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 and thrombus formation within the coronary artery are major factors in acute myocardial infarction (AMI) and unstable angina (UA), and continuing platelet activation is associated with an adverse prognosis. We assessed platelet activation by using flow cytometry to measure platelet surface expression of P-selectin and glycoprotein IIb/IIIa in 20 patients with AMI and 20 with UA, all of whom were treated with aspirin. Platelet studies were repeated after the infusion of a nitric oxide donor (glyceryl trinitrate or S-nitrosoglutathione) that produced a fall in mean arterial pressure of no more than 10 mm Hg. P-selectin was expressed on 2.5% (range, 1.4% to 6.3%) of platelets from AMI and 2.3% (range, 1.6% to 3.3%) from UA subjects compared with 1.0% (range, 0.6% to 1.9%) of platelets from 20 control volunteers without angina (P < .001). Glycoprotein IIb/IIIa expression was 101.6 +/- 2.7 arbitrary units of relative fluorescence in AMI and 100.2 +/- 3.3 in UA compared with 87.8 +/- 2.5 in control subjects (P < .01). In both AMI and UA, S-nitrosoglutathione reduced P-selectin (P < .001) and glycoprotein IIb/IIIa (P < .05) expression, as did glyceryl trinitrate (P < .02 and P < .01, respectively). In 3 of 20 patients receiving glyceryl trinitrate the lowest dose was not tolerated due to headache or hypotension. These findings show that platelet activation persists in AMI and UA despite aspirin treatment and that this can be inhibited by using glyceryl trinitrate or S-nitrosoglutathione. S-nitrosoglutathione is better tolerated at the doses required.
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PMID:Platelet activation in acute myocardial infarction and unstable angina is inhibited by nitric oxide donors. 854 26

Unstable angina occurs when atherosclerotic plaque ruptures. Recent evidence suggests a role for inflammation in this process. Leukocyte-endothelial cell interactions are important in inflammation and are regulated by cell adhesion molecules. This study was designed to examine the vascular expression of cell adhesion molecules and cytokines in patients with unstable angina. Directional coronary atherectomy was performed in patients with unstable and stable angina. Expression of the cell adhesion molecules P-selectin, E-selectin, and intercellular adhesion molecule-1 in the tissue obtained was examined using immunohistochemistry. In addition, expression of the cytokines tumor necrosis factor-alpha and interleukin-1beta, which participate in the regulation of cell adhesion molecule expression, was also examined. Atherectomy specimens had significantly greater P-selectin expression from patients with unstable angina than from patients with stable angina. P-selectin expression was observed primarily on endothelial cells. There were no differences in any of the other factors between patients with unstable and stable angina. In addition, other clinical and angiographic variables were not associated with differential expression of any of the cell adhesion molecules or cytokines. These results indicate a possible role for P-selectin in the process of unstable angina.
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PMID:Levels of expression of P-selectin, E-selectin, and intercellular adhesion molecule-1 in coronary atherectomy specimens from patients with stable and unstable angina pectoris. 907 May 52

Platelet activation state and responsiveness to physiological agonists were measured in 65 patients with documented coronary artery disease (54 male and 11 female; mean age, 58 years). Twelve patients (mean age, 52 years), selected at random from the male cohort, were compared with 12 age-matched male control subjects (mean age, 52 years) and with 10 normal, young male subjects (mean age, 25 years). Whole-blood flow cytometry was used to measure platelet activation status ex vivo and platelet responsiveness to physiological agonists in vitro. Peripheral blood samples were analyzed for bound fibrinogen and expression of P-selectin, GPIb, and GPIIb-IIIa at rest and in response to ADP (0.1 to 10 mumol/L) and thrombin (0.02 to 0.32 mu/mL). No significant differences were seen in the basal levels of fibrinogen binding between any of the groups, but P-selectin expression was significantly lower in patients compared with age-matched control subjects (P = .0005). When stimulated with agonists, patients' platelets had significantly decreased fibrinogen binding (P < .03) but no difference in P-selectin expression compared with the age-matched group. Both agonist-induced fibrinogen binding and P-selectin expression were, however, higher in the young subjects compared with either the older control group or the patients (P < .05). GPIb and GPIIb-IIIa expression were lowest in the patients with angina and highest in the young control subjects, with levels in the age-matched control subjects falling between these values. Data from the total patient cohort (n = 65) were identical to those in the smaller cohort (n = 12). In conclusion, atherosclerosis impairs platelet aggregatory responses (fibrinogen binding) over and above the decreased response seen with age. Platelet degranulation (P-selectin expression) is also impaired in patients with coronary artery disease, but only in comparison with younger subjects, not age-matched controls.
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PMID:Altered platelet function detected by flow cytometry. Effects of coronary artery disease and age. 935 70

The present study examines whether an acute inflammatory response occurs during acute myocardial infarction (AMI) by measuring soluble P-selectin levels. We examined plasma soluble P-selectin levels in 16 consecutive patients with AMI, in 15 patients with angina, and in 13 control subjects with chest pain but normal coronary arteries and no coronary spasm. In patients with AMI, blood samples were obtained immediately after admission and at 1, 4, 24, and 48 hours, and 1 week after initiation of reperfusion therapy. The plasma soluble P-selectin levels were significantly higher in the AMI group on admission than in the other 2 groups (83 +/- 13 ng/ml, p < 0.01). The plasma soluble P-selectin levels at baseline were not significantly different between the angina and control groups (28 +/- 4 vs 24 +/- 5 ng/ml, p = NS). Plasma soluble P-selectin levels reached their peak significantly at 4 hours after initiation of the reperfusion therapy in patients with AMI. The peak level was significantly higher than the level on admission (115 +/- 17 vs 83 +/- 13 ng/ml, p < 0.05). The plasma soluble P-selectin levels were higher in the AMI group than in the angina and control groups over the time course (p < 0.01). Our data indicate that the plasma soluble P-selectin levels are increased in patients with AMI, and that the levels are increases after reperfusion therapy more than before reperfusion. We suggest that the increase in the plasma soluble P-selectin levels may be caused by the activation of endothelial cells and platelets after myocardial ischemia and reperfusion during AMI.
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PMID:Serial changes in plasma levels of soluble P-selectin in patients with acute myocardial infarction. 948 26

Soluble (s) P-selectin, sE-selectin, sL-selectin and soluble intercellular adhesion molecule-1 (sICAM-1) levels were examined by monoclonal antibody-based enzyme immunoassay on serum samples taken from nine patients with acute myocardial infarction (AMI) and eight patients with stable angina pectoris (SAP) before and after the successful percutaneous transluminal coronary angioplasty (PTCA). In patients with acute phase of AMI, the levels (mean +/- SEM) of sP-selectin (110 +/- 18 ng/ml) and sE-selectin (54 +/- 15 ng/ml) before PTCA, were significantly higher than those in the SAP group, the values being 44 +/ 27 and 21 +/- 4 ng/ml (p < 0.05), respectively. After recanalization, the levels of sE-selectin and sL-selectin were significantly decreased (sE-selectin 54 +/- 15 to 42 +/- 11 ng/ml, sL-selectin 1104 +/- 106 to 891 +/- 59 ng/ml, P < 0.05, respectively). These findings suggest that the presence of activated and/or injured endothelial cells, which may be involved in the plaque disruption or intraluminal thrombosis in AMI region and that the inflammatory process may be altered after reperfusion therapy.
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PMID:Soluble form of selectins in blood of patients with acute myocardial infarction and coronary intervention. 954 64

P-selectin in platelets and endothelial cells mediates adhesive interactions between platelet, leukocyte and endothelium to form thrombi. The purpose of the present study was to investigate the plasma level of soluble P-selectin (sP-selectin) in patients with coronary heart disease and the relationship between sP-selectin and plasma concentration of lipoprotein(a) [Lp(a)]. Levels of sP-selectin and Lp(a) were determined by enzyme-linked immunoabsorbent assay on plasma taken from patients with acute myocardial infarction (AMI), old myocardial infarction (OMI), unstable angina (UA), stable angina (SA) and the controls. In patients with AMI and UA, sP-selectin levels (79.62+/-3.82 ng/ml, 43.75+/-2.97 ng/ml, respectively) were significantly higher (P<0.01) than those in patients with OMI (15.92+/-1.34 ng/ml), SA (15.31+/-1.51 ng/ml), and the controls (14.93+/-1.33 ng/ml), but there was no difference between AMI and UA groups. Among all subjects studied, there was an inverse correlation between Lp(a) and sP-selectin (r=-0.315 P<0.001). These findings indicate that plasma levels of sP-selectin are increased in patients with AMI and UA, and high levels of soluble P-selectin may play a role in the pathogenesis of acute coronary events.
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PMID:Elevated plasma levels of soluble P-selectin in patients with acute myocardial infarction and unstable angina. An inverse link to lipoprotein(a). 967 5

The acute coronary syndromes represent a continuum of myocardial ischemia ranging from angina, reversible tissue injury --> unstable angina, frequently associated with minor myocardial damage --> myocardial infarction and extensive tissue necrosis. Historically, coronary artery disease assessment has been mainly binary, using WHO criteria of symptoms, electrocardiography, and biochemical markers. The creatine kinase-MB isoenzyme (CK-MB) has been a benchmark for markers, but it is not specific for myocardium. Cardiac-specific isoforms of troponin T and I have emerged as sensitive myocardial infarction (MI) indicators and, importantly, for risk stratification of acute coronary syndrome patients. In addition to markers of myocardial cell necrosis, markers of plaque disruption (C-reactive protein and serum amyloid A), "angry" platelets (P-selectin), ischemia (glycogen phosphorylase-BB isoenzyme), and the procoagulant state and thrombosis (soluble fibrin) have potential use. Also, CK-MB and myoglobin have been combined with clinical indicators for monitoring reperfusion after thrombolytic therapy. Biochemical markers will continue to be an important clinical adjunct for MI diagnosis, risk assessment, and reperfusion monitoring in the future.
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PMID:Biochemical markers of the acute coronary syndromes. 970 95

P-selectin is translocated from platelets and endothelial cells to initiate the first step in a sequence of events leading to the adherence of leukocytes, possibly inducing reperfusion injury and the no-reflow phenomenon in acute myocardial infarction (AMI). This study was undertaken to investigate plasma P-selectin in AMI patients undergoing coronary recanalization therapy. A total of 40 patients were studied: 20 patients with AMI who underwent coronary recanalization by direct percutaneous transluminal coronary angioplasty (PTCA), 10 patients with AMI who underwent thrombolytic therapy by tissue-type plasminogen activator (TPA), and 10 patients with stable angina pectoris who underwent elective PTCA. Blood samples were obtained from systemic arteries before and immediately after PTCA or thrombolytic therapy. Plasma-soluble P-selectin was measured by enzyme immunoassay. Plasma P-selectin was significantly higher in AMI than in stable angina pectoris (176.6 +/- 12.9 ng/mL vs 91.4 +/- 9.5 ng/mL, p<0.001). Plasma P-selectin did not change significantly as a result of elective PTCA in patients with stable angina (from 91.4 +/- 9.5 ng/mL to 87.9 +/- 7.9 ng/mL). Plasma P-selectin was decreased by direct PTCA in all of the 20 patients with AMI (from 176.2 +/- 17.7 ng/mL to 141.7 +/- 12.6 ng/mL; p<0.001, paired t-test), whereas it was increased by thrombolysis using TPA in nine of the 10 AMI patients (from 177.4 +/- 17.2 ng/mL to 248.8 +/- 17.3 ng/mL, p<0.005). Increased P-selectin activity in AMI appeared to be attenuated by direct PTCA, but augmented by thrombolysis, possibly due to direct stimulatory effects of TPA on P-selectin expression. This may lead to less favorable results in salvaging the ischemic myocardium by thrombolytic than mechanical coronary recanalization therapy in AMI.
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PMID:Plasma soluble P-selectin in acute myocardial infarction: effects of coronary recanalization therapy. 978 45

P-selectin, an adhesion molecule, is involved in the alpha-granules of platelets with several factors such as platelet factor 4 (PF-4) and in Weibel-Parade bodies of endothelial cells with von Willebrand factor. The levels of the soluble form of P-selectin increase after angina episodes in patients with unstable angina, indicating that soluble P-selectin is associated with platelet activation and thrombogenesis in the coronary circulation. To evaluate the effect of successful coronary angioplasty on platelet activation or thrombogenesis in the coronary circulation, plasma soluble P-selectin, PF-4 and von Willebrand factor antigen levels were measured in blood obtained from the coronary sinus before and after successful coronary angioplasty in 15 patients with unstable angina. Fifteen patients with normal coronary angiograms served as controls. Plasma P-selectin, PF-4 and von Willebrand factor antigen levels were determined by sandwich enzyme-linked immunosorbent assays. Increased plasma soluble P-selectin (159.7 +/- 74.5 vs 78.7 +/- 26.4 ng/ml, p < 0.01) and PF-4 (456.5 +/- 87.0 vs 118.7 +/- 62.3 IU/ml, p < 0.01) levels were found in patients with unstable angina compared with those in controls, and were significantly decreased after angioplasty (147.8 +/- 69.6 ng/ml, p < 0.05; 401.6 +/- 108.5 IU/ml, p < 0.05), whereas von Willebrand factor antigen was unchanged. The ratio of plasma soluble P-selectin levels after and before angioplasty correlated with the corresponding ratio of plasma PF-4 levels (r = 0.53, p < 0.05), but not with the ratio of plasma von Willebrand factor antigen levels. The plasma levels of soluble P-selectin, which increase in the coronary circulation in patients with unstable angina, decrease after successful coronary angioplasty. Such data indicate that soluble P-selectin is associated with platelet activation and the therapeutical procedure improves the thrombogenic state in the coronary circulation.
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PMID:[Decreased plasma soluble P-selectin level in coronary sinus after successful coronary angioplasty in patients with unstable angina]. 1035 52

We have evaluated the activation of platelets in blood samples taken from patients with stable angina undergoing balloon angioplasty (percutaneous transluminal coronary angioplasty [PTCA]) (n=11) or coronary artery bypass grafting (CABG) under hypothermic (n=11) or normothermic conditions (n=11). We have found that surface expression of P-selectin on platelets in whole blood from PTCA patients upon thrombin treatment was significantly reduced, as compared with control platelets from healthy subjects. This effect was partially reversed when platelets washed from the same blood sample were used, but even then P-selectin expression was significantly lower in PTCA patients than it was in control subjects. There was a significant increase in basal expression of P-selectin in blood platelets taken from patients who underwent CABG under normothermic conditions (warm blood cardioplegia) as opposed to hypothermic patients (cold crystalloid cardioplegia). These platelets retain the ability to respond to agonists, although to a much lower extent than do those from healthy control donors. The surface exposure of P-selectin on resting and thrombin-treated platelets isolated from CABG surgery patients was not different from that of the control platelets. The adhesion to fibrinogen of resting and thrombin-treated platelets from patients who underwent balloon angioplasty as well as CABG surgery under normothermic and hypothermic conditions was significantly reduced when compared with the fibrinogen of the control platelets. These results suggest that the function of platelet fibrinogen receptor is impaired in patients with stable angina pectoris and that PTCA and CABG surgery activates platelets.
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PMID:Activation of blood platelets after percutaneous transluminal coronary angioplasty and coronary artery bypass graft surgery. 1112 46


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