Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Blood was obtained from 63 consecutive patients within 24 h period after the admission to a coronary care unit for the determination of plasma platelet factor 4 (PF-4) concentration. 28 of the subjects proved to have an acute myocardial infarction (MI), 24 had evidence of ischaemic heart disease (IHD) but no MI, and the remaining 11 patients had no signs of IHD. 40 healthy subjects served as controls. The mean PF-4 value in the MI group was 10.5 +/- 0.8 ng/ml. The corresponding values for patients with and without IHD were 8.7 +/- 0.6 and 8.3 +/- 0.6 ng/ml, respectively. The control mean (5.4 +/- 0.3 ng/ml) was significantly lower (P less than 0.001) than the means for all 3 groups of patients studied. The difference between the group of MI patients and patients with IHD as well as patients without IHD was only of borderline significance (0.10 greater than P greater than 0.05).
 ...
PMID:Plasma levels of platelet factor 4 in patients admitted to a coronary care unit. 723 87

The aim was to investigate whether in the acute stage of myocardial infarction (MI) platelet activation, as measured by plasma platelet factor 4 (PF-4), excluding that in ischaemic heart disease (IHD) is taking place. Over a period of 4 d the plasma levels of PF-4 were determined on 44 consecutive patients admitted to a coronary care unit with suspected MI. 21 of them had a definite acute MI (group 1), and 13 had evidence of IHD but no MI (group 2). In the remaining 10 subjects there was no evidence of either MI or IHD. On the first day the mean plasma PF-4 concentrations in group 1 and 2 patients were 11,8 +/- 1.1 and 15.0 +/- 2.3 ng/ml, respectively; the difference between means was not statistically significant. A peak mean PF-4 for group 1 patients (17.5 +/- 4.6 ng/ml) was recorded on the second day of study. The corresponding value for group 2 patients was lower, but not significantly so. In the latter subjects no peak PF-4 was recorded. During the last 2 d of study the plasma PF-4 concentrations tended to decrease, but the means for the 2 groups did not differ statistically. Thus, at no point in time was there a significant difference between the PF-4 values for MI and IHD patients present.
 ...
PMID:Plasma concentrations of platelet factor 4 in acute myocardial infarction. 733 49

Because platelet activation may be important in the worsening of coronary atherosclerosis, we used a radioimmunoassay for platelet factor 4 to study platelet behavior in patients with coronary-artery disease. Forty patients had paired blood samples withdrawn for measurement of the plasma level of platelet factor 4 before and after a standardized exercise-tolerance test. Twenty patients had positive tests, and 19 of those 20 had clinical or angiographic evidence of coronary-artery disease. Eleven of the 20 had a greater than 50 per cent increase in platelet factor 4 after exercise. The remaining nine had positive exercise tests without rises in platelet factor 4. Elevated levels returned to normal within 15 minutes of exercise. Eighteen of 20 patients with negative exercise tests had no rise in platelet factor 4 after exercise. We conclude that a subset of patients with coronary-artery disease and exercise-induced myocardial ischemia had evidence of platelet activation and secretion. (N Engl J Med 302:193-197, 1980).
 ...
PMID:Platelet activation during exercise-induced myocardial ischemia. 735 Apr 60

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.
 ...
PMID:[The effect of quantum hemotherapy on the plasma hemostatic indices and fibrinolysis in patients with unstable angina]. 783 73

The purpose of this study was to investigate the effects of beraprost sodium, a stable prostacyclin analog, on the parameters of hemostasis, fibrinolysis, and myocardial ischemia in patients with exertional angina. Thirty-one patients with exertional angina who had significant organic coronary artery stenosis in at least one of the three major coronary arteries were selected. All patients underwent quantitative exercise thallium-201 emission computed tomography before and 1 month after 120 micrograms per day of beraprost sodium administration. Before exercise, blood samples were collected from 8:30 a.m. to 9:30 a.m. after the patients had been lying in bed undisturbed for at least 10 minutes. Plasma platelet factor 4 (PF4), fibrinopeptide A (FPA), tissue plasminogen activator antigen (t-PA), and plasminogen activator inhibitor-1 activity (PAI-1) were measured. There were no significant differences in exercise parameters on both exercise tests. However, both the extent and severity scores of ischemia were significantly aggravated (p < 0.05 for both) during beraprost sodium administration. Plasma FPA levels decreased significantly during beraprost sodium administration (p < 0.01). Likewise, plasma PF4 levels decreased significantly during beraprost sodium administration (p < 0.05). As for plasma t-PA antigen levels, there was no significant difference before versus during beraprost sodium administration. Plasma PAI-1 activity levels decreased significantly during beraprost sodium administration (p < 0.05). The results indicate that beraprost sodium has strong antithrombogenic properties. However, its aggravation of myocardial ischemia may limit clinical usage.
 ...
PMID:Effects of beraprost sodium, a new prostaglandin I2 analog, on parameters of hemostasis, fibrinolysis, and myocardial ischemia in patients with exertional angina. 854 11

Platelet activation, impairment of fibrinolysis and dyslipidemia are important factors in the pathogenesis and progression of ischemic heart disease. Aspirin therapy will reduce platelet activation both by its negative effect on platelet aggregation (SPA) and by inhibition of granule release which liberates such mediators as platelet factor 4 (PF4) and plasminogen activator inhibitor 1 (PAI-1). The present study was performed in 57 patients with ischemic heart disease (IHD), divided into groups depending on coexistent hyperlipoproteinemia (HLP) and aspirin treatment. The control group included 21 healthy individuals, matched for age and sex. Parameters of hemostasis (SPA, PF4, PAI-1) and concentration of lipid fractions (TC, TG, LDL, HDL) were measured in plasma. Increased PF4 levels were found in all groups with IHD, irrespective of hyperlipoproteinemia or aspirin treatment. Enhanced SPA and higher PAI-1 were limited to group IHD-HLP without aspirin. Highest PAI-1 activities were observed after stimulation of platelets in vitro. In conclusion, patients with IHD and hyperlipoproteinemia presented most pronounced platelet activation and impairment of fibrinolysis. Aspirin had a beneficial effect on these changes. Lower activities of PAI-1, in patients treated with aspirin, can be ascribed to its reduced release from platelets. Aspirin did not satisfactorily reduce the level of PF4, although it strongly inhibited SPA.
 ...
PMID:[Evaluation of platelet function and tissue plasminogen activator activity in ischemic heart disease depending on concurrence with hyperlipoproteinemia and aspirin therapy]. 964 79

This study investigated the effects of antidepressant treatment on platelet activation in depressed patients with ischemic heart disease (IHD). Plasma levels of platelet alpha-granule release products beta-thromboglobulin (BTG) and platelet factor 4 (PF4) were measured in 17 depressed patients with IHD who were treated in a 6-week, double-blind trial with either paroxetine (10 patients) or nortriptyline (7 patients). Baseline measurements of BTG and PF4 were significantly elevated in both drug treatment groups before the initiation of antidepressant therapy compared with those of healthy control subjects. In the paroxetine group, mean PF4 and BTG levels significantly decreased from these elevated baseline values within 1 week of treatment and remained low at 3- and 6-week measurements. In contrast, the nortriptyline group did not exhibit a significant decrease in PF4 or BTG plasma levels after 1, 3, or 6 weeks of treatment. Therefore, platelet activation in depressed patients with IHD seems to be inhibited by the selective serotonin reuptake inhibitor paroxetine. The effect of paroxetine on PF4 and BTG plasma levels suggests that it may reduce platelet aggregation in vivo and may positively impact IHD-related mortality in this population.
 ...
PMID:Evaluation of platelet activation in depressed patients with ischemic heart disease after paroxetine or nortriptyline treatment. 1077 Apr 50

Several studies have demonstrated an increased level of plasma plasminogen activator inhibitor-1 (PAI-1) in patients with coronary artery disease (CAD). However, the concentration of PAI-1 in platelets, which accounts for more than 90% of the blood PAI-1, is unknown in these patients. The present study evaluated the concentrations of PAI-1 and several fibrinolytic factors in the plasma and platelets of patients with CAD and the serial changes in patients with acute myocardial infarction (AMI). All 72 subjects had coronary angiography and were divided into 3 groups: CAD(-) group without coronary artery stenosis or myocardial ischemia (n=20), CAD(+) group with either stable angina pectoris (n=18) or old myocardial infarction (n=12) with coronary artery stenosis, and the AMI group admitted within 24h of symptom onset who underwent successful percutaneous transluminal coronary angioplasty (n=22). The concentrations of plasma PAI-1, tissue plasminogen activator (t-PA), and t-PA x PAI-1 complex were similar in the CAD(-) and CAD(+) groups, but were greater on day 1 in the AMI group compared with the 2 CAD groups. There were no significant differences between the 3 groups in the plasma concentrations of thrombin antithrombin III complex (TAT), alpha2-plasmin inhibitor-plasmin complex (PIC), beta-thromboglobulin (beta-TG), and platelet factor 4 (PF-4). The platelet PAI-1 concentrations did not differ between the CAD(-) and CAD(+) groups, but was greater on day 1 in the AMI group compared to the CAD groups. The platelet beta-TG and PF-4 were similar between the 3 groups. In the AMI group, both the plasma and platelet PAI-1 concentrations were greater on day 1, but the plasma PAI-1 rapidly decreased by day 5 and remained low on day 28 compared with day 1. The platelet PAI-1 concentration gradually decreased by day 5 and was further decreased by day 28. The serial changes of the plasma t-PA and t-PA PAI-1 complex during the course of AMI were similar to those of the plasma PAI-1. A positive correlation was found between the plasma and platelet PAI-1 in all 72 patients, but not in the AMI group alone. These results suggest that the PAI-1 that has accumulated in platelets at the onset of AMI might be released in large amounts into the plasma, resulting in an increase in thrombus formation.
 ...
PMID:Plasma and platelet plasminogen activator inhibitor-1 in patients with acute myocardial infarction. 1095 48

The deadliest manifestations of ischemic heart disease are initiated and propagated by intra-coronary thrombin generation. Thrombin is resistant to inactivation by heparin when it is bound to fibrin, fibrin degradation products or subendothelial collagen. Recognition of these limitations has led to development of a new class of antithrombin agents which directly target the active sites on the surface of thrombin molecule and are therefore designated as direct antithrombins. These agents do not need mediation of antithrombin III for their action and are not inhibited by platelet factor 4. This report focuses on bivalirudin, a new agent of promising impact on both interventional as well as non-interventional cardiology. It is a short acting anticoagulant which bivalently and directly inhibits thrombin (coagulation factor II). It binds the active (catalytic) site and the fibrinogen-binding site (exosite I). This provides high affinity and specificity for thrombin. Slow cleavage at the Arg3-Pro4 bond results in recovery of thrombin activity after discontinuation of bivalirudin. Bivalirudin inhibits both protease activated receptor 1 and 4 (PAR 1 and PAR 4) thereby effectively inhibiting acute thrombin mediated platelet aggregation. Clinical efficacy has been assessed and proved in over 20 published patient series focussing on patients with acute coronary syndrome with or without myocardial infarction, patients undergoing percutaneous coronary interventions, patients receiving various adjunctive anti-platelet medications, patients with heparin induced thrombocytopenia or patients undergoing cardiac surgery. In contrast to the well established unfractionated heparin, bivalirudin lacks the risk of heparin induced thrombocytopenia. It shows a tendency to lower bleeding risks without reduction of efficacy when compared with the two-pronged treatment with unfractionated heparin and glycoprotein IIb/IIIa inhibitors.
 ...
PMID:Bivalirudin: a new promising direct antithrombin. 1912 43


<< Previous 1 2 3