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)

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

The hypothesis that exercise-induced myocardial ischemia is associated with abnormal platelet activation and fibrin formation or dissolution was tested in patients with coronary artery disease undergoing upright bicycle stress testing. In vivo platelet activation was assessed by radioimmunoassay of platelet factor 4, beta-thrombo-globulin and thromboxane B2. In vivo fibrin formation was assessed by radioimmunoassay of fibrinopeptide A, and fibrinolysis was assessed by radioimmunoassay of thrombin-increasable fibrinopeptide B which reflects plasmin cleavage of fibrin I. Peripheral venous concentrations of these substances were measured in 10 normal subjects and 13 patients with coronary artery disease at rest and during symptom-limited peak exercise. Platelet factor 4, beta-thromboglobulin and thromboxane B2 concentrations were correlated with rest and exercise catecholamine concentrations to determine if exercise-induced elevation of norepinephrine and epinephrine enhances platelet activation. Left ventricular end-diastolic and end-systolic volumes, ejection fraction and segmental wall motion were measured at rest and during peak exercise by first pass radionuclide angiography. All patients with coronary artery disease had documented exercise-induced myocardial ischemia manifested by angina pectoris, ischemic electrocardiographic changes, left ventricular segmental dyssynergy and a reduction in ejection fraction. Rest and peak exercise plasma concentrations were not significantly different for platelet factor 4, beta-thromboglobulin, thromboxane B2, fibrinopeptide A and thrombin-increasable fibrinopeptide B. Peripheral venous concentrations of norepinephrine and epinephrine increased significantly (p less than 0.001) in both groups of patients. The elevated catecholamine levels did not lead to detectable platelet activation. This study demonstrates that enhanced platelet activation, thromboxane release and fibrin formation or dissolution are not detectable in peripheral venous blood of patients with coronary disease during exercise-induced myocardial ischemia.
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PMID:Exercise-induced myocardial ischemia in patients with coronary artery disease: lack of evidence for platelet activation or fibrin formation in peripheral venous blood. 633 91

In 19 patients with unstable angina pectoris at rest, plasma levels of the platelet-derived proteins beta-thromboglobulin and platelet factor 4 were significantly elevated in blood samples obtained during or within 4 hours after episodes of angina, but were usually normal during quiescent intervals. Plasma levels of the arachidonic acid metabolite thromboxane B2 were less clearly related to angina, and there was no association of angina with levels of the coagulation product fibrinopeptide A. This demonstration of an association of platelet activation and secretion with unstable angina pectoris by radioimmunoassay of circulating platelet constituents offers a new approach to assessment of therapy in ischemic heart disease and suggests that agents that alter platelet function should be evaluated in patients with unstable angina.
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PMID:Circulating platelet products in unstable angina pectoris. 645 1

Previous studies have shown that there is both a significant shortening in platelet survival and a measured hyperactivity to platelet-aggregating agents in patients with documented coronary artery disease compared with control groups. We used a recently described radioimmunoassay for the platelet-secreted protein platelet factor 4 (PF4) to study 162 patients with documented coronary artery disease. There was a significant increase in plasma PF4 concentrations in patients with documented coronary artery disease compared with angiographically normal patients (8.7 vs 16 ng/ml, respectively, n = 121), but as in previous studies of platelet survival, we could not correlate elevated plasma PF4 concentration and the severity or site of the coronary artery disease. In addition, there was no correlation with left ventricular function, serum cholesterol or the type of angina. Patients with confirmed acute myocardial infarction had no significant difference in mean plasma PF4 concentrations compared with similar groups of coronary disease patients who had prolonged chest pain or chronic stable angina. Coronary artery bypass grafting in a subgroup of patients did not affect the mean plasma PF4 concentration during 1 year of follow-up after bypass surgery, but medical therapy for angina with increasing doses of propranolol and nitrates significantly reduced PF4 concentration in another subgroup of patients who were not considered to be candidates for surgical therapy.
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PMID:Increased plasma concentrations of platelet factor 4 in coronary artery disease: a measure of in vivo platelet activation and secretion. 697 19

Increases in endogenous free fatty acids (FFA) induced by several stimuli are associated with increases in platelet aggregates and platelet factor 4 in man. To determine if thromboxane (TxB) release is also an associated event, we measured plasma FFA and TxB2 levels before and 5 min after bolus injection of 2,500 U of heparin prior to coronary arteriography in 27 patients with angina. Significant increases in FFA occurred in all patients (p less than 0.02) and those with critical lesions (p less than 0.01), while TxB2 levels also rose (p less than 0.02, p less than 0.05, respectively). However, linear regression showed increases in FFA and TxB2 were independent. The observed TxB2 release may be due to lipolysis-induced exposure of vascular collagen or direct inhibition of platelet adenylate cyclase by heparin.
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PMID:Effect of elevated plasma-free fatty acids on thromboxane release in patients with coronary artery disease. 737

Adrenergic responsiveness after abrupt propranolol withdrawas during exogenous and esdogenous catecholamine stimulation was assessed in 10 normal subjects and 10 patients with angina pectoris. Propranolol, 160 mg/day, was administered for 2 weeks and then stopped. During an epinephrine infusion, period (p < 0.005). There were no differences from control 96 hours after the drug had been stopped in both groups or at 144 hours in the angina patients who were studied for a longer time. At 48 hours of heart rate and the pressure-rate product were significantly less than control level in the angina patient, but not in the normal subjects. Similar results were observed during exercise in both groups. The epinephrine-induced increase in free fatty acids was blocked by propranolol (p < 0.005), was still attenuated at 48 hours of withdrawals (p < 0.05), but returned to control levels thereafter in both groups. Resting serum triiodothyromine levels decreased with propranolol ( < 0.005) and remaind low throughout the withdrawal period. Measurements of dopamine beta-hydroxylase, plasma platelet factor 4, and platelet aggregation at rest and after exercise did not change significantly during or after propranolol administration. Plasma norepinephrine and epinephrine values were not changed from control during the withdrawal period at rest or after exerise. We conclude that there is no evidence of hypersensitivity to beta-adrenergically mediated responses after abrupt propranolol withdrawal.
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PMID:Adrenergic responsiveness after abrupt propranolol withdrawal in normal subjects and in patients with angina pectoris. 740 43

An evaluation was done in 172 patients with progressive stenocardia. The use of intracardiac laser light irradiation of blood in combined treatment was found to improve the clinical course of the illness and to have a beneficial effect on the factors of plasma haemostasis and fibrinolysis which play a pathogenetic role in the destabilization of the ischemic heart disease course, this being manifest by a significant decrease in the activity of factor XIII, platelet factor 4, and an increase in fibrinolysis.
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PMID:[The effect of quantum hemotherapy on the plasma hemostatic indices and fibrinolysis in patients with unstable angina]. 783 73

The variability of haemostatic factor measurements in patients presenting with angina pectoris is investigated. In all, 219 middle aged patients (almost all men) provided repeat measurements 2.5 years apart on a battery of haemostatic and haematological tests and other cardiovascular risk factors. Correlations between repeat measurements were lower than might be expected in a healthy population, reflecting a relatively large degree of variability within individuals over time. The highest correlations observed for haemostatic factors were for von Willebrand factor related antigen (r = 0.48) and fibrinogen (r = 0.45). The correlations were generally lower amongst patients who had undergone coronary surgery or angioplasty between the two measurements. We conclude that the underlying relationship of fibrinogen to coronary risk must be much greater than is generally appreciated, since even single measurements are found to be important predictors of risk, despite only moderate stability over time. The very low correlations for beta-thromboglobulin (r = 0.10) and platelet factor 4 (r = 0.03) which were observed in this study casts doubt on their potential usefulness as predictors of long-term cardiovascular risk.
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PMID:Variability over time of haemostatic and other cardiovascular risk factors in patients suffering from angina pectoris. ECAT Angina Pectoris Study Group. 812 28

In an attempt to discern biological (such as thrombotic or fibrinolytic) risk factors in patients developing restenosis after percutaneous transluminal coronary angioplasty, the following factors were measured prior to angiography in a population of 23 patients (20 men, 3 women, mean age 57 +/- 5 yr) treated by a successful angioplasty (gain > 20% and residual stenosis < 50%) for stable angina pectoris and who had a routine angiographic restudy. The following factors were thus assessed: lipid factors: cholesterol, triglycerides, high density lipoprotein cholesterol, low density lipoprotein cholesterol, apolipoprotein AI, apolipoprotein B; coagulation factors: fibrinogen, antithrombin III, fibrinopeptide A, factor VIII coagulant, factor VIII antigen, protein C; factors of physiological fibrinolysis: plasminogen, alpha 2-antiplasmin, tissue plasminogen activator and euglobulin clot lysis time before and after venous occlusion, plasminogen activator inhibitor before venous occlusion; and factors of platelet release: beta-thromboglobulin, platelet factor 4. Also studied were clinical characteristics: age, gender, diabetes, hypertension, smoking habits, previous myocardial infarction; angiographic data: global extent of coronary artery disease, location of the stenosis in a bend or branch point, complexity of the lesion, initial and residual stenosis and treatment during follow-up. The coronary angiograms were analyzed by a computer-assisted method with automatic edge detection. On angiographic criteria, 6 patients (restenosis group) were judged to have developed a restenosis (30% decrease in diameter and/or return to a 50% stenosis). The other 17 patients (those without restenosis) were considered to have a persistent success. Apart from age (group without restenosis: 55 +/- 6; restenosis group 61 +/- 5, p < 0.04), there were no differences in clinical, angiographic or treatment variables. There were no differences in lipid factors, but significant differences were observed in hemostatic variables: fibrinogen (without restenosis: 3.18 +/- 0.83; restenosis: 3.83 +/- 0.51 milligrams, p = 0.05), tissue plasminogen activator before venous occlusion (without restenosis: 10.9 +/- 26.8; restenosis: 232.5 +/- 371.2 IU, p < 0.04), euglobulin clot lysis time after venous occlusion (without restenosis: 176.5 +/- 100.5; restenosis: 78.6 +/- 40.2 min, p < 0.05) and for marker of the platelet release: platelet factor 4 (without restenosis: 10.8 +/- 7.9; restenosis: 20.5 +/- 7.5 ng/l, p < 0.04). These findings indicate that patients developing restenosis after coronary angioplasty tend to have an imbalance in the prothrombotic-antithrombotic equilibrium prior to the procedure.
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PMID:Biological risk factors for restenosis after percutaneous transluminal coronary angioplasty. 844 4

To characterize the vasospastic angina patients with exercise-induced ischemia, we measured hemostasis (platelet factor 4; PF4, fibrinopeptide A; FPA) and fibrinolytic parameters (tissue plasminogen activator antigen; t-PA, free plasminogen activator inhibitor-1 antigen; free PAI-1) in 15 normal subjects and 33 vasospastic angina patients without significant coronary artery stenosis (less than 50% stenosis). All of the vasospastic angina patients began to feel chest pain within 3 months before diagnostic coronary angiography. Blood samples were obtained from all of the study patients at 8:30-9:30 am before exercise 201Tl emission computed tomography. Vasospastic angina patients were divided into 2 groups; 15 patients with exercise-induced ischemia (group 1) and 18 patients without exercise-induced ischemia (group 2). On coronary angiography, the severity of coronary artery stenosis at the site of spasm in group 1 (34 +/- 5%) was greater than that in group 2 (18 +/- 3%). Plasma FPA and PF 4 levels in group 1 were also significantly higher than those in normal subjects and group 2. Plasma t-PA and free PAI-1 levels in group 1 were significantly higher than those in normal subjects and group 2. Plasma levels of free PAI-1 group 2 were also significantly higher than those in normal subjects. The present study demonstrated that all of the patients with vasospastic angina had impaired fibrinolysis, and these patients with exercise-induced ischemia showed enhanced platelet activation, an enhanced coagulation system, and advanced atherosclerotic lesions. These results suggest that vasospastic angina with exercise-induced ischemia puts patients at increased risk for thrombus formation.
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PMID:Characteristics of vasospastic angina with exercised-induced ischemia--analysis of parameters of hemostasis and fibrinolysis. 880 21


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