disease progression and future coronary events. 810 46

Thrombin, the final product of blood coagulation cascade, shows several effect on the vessel-wall cells. However the effects may be regulated by several thrombin receptors on the endothelium. They include thrombomodulin (TM), protease-Nexin, heparin-like molecule-antithrombin III complex. These binding sites do not transduce the signal of thrombin. Especially TM converts thrombin from a procoagulant protease to an anticoagulant. Recently new thrombin receptor was identified on the endothelium and platelets. Through this receptor, thrombin induces activations both on platelet end-endothelium. In brief platelets aggregate and release several factors including serotonin, PDGF, platelet factor4, beta-thromboglobulin on the stimulation by thrombin. The endothelium release t-PA inhibitor; PAI-1, prostacyclin and endothelin. Thus the activations of these cells by thrombin is a key events in hemostasis, wound healing, inflammation, atherosclerosis and restenosis of coronary artery after PTCA.
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PMID:[Regulation of the endothelial function by thrombomodulin and/or thrombin receptor]. 815 41

The aim of this study was to determine differences between cases of peripheral arterial disease and healthy controls in levels of haemostatic factors and lipid peroxides and the influence of cigarette smoking. The study groups were selected from the Edinburgh Artery Study which is a random sample survey of men and women aged 55-74 years. Mean levels of plasma fibrinogen, von Willebrand factor, beta-thromboglobulin, plasminogen activator inhibitor (type I), cross-linked fibrin degradation products and lipid peroxides were markedly elevated in 121 study cases compared with 126 age- and sex-matched controls. For example, cross-linked fibrin degradation products had a geometric mean of 106.8 ng/ml (95% confidence interval (CI) 95.3, 119.8) in study cases and 74.7 ng/ml (95% CI 67.0, 83.4) in controls (P < 0.001). Inclusion of smoking in logistic regressions of each factor on peripheral arterial disease significantly reduced the odds of disease for von Willebrand factor and for cross-linked fibrin degradation products, but had little effect on the increased odds associated with fibrinogen, beta-thromboglobulin, plasminogen activator inhibitor and lipid peroxides. We conclude that, in men and women in Edinburgh, peripheral atherosclerosis is associated with lipid peroxidation, endothelial disturbance, platelet activation, elevated fibrinogen, fibrin formation and increased inhibition of fibrinolysis. The most important effects of cigarette smoking in promoting atherosclerosis may be endothelial disturbance and fibrin formation.
Atherosclerosis 1993 Sep
PMID:Smoking, haemostatic factors and lipid peroxides in a population case control study of peripheral arterial disease. 825 Oct 1


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