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

46 patients with ischaemic heart disease were treated with Micristin (20-40 mg/kg) or a combination of Micristin and Propranolol (80-120 mg/die). The values of bleeding time, the platelet factor 4 in lysate of thrombocytes or in plasma of patients as well as the soluble fibrin monomer complexes were investigated. They showed no obvious correlation to the clinical findings.
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PMID:[Clinical aspects of control in therapy with platelet inhibitors]. 9 69

In vivo activation of platelets can be accurately measured by radioimmunoassays of platelet factor 4 (PF4) and beta thromboglobulin (beta TG). Studies that attempt to correlate increases in PF4 and beta TG levels with exercise-induced myocardial ischemia have yielded conflicting results. To further examine the natural history of release of PF4 and beta TG we used a method of serial samplings of these proteins during and after exercise in nine normal subjects and 24 patients with coronary artery disease (CAD). Mean values for PF4 and beta TG at rest, during each stage, and immediately after treadmill exercise were the same for normal subjects and for patients with positive and negative responses to exercise-tolerance tests (ETTs). However, nonparametric analysis and regression equations disclosed differences in trends of PF4 level during exercise; PF4 levels increased in normal subjects during exercise, while patients with positive ETTs had no change in PF4 levels and patients with negative ETTs actually showed a decrease in PF4. This investigation confirmed that exercise-induced myocardial ischemia is not associated with platelet aggregation as manifested by the release of the platelet-specific proteins PF4 and beta TG. Statistical analysis suggested that prior reports of elevated levels of PF4 during exercise could have been caused by technical and methodologic difficulties that were associated with the collection and handling of the samples.
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PMID:Serial studies of platelet factor 4 and beta thromboglobulin during exercise in patients with coronary artery disease. 241 Nov 21

Platelet behaviour (activation) in ischemic heart disease (stable angina) during pacing-induced tachycardia was studied. ECG was recorded during the trial. Ischemic heart disease (IHD) subjects had 75% or more narrowing of the luminal diameter of a coronary artery, demonstrated by coronary angiography. Eight subjects needing cardiac catheterism because of supraventricular rhythm disturbances with no evidence of IHD were studied as controls. Beta-thromboglobulin (beta-tg) and platelet factor 4 (PF4) were studied as platelet activation markers; beta-tg and PF4 were evaluated before atrial pacing in peripheral venous blood and, by catheterism, before and at maximum pacing rate in coronary venous sinus (CVS) and in ascending aorta (AA). Catheterism and blood withdrawals were performed in order to reduce platelet activation in vivo. No significant difference in platelet activation between IHD patients and control group in peripheral venous blood were found. No trans-myocardial gradient neither in IHD subjects nor in controls were observed. In conclusion, no platelet activation in IHD patients during pacing-induced tachycardia could be observed.
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PMID:No evidence of platelet activation during atrial pacing in subjects with stable angina. 252 53

The effect of pacing-induced myocardial ischemia on platelet activation and fibrin formation was investigated in seven patients with severe proximal lesions of the left anterior descending coronary artery to determine if acute ischemia activates the coagulation system. Fibrin formation was assessed from plasma levels of fibrinopeptide A. Platelet activation was assessed by levels of platelet factor 4, beta-thromboglobulin and thromboxane B2. Plasma levels were measured before, during and after acute myocardial ischemia induced by rapid atrial pacing. Blood samples were collected from the ascending aorta and from the great cardiac vein through heparin-bonded catheters. The occurrence of anterior myocardial ischemia was established by electrocardiography and by myocardial lactate extraction. No significant transmyocardial gradients in the levels of fibrinopeptide A, platelet factor 4, beta-thromboglobulin or thromboxane B2 were found at rest, during ischemia or in the recovery period, and levels in the great cardiac vein did not change in response to ischemia. These data indicate that pacing-induced myocardial ischemia does not result in release of fibrinopeptide A, platelet factor 4, beta-thromboglobulin or thromboxane B2 into the coronary circulation, and imply that acute ischemia does not induce platelet activation or fibrin formation in the coronary circulation.
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PMID:Effect of pacing-induced myocardial ischemia on platelet activation and fibrin formation in the coronary circulation. 295 18

Unstable coronary artery disease (CAD) might be related to obstructions of coronary blood flow by platelet aggregates. In 121 men and 43 women admitted to the coronary care unit with suspected unstable CAD, blood samples for tests of platelet function were obtained within 24 hours after admission. Platelet reactivity was tested in vitro in platelet rich plasma as the aggregability towards ADP 1 microM and collagen 1 mg/ml and as the sensitivity to prostacyclin (PSP). The levels of beta-thromboglobulin and platelet factor 4 were determined ex vivo in platelet poor plasma. Patients who developed a nontransmural myocardial infarction (n = 39) or had signs of myocardial ischemia at an exercise test performed within a week (n = 39) were considered to have unstable CAD while patients without signs of ischemia constituted the control group. In the acute phase the PSP was reduced in patients with unstable CAD without any difference between genders. The aggregability towards ADP was higher in women than men but otherwise there were no differences between groups or sexes in any other test in the acute phase. After 12 months there were no differences in PSP between the groups but women had a lower PSP than men. Thus, in the acute phase of unstable CAD, the platelet sensitivity to the inhibitory effects of prostacyclin was reduced which might contribute to the risk for further platelet aggregation, coronary occlusion and myocardial infarction.
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PMID:Platelet reactivity in unstable coronary artery disease. 295 54

Platelet suppressive agents have been shown to improve the prognosis of coronary diseases such as myocardial infarction and unstable angina. Several markers of platelet activation during myocardial ischemia have been found to be increased. Platelet granule constituents (beta thromboglobulin or platelet factor 4) or thromboxane B2 have been reported to be enhanced and, in some studies, to be correlated with the ischemia. Molsidomine or its active metabolite SIN-1 have antithrombotic properties in experimental models. This effect seems to be at least partly related to their antiplatelet activities. SIN-1A inhibited platelet aggregation and release reaction. Specific investigations have demonstrated that SIN-1A acts at a early stage of platelet activation inhibiting calcium influx and phospholipase activity which lead to inhibition of thromboxane formation and fibrinogen binding. Antiplatelet properties were also observed after oral administration of molsidomine but the extent of inhibition appeared to vary with the subjects.
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PMID:[Role of molsidomine on platelet activation in coronary ischemia]. 296

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

To determine changes in platelet activity, prostaglandin metabolism and catecholamine release along with changes in hemodynamics during exercise, we measured these parameters before and immediately after treadmill exercise. Measurements were made on peripheral arterial blood simultaneously with a direct aortic pressure recording in 30 patients with coronary artery disease (Group 1), in 20 patients without significant coronary disease (Group 2), and in 11 young healthy volunteers as controls. At the peak of the exercise regimen, the ST segment depression was found to be significantly lower in Group 1 than in Group 2, whereas the changes in the DPTI/TTI ratio in Group 2 and the controls decreased with the increase in the duration of exercise. The increased serum lactate level at the intermediate level of exercise (420 +/- 20 sec) was significantly lower in the controls than in the other 2 groups. Changes in beta thromboglobulin, platelet factor 4, and plasma norepinephrine were similarly increased in all 3 groups by exercise. At the termination of exercise, however, 6 keto-prostaglandin F1 alpha in Group 1 was insignificantly elevated, whereas it increased from 42.9 +/- 7 pg/ml to 55.7 +/- 7.1 (p less than 0.05) in Group 2 and from 38.2 +/- 5.7 pg/ml to 45.1 +/- 6.8 (p less than 0.01) in the controls. These results suggest that decreased prostacyclin production in the vessel wall might be an indicator of myocardial ischemia, and that the administration of prostacyclin may modulate the coronary vascular tone exaggerated by exercise.
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PMID:The role of prostacyclin during exercise in patients with chronic angina pectoris. 305 98

We studied the levels of thromboxane B2 (TXB2), 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), platelet aggregability, beta-thromboglobulin and platelet factor 4 in 30 coronary artery disease (CAD) patients and 21 normal subjects during exercise. During treadmill exercise, 13 of 30 CAD patients reported chest pain. We administered a selective thromboxane synthetase inhibitor (OKY-046) for 2 weeks to 10 CAD patients with exercise-induced chest pain and studied its effects. At rest, the plasma TXB2 levels and platelet aggregation were significantly lower in normal subjects than in CAD patients, and there was no difference between CAD patients with and without exercise-induced chest pain. On treadmill testing, plasma TXB2 levels and platelet aggregation increased significantly only in the CAD patients with exercise-induced chest pain. Plasma 6-keto-PGF1 alpha levels in normal subjects were significantly higher than those in CAD patients both at rest and during exercise. After administration of OKY-046, mean exercise time increased significantly from 7.5 to 8.6 min (p less than 0.001). Plasma TXB2 level and platelet aggregation decreased significantly after OKY-046 administration both at rest and during exercise. These results suggest that a marked increase in TXA2, with only a minimal change in PGI2, during exercise may contribute to exercise-induced myocardial ischemia, and that OKY-046 is useful in the treatment of CAD patients.
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PMID:Effects of a selective thromboxane synthetase inhibitor (OKY-046) in patients with coronary artery disease during exercise. 332 62

Plasma levels of platelet factor 4 have been measured in the aortic and coronary sinus blood of 35 patients: group I (n = 12) with normal coronary arteriograms; group II (n = 15) with angiographically proven coronary artery disease; and group III (n = 8) composed of patients with ischemic heart disease who were being treated with the antiaggregant agent ticlopidine at the time of cardiac catheterization. The mean increase in platelet factor 4 levels through the coronary circulation was 27.4 +/- 21.9 ng/ml (mean +/- standard deviation) in group II, compared with -1 +/- 4.5 ng/ml in group I (p less than 0.01). In group III plasma levels of platelet factor 4 in aortic and coronary sinus samples were all within the normal range. Thus, we conclude that platelet activation constantly occurs in the coronary circulation of patients with stable coronary artery disease, and can be prevented with ticlopidine.
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PMID:Intracoronary platelet activation in ischemic heart disease: effects of ticlopidine. 398 29


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