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)

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

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

Platelets play a key role in the progression of acute coronary syndromes (ACS). Clinical depression alone is also associated with enhanced platelet activation. The purpose of this study was to compare concentrations of established biomarkers of enhanced platelet/endothelial activation in clinically depressed versus non-depressed patients enrolled in recent clinical trials for ACS. Two hundred and eighty-one baseline plasma samples from patients with acute myocardial infarction (ASSENT-2; n = 41), with ACS (PRONTO; n = 126) and with clinical depression plus previous acute coronary syndrome within 6 months (SADHART; n = 64), and from normal healthy controls (n = 50) were analyzed. Blood was drawn before applying any therapeutic strategies including interventions, thrombolytics, infusions, and selective serotonin re-uptake inhibitors. Platelet factor 4, beta-thromboglobulin, platelet/endothelial cell adhesion molecule-1, P-selectin, thromboxane, prostacyclin, vascular cell adhesion molecule-1, and E-selectin were measured by enzyme-linked immunosorbent assay by a single core laboratory. Patients with ACS exhibited a higher degree of platelet activation than controls independently of the presence of depression. Plasma levels of P-selectin, thromboxane, prostacyclin, and vascular cell adhesion molecule-1 were the highest in the acute myocardial infarction group when compared with ACS despite the presence or absence of clinical depression. Surprisingly, patients with ACS and depression exhibited the highest levels of platelet factor 4, beta-thromboglobulin, and platelet/endothelial cell adhesion molecule-1 when compared with myocardial infarction or angina patients without clinical depression. E-selectin plasma level was constantly elevated compared with controls but did not differ among the groups dependent on the incidence of depression. The depressed plus ACS group had higher plasma levels of all biomarkers compared with the non-depressed patients. Retrospective analysis of the data from several clinical trials reveals that clinical depression is associated with enhanced activation of platelet/endothelial biomarkers even above the level expected in ACS. These findings may contribute to the unfavorable outcome associated with clinical depression in patients with ACS.
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PMID:Enhanced platelet/endothelial activation in depressed patients with acute coronary syndromes: evidence from recent clinical trials. 1296 Jun 10