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      Plasma Apolipoprotein B Levels Predict Platelet-Dependent Thrombosis in Patients with Coronary Artery Disease


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          Elevated plasma apolipoprotein B is a known risk factor for atherosclerotic coronary artery disease (CAD), however its relationship to arterial thrombosis is unexplored. We prospectively assessed apolipoprotein B and platelet-dependent thrombosis (PDT) in 42 CAD patients (37 men, 5 women, mean age 68 ± 9 years), by exposing porcine aortic media to their flowing unanticoagulated venous blood for 5 min using an ex vivo perfusion (Badimon) chamber. PDT was significantly correlated with apolipoprotein B (r = 0.41, p = 0.009), intracellular magnesium levels (r = –0.46, p = 0.003) fasting blood glucose (r = 0.47, p = 0.002), and total cholesterol (r = 0.43, p = 0.006). PDT did not correlate with serum total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, apolipoprotein A-I or fibrinogen levels. These findings suggest that the positive relationship of elevated apolipoprotein B to CAD may be, in part, related to its prothrombotic effects.

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          The electronic aggregometer: a novel device for assessing platelet behavior in blood.

          A novel device for measuring platelet aggregation has been devised. The technique, which depends upon changes in electrical impedance caused by platelet accretion onto electrodes, is suitable for measurements of aggregation in either platelet-rich plasma (PRP) or blood. In PRP both turbidometric and electronic techniques give very similar responses to collagen, thrombin, prostaglandin endoperoxides, ADP, and arachidonic acid, although the electronic aggregometer gives no "shape-change" information and was somewhat more sensitive. In whole blood all these stimuli gave similar dose-related responses to those seen in PRP. The new technique is very suitable for investigating platelet pharmacology, since the inhibitors of aggregation, such as indomethacin and prostacyclin, can be conveniently quantitated in blood by using this technique.
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            Oral magnesium supplementation inhibits platelet-dependent thrombosis in patients with coronary artery disease.

            The use of magnesium in the treatment of acute myocardial infarction remains controversial despite preliminary experimental evidence that magnesium plays a beneficial role as a regulator of thrombosis. This study examines whether oral magnesium treatment inhibits platelet-dependent thrombosis (PDT) in patients with coronary artery disease (CAD). In a randomized prospective, double-blind, crossover, and placebo-controlled study, 42 patients with CAD (37 men, 5 women, mean age 68 +/- 9 years) on aspirin received either magnesium oxide tablets (800 to 1,200 mg/day) or placebo for 3 months (phase 1) followed by a 4-week wash-out period, and the crossover treatment for 3 months (phase 2). PDT, platelet aggregation, platelet P-selectin flow cytometry, monocyte tissue factor procoagulant activity (TF-PCA), and adhesion molecule density were assessed before and after each phase. PDT was evaluated by an ex vivo perfusion model using the Badimon chamber. Median PDT was significantly reduced by 35% in patients who received magnesium versus placebo (delta change from baseline -24 vs 26 mm2/mm; p = 0.02, respectively). There was no significant effect of magnesium treatment on platelet aggregation, P-selectin expression, monocyte TF-PCA, or adhesion molecules. Oral magnesium treatment inhibited PDT in patients with stable CAD. This effect appears to be independent of platelet aggregation or P-selectin expression, and is evident despite aspirin therapy. These findings suggest a potential mechanism whereby magnesium may beneficially alter outcomes in patients with CAD.
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              Apolipoproteins and ischaemic heart disease: implications for screening


                Author and article information

                S. Karger AG
                February 2000
                23 March 2000
                : 92
                : 3
                : 151-155
                Preventive & Rehabilitative Cardiac Center and Atherosclerosis Research Center, Cedars-Sinai Burns and Allen Research Institute, Department of Medicine, Division of Cardiology, Cedars-Sinai Medical Center and UCLA School of Medicine, Los Angeles, Calif., USA
                6964 Cardiology 1999;92:151–155
                © 2000 S. Karger AG, Basel

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                Page count
                Figures: 2, Tables: 2, References: 20, Pages: 5
                General Cardiology

                General medicine,Neurology,Cardiovascular Medicine,Internal medicine,Nephrology
                Thrombosis,Coronary disease,Platelets,Apolipoproteins


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