Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Coronary blood flow might be reduced by platelet aggregates or by vasospasm induced by platelet-produced thromboxane A2. Therefore the effects of the platelet inhibitor ticlopidine (500 mg daily) on platelet function and on exercise tolerance were investigated in a double-blind placebo-controlled study in 38 middle-aged men with stable incapacitating angina pectoris. Before and after 4 and 8 weeks of treatment, exercise tests were performed in warm and cold environments. The in vitro platelet reactivity to ADP was determined at rest and the plasma levels of beta-thromboglobulin (BTG) and platelet factor 4 (PF4) were measured before and immediately after exercise. There were no signs of increased platelet activity at rest or after exercise as judged by the levels of BTG and PF4. Despite a potent inhibition of platelet reactivity to ADP in vitro during ticlopidine treatment, the exercise tolerance was reduced in exercise tests in both warm and cold environments and in daily life. Therefore platelet activity does not seem to play any significant role in exercise tolerance in the stable phase of angina pectoris.
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PMID:Effects of the platelet inhibitor ticlopidine on exercise tolerance in stable angina pectoris. 294 74

Two different methods of causing myocardial oxygen demand and supply imbalance; symptom limited treadmill exercise and right atrial pacing stimulation, were used to examine the alteration of hemodynamics and the effects upon sympathetic nerve activities, platelet functions and prostaglandin synthesis in patients with coronary artery disease (CAD). Age and sex distributions, the cardiothoracic ratio, left ventricular end-diastolic pressure, ejection fraction and coronary artery obstructions of the patients did not differ significantly between the two tests. Arterial blood samples were obtained to assay for plasma catecholamine, beta-thromboglobulin (beta TG), platelet factor 4 (PF4), TXB2 (thromboxane B2) and 6 keto-PGF1-alpha (6 ketoprostaglandin F1-alpha) without any difficulties before and immediately after testing. The arterial systolic pressure and pressure rate product (PRP) were changed more significantly by treadmill exercise than pacing, while the DPTI/TTI (diastolic pressure time index/tension time index) ratio and ST segment deviations showed similar changes with both tests. The plasma NE (norepinephrine) level, beta TG, PF4, and TXB2/6 keto-PGF1-alpha were significantly elevated by treadmill exercise, but not by pacing. 6 keto-PGF1-alpha was not markedly affected by either tests. There were no significant differences between the patients with and without anginal pain either in hemodynamics or metabolites. Significant relationships were observed between changes in plasma NE levels and the PRP (r = 0.76, n = 26, p less than 0.01) and also changes in the arterial systolic pressure (r = 0.64, n = 26, p less than 0.01), but there were no significant correlations between any other hemodynamic parameters with plasma NE, platelet function, prostaglandin activity, or between each metabolite.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of treadmill and pacing stress testing on peripheral arterial thromboxane, platelet function and catecholamine activities in patients with chronic coronary artery disease. 295 24

Indexes of in vivo platelet activation, beta-thromboglobulin and platelet factor 4 were measured in triplicate in plasma from venous blood of 69 patients with proven ischaemic heart disease (IHD), discarding samples with a ratio of the plasma concentrations of the two proteins less than 2.6, in order to rule out sampling artifacts. Compared with 60 control volunteers, differences were not significant [for beta-thromboglobulin controls (ng ml-1, mean +/- SD) 27.8-8.6, ischaemic patients 32.3 +/- 17.1; for platelet factor 4 controls 4.3 +/- 1.4, ischaemic patients 5.9 +/- 5.7]. However, when patients were stratified according to disease activity (Group I--patients without spontaneous ischaemic episodes at rest during 4 days of continuous electrocardiographic monitoring; Group II--patients with less than 1 ischaemic episode/day; Group III--patients with greater than 1 episode/day), these indexes were increased in 'active' patients (for beta-thromboglobulin, in Group II--32.4 +/- 10.5 ng ml-1, P less than 0.05 vs. Group I; in Group III--42.6 +/- 14.6 ng ml-1, P less than 0.01 vs. Group I, P less than 0.05 vs. control. Platelet factor 4 was increased only in Group III--8.9 +/- 7.2 ng ml-1, P less than 0.05 vs. control). Beta-thromboglobulin and platelet factor 4 were 25.0 +/- 6.7 ng ml-1 and 4.9 +/- 4.8 ng ml-1, respectively, in Group I (P = NS vs. control). A relationship with the number of spontaneous ischaemic episodes at rest was confirmed by linear regression analysis (in Group III patients for beta-thromboglobulin: r = 0.76, P less than 0.01, and for platelet factor 4 r = 0.62, P less than 0.01). Levels were not elevated in patients with previous myocardial infarction without ischaemia at rest and/or patients with stable angina, and were not influenced by the occurrence of a positive exercise stress test. Coronary angiograms of ischaemic patients were analyzed to assess the extent and severity of atherosclerotic involvement: for both extent and severity, involvement was similar in the three groups. These data support the hypothesis of the occurrence of platelet activation in patients with spontaneous angina at rest, but not in other subsets of IHD patients, and establish the possibility of detecting in vivo platelet activation in IHD by means of such circulating markers.
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PMID:Platelet activation in angina at rest. Evidence by paired measurement of plasma beta-thromboglobulin and platelet factor 4. 297 44

Platelet function (aggregation, circulating platelet aggregates, platelet factor 4, beta-thromboglobulin, thromboxane B2, 6-keto-PGF1 alpha, platelet count) was evaluated in patients with angina of new onset, as compared to individuals without coronary heart disease, and patients with angina of long standing (28 +/- 4.6 months). Some of the patients with angina of new onset were examined repeatedly 6 to 12 months after the onset of angina. Platelet activity was shown to be significantly higher in patients with stable angina of new onset, as compared to patients with lasting angina, where ADP and serotonin were used as inductors. Platelet aggregation, induced by platelet activation factor and collagen, was similar in all groups. Repeated investigation 6 to 12 months after the first anginal attacks demonstrated that most of platelet functional parameters declined or tended to decline.
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PMID:[Newly developed stenocardia: functional activity of thrombocytes]. 297 4

Twenty-three patients with essential hypertension and diabetes mellitus type II were treated with the calcium antagonist diltiazem (120 to 180 mg twice daily). The mean dose was 307 mg/day. The study was a double-blind, placebo-controlled, crossover design. All measurements were performed 12 to 14 hours after drug intake. Blood pressure, heart rate and forearm blood flow were measured noninvasively. Platelet function was studied by measuring adenosine diphosphate-induced platelet aggregation and the platelet specific proteins, beta thromboglobulin and platelet factor 4. Thromboxane B2 formation in serum and the plasma concentration of diltiazem and its metabolites N-demethyldiltiazem, deacetyldiltiazem and N-demethyldeacetyldiltiazem were measured both during placebo and diltiazem treatment. Diabetic control was evaluated by following HbA1C, fasting blood glucose and urinary glucose. Diltiazem reduced both systolic and diastolic (supine and standing) blood pressure significantly. Forearm blood flow was significantly increased by 32%, p less than 0.05. Supine heart rate decreased significantly, while no such change was seen in the standing position. No significant changes were observed in platelet function during diltiazem treatment. There was no relation between the observed blood pressure reduction and the plasma concentration of diltiazem or its metabolites. A positive correlation between the change in heart rate and the metabolite N-demethyldeacetyldiltiazem was observed (r = 0.647, p = 0.005). Three patients were excluded during diltiazem treatment (skin exanthema, headache and atrial fibrillation) and 1 during placebo treatment (angina pectoris). No negative effect on diabetes control was observed. Thus, diltiazem could be used for treatment of hypertension in diabetic patients.
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PMID:Diltiazem in hypertensive patients with type II diabetes mellitus. 317 28

Blood samples were taken for haemostatic analysis from 225 patients with angina pectoris who were admitted to hospital for coronary angiography. beta thromboglobulin, platelet factor 3, platelet factor 4, factor VII:C, factor VIII:C, von Willebrand factor antigen, activated partial thromboplastin time, fibrinogen, antithrombin III, protein C:Ag, plasminogen, and antiplasmin were measured before angiography. Patients who had had a myocardial infarction in the two months before the investigation were excluded from the study. Multiple linear regression analysis showed that none of the haemostatic variables contributed independently to the prediction of an angiographic score that indicated the extent of coronary atherosclerosis. History of myocardial infarction, male sex, worsening of angina pectoris, serum triglycerides, and ejection fraction were independently associated with the angiographic score. There were some significant correlations between haemostatic variables and conventional risk factors for coronary heart disease. Thus data obtained from haemostatic analyses of peripheral venous blood do not permit the presence or the extent of atherosclerosis in coronary arteries to be predicted.
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PMID:Lack of association between haemostatic variables and the presence or the extent of coronary atherosclerosis. 325 21

Ticlopidine is an inhibitor of platelet action that has been used in the treatment of a variety of disease states in which platelets play a prominent role. Studies in animals and man have demonstrated that ticlopidine is a potent inhibitor of platelet aggregation induced by adenosine diphosphate (ADP), and variably inhibits aggregation due to collagen, adrenaline (epinephrine), arachidonic acid, thrombin, and platelet activating factor. Inhibition of platelet aggregation is both dose- and time-related, with its onset of activity being 24 to 48 hours, its maximal activity occurring after 3 to 5 days, and its activity still being present 72 hours after a final dose. Ticlopidine also inhibits the release reaction of platelets, prolongs bleeding time, reduces plasma levels of platelet factor 4 and beta-thromboglobulin in patients in whom these proteins are elevated, and may also inhibit platelet adhesion, increase red cell filtrability and decrease whole blood viscosity. In a large number of animal models, ticlopidine markedly inhibits thrombus formation or graft occlusion. Ticlopidine is well absorbed after oral administration. It is extensively metabolised and at least one of its metabolites is pharmacologically active. Therapeutic trials in patients with chronic arterial occlusion due to thrombangitis obliterans or arteriosclerosis obliterans, post-myocardial infarction, cerebrovascular thromboembolic disease, subarachnoid haemorrhage, vascular shunts or fistulas for haemodialysis, and sickle cell disease have shown promise for the use of ticlopidine. However, trials of patients with intermittent claudication, angina pectoris, diabetes mellitus with microvascular disease, aortocoronary bypass grafts, and vascular prostheses have had conflicting results or have shown an unfavourable side effect profile. Further studies are clearly required to establish the role of ticlopidine in many of these areas, some of which are already in progress. Overall, side effects occur in 10 to 15% of patients receiving ticlopidine. The most common side effects are gastrointestinal disturbances and skin rashes. Neither of these necessarily require discontinuation of therapy in most patients. Agranulocytosis, thrombocytopenia, and cholestatic jaundice have also been reported. Bleeding is infrequent except possibly in patients receiving ticlopidine prior to some surgical procedures.
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PMID:Ticlopidine. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic efficacy in platelet-dependent disease states. 330 67

The effects of ticlopidine (T) (500 mg daily) on platelet function were investigated in a double-blind placebo-controlled study in 38 middle-aged men with stable incapacitating angina pectoris. The in vitro platelet reactivity to aggregating agents, the platelet sensitivity to prostacyclin and the plasma levels of platelet specific proteins and fibrinogen were determined before and after 4 and 8 weeks of treatment. T exerted a potent inhibitory effect on ADP-and collagen-induced platelet aggregation. The effect of T was proportional to the pretreatment reactivity to ADP and collagen. The inhibitory effect of T on the epinephrine response was less pronounced. The plasma levels of beta-thromboglobulin, platelet factor 4 and fibrinogen were not influenced by T. The platelet inhibition of prostacyclin was potentiated by T, and it was demonstrated that T and prostacyclin had synergistic inhibitory effects on platelet aggregation.
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PMID:Effects of ticlopidine of platelet function in men with stable angina pectoris. 391 81

Pathologic and experimental evidence indicates that platelet activation and fibrin formation contribute to the pathogenesis of angina pectoris, coronary vasospasm and myocardial infarction. Detection of localized intravascular platelet activation and fibrin formation in vivo by selective blood sampling requires catheters that do not induce coagulation ex vivo. We studied the effect of heparin bonding of catheter surfaces on activation of the coagulation system by cardiovascular catheters. Woven Dacron, polyvinylchloride, and polyurethane catheters were tested and compared with identical catheters with heparin-bonded surfaces in 47 patients undergoing percutaneous cardiac catheterization. Platelet activation was measured by radioimmunoassay of plasma platelet factor 4 (PF4), beta-thromboglobulin (BTG), and thromboxane B2 (TXB2) in blood samples withdrawn through catheters, and fibrin formation was assessed by determination of fibrinopeptide A (FPA) levels. In blood samples collected through conventional catheters, FPA, PF4, BTG, and TXB2 levels were markedly elevated; blood sampling through heparin-bonded catheters had no significant effect on FPA, PF4, BTG, or TXB2 levels. Scanning electron microscopy disclosed extensive platelet aggregates and fibrin strands adherent to the surface of conventional catheters but not to heparin-bonded catheter surfaces. This study demonstrates that (1) collection of blood samples through cardiovascular catheters causes artifactual elevation of FPA, PF4, BTG, and TXB2 levels, and (2) heparin-bonded catheter surfaces effectively prevent catheter-induced platelet alpha-granule release and fibrin formation on catheter surfaces. Heparin-bonded catheters will facilitate investigation of the role of intravascular coagulation in coronary artery disease by eliminating catheter-induced fibrin formation and platelet activation.
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PMID:Effect of heparin bonding on catheter-induced fibrin formation and platelet activation. 623 7

Radio-immunological assay of specific platelet substances in the serum allows assessment of in vivo platelet function at a given moment. Plasma levels of beta thromboglobulin (beta TG) platelet factor 4 (PF4) and thromboxane B2 (TXB2) were measured at rest and during exercise stress testing in 39 patients with known coronary artery disease with stable effort angina. The patients were divided into two groups according to the results of exercise ECG and thallium 201 myocardial scintigraphy: ischaemic (n = 28) and non-ischaemic (n = 11). Resting and exercise levels of the three platelet substances were compared with a group of normal controls (n = 14). The average control values at rest and on exercise were, respectively: PF4: 8.5 +/- 5 and 22 +/- 14 ng/ml; beta TG: 36 +/- 17 and 68 +/- 36 ng/ml and TXB2: 112 +/- 41 and 201 +/- 81 pg/ml. The average values of the non-ischaemic patients did not differ significantly, either at rest or during exercise. The variation of pathological values was higher in the ischaemic group. This seems to reflect the absence of univocal platelet behaviour and does not allow statistical comparison of mean values. Our results suggest the existence of an "unstable platelet syndrome", which seems to be associated with poor effort tolerance especially when present under resting conditions. There would seem to be a causal relationship between platelet instability and myocardial ischaemia, which would justify anti-platelet aggregation therapy in primary and secondary prophylaxis of myocardial infarction.
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PMID:[Platelet function and coronary disease: demonstration of a so-called unstable platelet syndrome]. 623 99


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