Plasma Levels Of Β-thromboglobulin Research Articles

Persistence of subsyndromal residual symptoms after remission of major depression in patients without cardiovascular disease may condition maintenance of elevated platelet factor 4 and β-thromboglobulin plasma levels

BackgroundDepressive patients show a state dependent platelet activation that may heighten their cardiovascular risk, specially when comorbid with Coronary Artery Disease (CAD). We still have little information however on the possibility that residual symptoms that often persist after recovery from a major depressive episode may contribute to drive forward platelet activation, thus extending the exposure to the associated cardiovascular risk. MethodsNineteen major depressed inpatients treated with electroconvulsive therapy (ECT) were enrolled and tested for platelet aggregation by measuring platelet factor-4 (PF4) and β-thromboglobulin (β-TG) plasma levels, and for psychometric evaluation by using the 20-item Hamilton Depression Rating Scale (HDRS) and the Symptom Checklist 90 Revised (SCL-90R). Subjects were tested at the beginning of treatment (baseline) and after clinical remission (endpoint). ResultsAt baseline the patients showed high HDRS (31±6) and total SCL-90R (200±38) scores, followed by a significant decrease at endpoint. However, even if all patients showed full syndromal recovery, SCL-90R “Hostility” and “Psychoticism” subscores showed no significant reduction from baseline, indicating the persistence of subtle residual symptoms. Baseline PF4 and β-TG plasma levels were found remarkably higher and no significant reduction was observed at the endpoint. LimitationsSmall study population. No follow-up evaluation. ConclusionsDespite of clinical remission obtained with ECT in patients with major depression, persistence of subsyndromal residual symptoms may contribute to maintain a condition of platelet hyperactivation at the endpoint, increasing their cardiovascular risk and making them more vulnerable to develop cardiovascular disease.

Are Mood Disorders a Stroke Risk Factor?

See related article, pages 16–21 A growing body of evidence suggests that biological mechanisms underlie a bidirectional link between depression and many neurological illnesses, and that mood disorders can affect the course of the diseases.1 Depression commonly occurs after a stroke, with an estimated prevalence as high as 30% in the first year after the event.2 It is well known that poststroke depression affects quality of life, functional recovery, cognitive function and health care use in stroke survivors.3 Inversely, does any association exist between a history of a previous affective disorder and future risk of cardiovascular events? Recent prospective studies have shown an association between depression and incidence of hypertension,4,5 coronary heart disease,6,7 and cardiovascular mortality.8–11 In the Multiple Risk Factor Intervention Trial, 12 866 men were followed for 18 years; those with greater depressive symptoms, as measured by the Center for Epidemiologic Studies Depression Scale (CES-D), were associated with a significant higher risk of cardiovascular mortality (hazard ratio=1.21; 95% CI, 1.03 to 1.41; P <0.05) and stroke mortality (hazard ratio= 2.03; 95% CI, 1.20 to 3.44; P <0.01).12 The NHANES I Epidemiologic Study13 showed that individuals reporting 5 or more symptoms of depression at baseline were 50% more likely to die of a stroke-related cause during a 29-year follow-up. The Baltimore Epidemiologic Catchment Area Study showed that individuals with a history of depressive disorder, measured with the diagnostic interview schedule, were 2.6 times more likely to report stroke.14 Depressive symptoms, measured by the Zung Self-rating Depression Scale, were also associated with an increased incidence of ischemic stroke in a Japanese 10-year follow study.15 Self-reported depression scores significantly predicted stroke in an Australian cohort of people …

Whole blood serotonin and platelet activation in depressed post-myocardial infarction patients

Depression is an independent risk factor for post myocardial infarction (MI) mortality. Abnormalities in platelet function have been proposed as one of the mechanisms involved in increased cardiovascular risk among patients with depression post-MI. Depression in somatically healthy patients has been associated with increased platelet activation. Some but not all studies showed changes in blood serotonin level. Increased platelet activation and blood serotonin level have been associated with increased risk of cardiac events in patients with MI. The goal of this study was to investigate whether 1) depressed post-MI patients have higher markers of platelet activation as measured by plasma levels of β-thromboglobulin (βTG), platelet factor 4 (PF4) and soluble CD40 ligand (sCD40L) and higher serotonin (5-HT) levels than non-depressed post-MI patients and 2) treatment with the antidepressant mirtazapine decreases platelet activation. In this study, 25 depressed post-MI patients were asked for blood collection before start as well as after 8 weeks treatment with mirtazapine or placebo. The control group (n=22) consisted of non-depressed post-MI patients, matched for age, gender and time elapsed since MI. Plasma levels of βTG, PF4 and sCD40L were not statistically different between the groups, but 5-HT levels were significantly higher in depressed patients. Treatment with mirtazapine resulted in a non-significant decrease in βTG and PF4 and platelet 5-HT levels. Platelet and whole blood 5-HT, but not platelet activation was significantly increased in depressed post-MI patients. Treatment with mirtazapine showed a non-significant decrease in platelet activation and platelet 5-HT.

W12.289 PPARγ activation lowers postprandial but not fasting triglyceride concentrations in type 2 diabetes: An investigation of tissue-specific mechanisms in humans

The present study was conducted to determine whether alimentary lipemia alters platelet activity in vivo. Normolipidemic volunteers were given a fatty meal and platelet function was assessed before, and 3 and 6 h after the meal. Platelet aggregability and secretion was determined using whole blood flow cytometry (expression of platelet P-selectin and fibrinogen binding), filtragometry ex vivo (reflecting platelet aggregability in vivo) and by measurements of platelet specific products in plasma (β-thromboglobulin and platelet factor 4). Plasma triglycerides increased from 0.8 (0.6:1.1; median, 25th and 75th percentiles) to 1.7 (1.0:2.3) mmol/l at 3 h and returned to baseline after 6 h (P<0.001, one-way ANOVA). Apo B-100 and apo B-48 were both markedly increased 3 h postprandially in the Sf 60–400 fraction (large VLDLs, P<0.001 for both), whereas the Sf 20–60 (small VLDLs) and Sf 12–20 fractions (IDL) did not change. The platelet function assessments revealed that the percentage of platelets expressing P-selectin increased by 40% (5%; 64%) after 3 h and by 51% (−7%; 85%) 6 h postprandially in unstimulated samples (P<0.05 for both). In samples stimulated by ADP in vitro P-selectin expression increased by 45% (6%; 58%) after 3 h and by 30% (12%; 58%) (P<0.01 for both) after 6 h at 0.1 μM. Platelet P-selectin expression was less influenced at higher ADP concentrations. The plasma levels of β-thromboglobulin (≈20 ng/ml) and platelet factor 4 (≈0.3 ng/ml) were not affected by the fat load. Flow cytometric analyses of fibrinogen binding and filtragometry measurements also failed to reveal any postprandial alterations. The present finding of enhanced platelet P-selectin expression suggests that platelets are mildly sensitized postprandially. Whether this is of importance for thrombus formation and atherosclerosis needs to be studied further.

SMA circuits reduce platelet consumption and platelet factor release during cardiac surgery

Background. Platelet count and function are particularly damaged by cardiopulmonary bypass (CPB). This study evaluated the effects of a novel CPB circuit in terms of platelet count and activation, and postoperative need for blood products. Methods. One hundred patients undergoing coronary grafting were randomized in two groups: control group (n = 50) and test group (n = 50, surface modifying additives circuit, SMA group). Blood samples were taken before, during, and after CPB. Postoperative blood loss, number of transfused blood products, and postoperative variables were recorded. Results. The platelet count decreased less in the SMA group compared to the control group (end of CPB: respectively, 165 ± 9 × 10 3/mm 3 vs 137 ± 8 × 10 3/mm 3; p < 0.01). This was paralleled by a reduction in β-thromboglobulin plasma levels in the SMA group. There was a trend to decreased blood loss in the SMA group, but the difference was significant only in patients taking aspirin preoperatively ( p < 0.05). In the SMA group nearly 50% less fresh frozen plasma and platelet units were administered ( p < 0.01). No operative deaths were observed. Conclusions. The use of circuits with surface additives is clinically safe, preserves platelet levels, and attenuates platelet activation. This may lead to a reduced need for blood products.

Plasma adenosine levels and platelet activation in patients with atrial fibrillation

Platelet activation is observed in patients with atrial fibrillation (AF). P-selectin, which is expressed on platelet activation, plays an important role in the formation of thromboemobli. Because adenosine is known to attenuate platelet activation, we evaluated adenosine levels and 2 indicators of platelet activation, i.e., expression of P-selectin on platelets and plasma levels of β-thromboglobulin, in 28 patients with AF (20 men and 8 women, age range 64 ± 2 years) with sex- and age-matched (± 2 years) subjects with sinus rhythm. The incidence of risk factors for stroke except for coronary heart disease and in echocardiographic parameters did not differ between the 2 groups. Plasma adenosine levels were lower (p <0.05) in patients with AF than in controls (mean [interquartile range] 13.4 [19.3–9.3] vs 19.1 [30.8–11.9] nmol/L). The expression of P-selectin on platelets (6.8% [13.6–3.4] vs 4.0% [8.8–1.8]) and plasma levels of β-thromboglobulin were higher (p <0.05) in patients with AF. Flow cytometric analysis revealed that an antagonist of adenosine receptors, 8-sulfophenyltheophylline, increased the expression of P-selectin on platelets in a dose-dependent manner in the in vitro study. These results suggest that decreased plasma levels of adenosine were associated with platelet activation in patients with AF. Substitution of adenosine may provide a strategy for preventing platelet activation in these patients.

Alimentary lipemia enhances the membrane expression of platelet P-selectin without affecting other markers of platelet activation

The present study was conducted to determine whether alimentary lipemia alters platelet activity in vivo. Normolipidemic volunteers were given a fatty meal and platelet function was assessed before, and 3 and 6 h after the meal. Platelet aggregability and secretion was determined using whole blood flow cytometry (expression of platelet P-selectin and fibrinogen binding), filtragometry ex vivo (reflecting platelet aggregability in vivo) and by measurements of platelet specific products in plasma ( β-thromboglobulin and platelet factor 4). Plasma triglycerides increased from 0.8 (0.6:1.1; median, 25th and 75th percentiles) to 1.7 (1.0:2.3) mmol/l at 3 h and returned to baseline after 6 h ( P<0.001, one-way ANOVA). Apo B-100 and apo B-48 were both markedly increased 3 h postprandially in the Sf 60–400 fraction (large VLDLs, P<0.001 for both), whereas the Sf 20–60 (small VLDLs) and Sf 12–20 fractions (IDL) did not change. The platelet function assessments revealed that the percentage of platelets expressing P-selectin increased by 40% (5%; 64%) after 3 h and by 51% (−7%; 85%) 6 h postprandially in unstimulated samples ( P<0.05 for both). In samples stimulated by ADP in vitro P-selectin expression increased by 45% (6%; 58%) after 3 h and by 30% (12%; 58%) ( P<0.01 for both) after 6 h at 0.1 μM. Platelet P-selectin expression was less influenced at higher ADP concentrations. The plasma levels of β-thromboglobulin (≈20 ng/ml) and platelet factor 4 (≈0.3 ng/ml) were not affected by the fat load. Flow cytometric analyses of fibrinogen binding and filtragometry measurements also failed to reveal any postprandial alterations. The present finding of enhanced platelet P-selectin expression suggests that platelets are mildly sensitized postprandially. Whether this is of importance for thrombus formation and atherosclerosis needs to be studied further.

Elevated platelet factor 4 and β-thromboglobulin plasma levels in depressed patients with ischemic heart disease

Clinical depression has recently been recognized as an independent risk factor for cardiac mortality in patients after myocardial infarction. The underlying mechanisms of this increased mortality remain unclear. This study investigated the hypothesis that patients suffering from ischemic heart disease (IHD) and depression concurrently may have abnormal platelet activation resulting in an increased risk of thrombosis. Platelet factor 4 (PF4) and beta-thromboglobulin (beta-TG) were measured in young healthy control subjects, in nondepressed patients with IHD, and in depressed patients with IHD. Mean PF4 and beta-TG plasma levels in the IHD group with depression were found to be significantly higher than those of the control and IHD groups. This increase was not related to age, gender, racial difference, aspirin use, or severity of cardiac disease. This finding suggests that in depressed patients with IHD there is greater platelet activation, and may indicate an increased risk of thrombotic complications.

Increased heparin-releasable platelet factor 4 and D dimer in patients one month after the onset of acute myocardial infarction: persistent activation of platelets and the coagulation/fibrinolytic system

To evaluate the activity of platelets and the coagulation/fibrinolytic system 1 month after the onset of acute myocardial infarction, we measured the plasma levels of molecular markers, i.e. β-thromboglobulin, platelet factor 4, thrombin-antithrombin III complex and D dimer, in 16 patients with acute myocardial infarction and in 11 normal subjects. Blood was drawn through a catheter placed in the pulmonary artery before heparin injection. The heparin-releasable platelet factor 4 was calculated by subtracting the level before the injection of 5000 U of heparin, from the level 5 min after injection. The plasma β-thromboglobulin, thrombin-antithrombin III complex and the D dimer levels in the acute phase of myocardial infarction were 134.9 ± 121.2, 11.2 ± 7.1 and 164.4 ± 115.3 ng/ml, respectively. These values were significantly higher than those in the normal subjects. The plasma levels of β-thromboglobulin and thrombin-antithrombin III complex, 1 month after the onset (36.6 ± 16.4 and 4.6 ± 2.3 ng/ml, respectively) were not significantly different from those of the normal subjects. In contrast, D dimer and heparin-releasable platelet factor 4 were 216.9 ± 176.9 and 80.5 ± 29.3 ng/ml, respectively, and significantly higher than in the normal subjects. These findings suggest a latent but persistent activation of the platelets and the coagulation/ fibrinolytic system 1 month after the onset or acute myocardial infarction.

β-Thromboglobulin plasma levels in the first week after myocardial infarction: Influence of thrombolytic therapy

In vitro and in vivo studies have shown both an inhibition and an activation of platelets after thrombolysis in acute myocardial infarction. Plasma β-thromboglobulin, a marker of platelet activity, was evaluated daily during the first week after myocardial infarction in 24 patients who received intravenous streptokinase (group 1) and 26 who did not (group 2). On admission, levels of β-thromboglobulin, as compared to those in healthy subjects (35 ± 9 IU/ml), were similarly augmented in group 1 (105 ± 27 IU/ml) and in group 2 (115 ± 30 IU/ml); 3 hours later, values averaged 191 ± 58 IU/ml in group 1 ( p < 0.001 vs baseline) and 95 ± 28 IU/ml in group 2 (not significant vs baseline; p < 0.001 between the two groups). From the second to the seventh day, β-thromboglobulin augmented in those patients in both groups with postinfarction angina. From day 5 to day 7, patients of group 1 without angina had lower β-thromboglobulin levels than patients of group 2 who had no symptoms. The lowest levels of platelet activity were observed in group 1 reperfused patients. These data indicate that in myocardial infarction an early platelet activation takes place that is enhanced by thrombolytic treatment; recurrence of angina is associated with persistent activation; in the absence of recurrent angina, thrombolysis can limit late platelet activation.

Platelet activation in diabetic patients with asymptomatic atherosclerosis

We studied 27 non-insulin-dependent diabetics without apparent atherosclerosis (AS) to investigate whether abnormal platelet function is related to asymptomatic atherosclerosis in diabetes mellitus. The degree of AS was quantitatively evaluated by determining the intimal plus medial thickness (IMT) of the carotid artery wall with ultrasound high-resolution B-mode imaging. Based on our previous finding that the upper threshold of the IMT was 1.1 mm in healthy subjects, the patients were divided into the AS-positive group with the IMT > 1.1 mm, ( n = 17) and the AS-negative group with the IMT < 1.1 mm ( n = 10). Among five variables measured as the factors concerned with thrombogenesis, only plasma levels of β-thromboglobulin (β-TG) and platelet factor 4 (PF4) were significantly higher in the AS-positive group than in the AS-negative group. Chronic administration of pentoxifylline (300 mg/day) significantly reduced the abnormally high plasma levels of β-TG and PF4 in 7 patients of the AS-positive group to normal levels, without lowering the normal plasma β-TG and PF4 levels in the remaining 10 patients. Pentoxifylline treatment did not affect the plasma levels of the 3 other variables, von Willebrand factor, 6-keto prostaglandin F1α and thromboxane B2. This study suggests that the progress of atherosclerosis in diabetes mellitus is associated with in vivo platelet activation and platelet activation does not occur in diabetics without carotid atherosclerosis. Pentoxifylline may impede the vicious cycle in which atherosclerosis is accelerated by platelet activation.

Effect of Satigrel (E5510), a Novel Antiplatelet Agent, on Platelet Function and the Coagulation-Fibrinolytic System in Peripheral Arterial Occlusive Disease

A novel antiplatelet agent, satigrel (E5510), was administered to 9 patients with arteriosclerosis obliterans (ASO) and 6 patients with thromboangiitis obliterans (TAO) at a dosage of 4mg/day for 2 weeks followed by 8mg/day for another 2 weeks and its effect on platelet function and coagulation-fibrinolytic system as well as hemodynamics were evaluated. Satigrel significantly inhibited platelet aggregation induced by collagen (p<0.001), lowered plasma thromboxane B2 (TXB2) (p<0.01) and 11-dehydro TXB2 (p<0.1), and increased plasma antithrombin III (AT-III) (p<0.001). Hopwever, there were no significant change in plasma levels of β-thromboglobulin (β-TG), platelet factor 4 (PF4), 6-keto prostaglandin F1α (6-KF), thrombin-antithrombin III complex (TAT), fibrinopeptide A (FPA) and plasmin-α2 plasmin inhibitor complex (PIC). Plasma D-Dimer and fibrinopeptide Bβ15-42 (FPBβ15-42) levels were higher in ASO patients than in TAO patients before treatment and tended to increase in both groups following the administration of satigrel. Furthermore, satigrel improved tissue blood flow in the affected feet (p<0.05) even though clinical improvement and increase in ankle pressure index were not significant. These results suggest that satigrel is beneficial to a failed circulation in these arterial occlusive diseases.

Clopidogrel – a Platelet Inhibitor which Inhibits Thrombogenesis in Non-Anticoagulated Human Blood Independently of the Blood Flow Conditions

The goal of the present study was to investigate the effect of 7 and 14 days of daily oral administration of 75 mg clopidogrel on collagen-induced thrombogenesis in flowing non-anticoagulated human blood. Blood was drawn directly from an antecubital vein over immobilised collagen type III fibrils positioned in a parallel-plate perfusion chamber. The wall shear rates at the collagen surface were those characteristic for veins (100 s-1), and for medium sized (650 s-1) and moderately stenosed (2600 s-1) arteries. Clopidogrel ingestion reduced the thrombus volume significantly (p < 0.05) at 100 and 2600 s-1 (39 and 51% respectively). The beta-thromboglobulin plasma levels were reduced concomitantly. However, it was not possible to measure accurately the thrombus volume at 650 s-1, due to loose packing of the platelet thrombi. Transmission electron microscopy substantiated this observation and showed that clopidogrel profoundly reduced the platelet degranulation process (p < 0.005). The inhibitory effect of clopidogrel on platelet consumption by the growing thrombi resulted apparently in higher platelet concentration at the collagen surface, which enhanced the platelet-collagen adhesion at all three shear rates (p < 0.05). Despite the low deposition of fibrin on collagen, clopidogrel reduced significantly the fibrinopeptide A plasma levels and the fibrin deposition at shear rates below 650 s-1. This was apparently a consequence of the reduced platelet recruitment and the lower activation of platelets, since activated platelets in thrombi promote deposition of fibrin.(ABSTRACT TRUNCATED AT 250 WORDS)

The evidence of platelet activation in bronchial asthma

The possible involvement of platelets in bronchial asthma was investigated under three different conditions: (1) chronic asthma, (2) bronchial provocation inhaling house dust mite (HDM), and (3) status asthmaticus. Plasma levels of β-thromboglobulin (β-TG), platelet factor 4 (PF4), and in part, platelet-activating factor (PAF) were measured. Approximately one third of the subjects with symptomatic or asymptomatic chronic asthma showed an increased level of β-TG or PF4. Statistically significant differences occurred in β-TG and PF4 levels only between healthy controls and symptomatic subjects. Five out of six subjects showed no elevation of β-TG and PF4 during immediate asthmatic response. In two out of nine subjects with status asthmaticus, β-TG or PF4 was elevated, and statistically significant correlations occurred between the initial level of PAF and that of β-TG or PF4. Those results suggest that the platelet activation in the circulation is sometimes provoked in asthma, but plasma level of α-granule—derived proteins does not reflect the intensity or severity of asthma, and that PAF is likely to be a mediator responsible for the platelet activation.

Circadian variation in platelet function in healthy volunteers

Circadian variation in hemostatic factors may contribute to a higher frequency of cardiac events observed in the morning and with activity. Diurnal changes in these factors were investigated by measuring in vitro platelet aggregability in response to epinephrine and adenosine diphosphate together with β-thromboglobulin and platelet factor 4 as indexes of in vivo platelet activation. Activation of coagulation was measured by thrombin-antithrombin III complexes and D-Dimers. Tests were performed in 9 normal healthy subjects. Circadian changes occurred in β-thromboglobulin (p < 0.05) and platelet factor 4 (p < 0.06). Plasma levels of β-thromboglobulin and platelet factor 4 were lowest with patients supine and resting at 7 and 8 A.M., and increased with activity, with peak levels achieved at 3 P.M. (p < 0.01). Thrombin-antithrombin III complexes (p = 0.44), D-Dimer (p = 0.36) and in vitro platelet aggregability to adenosine diphosphate (p = 0.20) did not show diurnal variation. There was a trend toward circadian variation in vitro platelet aggregability to epinephrine, but these changes did not achieve statistical significance (p = 0.16). Circadian changes of in vivo release of β-thromboglobulin and platelet factor 4 correlated to patient activity and not to the morning peaks in ischemic events. These data indicate that changes in platelet function and not in coagulation have a diurnal occurrence.

Effects of varying dietary fatty acid ratios on plasma lipids and platelet function in the African green monkey

The influence of varying dietary fatty acid ratios on plasma lipids, platelet function and the potential for thrombosis was evaluated in the African green monkey ( Cercopithecus aethiops), an animal model widely used in cardiovascular research. Ten adult animals, 5 males and 5 females, at intervals of 2 months, were fed a series of 7 diets with fatty acid ratios (P:S) ranging from 3:1 to 1:4. Platelet aggregation in vitro, plasma levels of β-thromboglobulin and platelet factor 4, platelet membrane fatty acid composition and plasma lipids including total cholesterol, HDL and LDL were monitored at the end of each dietary period. Platelet hypersensitivity to ADP aggregation (3 and 10 μM) and plasma β-thromboglobulin were elevated in both males and females when dietary P:S exceeded 1.5:1 (β-TG = 45 ng/ml) as compared to control diets either reflecting current North American or that recommended as a desirable dietary goal (P: S = 1 : 1, β-TG = 10 ng/ml). Diets enriched in saturated fatty acids (P:S = 1:2) also altered platelet function, but the effects were most consistently observed in female animals (β-TG = 32 ng/ml). Platelet hypersensitivity was lost and (β-TG levels were at baseline when the animals were returned to the control diets. Platelet sensitivity did not correlate with membrane composition which generally reflected dietary composition. Both the saturated and the polyunsaturated fatty acid enriched diets lowered plasma HDL levels, and the saturated fatty acid diets elevated plasma LDL. In general, a positive relationship was observed between plasma LDL and β-TG; however, this was statistically significant ( P < 0.05) only with polyunsaturated fatty acid diets in female animals. Changes in either LDL or HDL were not consistently related to platelet function, suggesting independence of the platelet effects from plasma lipoproteins.

Platelet reactivity in human aortic grafts: A prospective, randomized midterm study of platelet adherence and release products in Dacron and polytetrafluoroethylene conduits

Platelet-related phenomena at the blood-surface interface of randomly placed knitted Dacron (n = 6) and polytetrafluoroethylene (ePTFE) (n = 6) interposition aortic grafts were studied in patients undergoing abdominal aortic aneurysmectomy. Luminal accumulation of platelets was assessed by infusing indium-111-oxine (400 μCi) labeled autologous platelets and imaging grafts at 1 week, 3 months, and 6 months after surgery. Image analysis included an indium ratio technique (comparing aortic graft radioactivity to that of an iliac artery) and a red blood cell technetium subtraction technique (excluding blood pool radioactivity from graft radioactivity, with the heart or iliac artery serving as reference regions). Plasma levels of β-thromboglobulin and platelet factor 4 were correlated with platelet accumulations on the aortic prostheses. Differences in graft radioactivity or platelet-release products were not evident 1 week after surgery. Three months after implantation, Dacron and ePTFE conduits exhibited 87% and 47% (p < 0.05) more radioactivity with the indium ratio technique than the iliac artery. Similary, increased Dacron compared with ePTFE graft radioactivity was noted using technetium subtraction techniques: 71% vs 30% with a heart reference and 26% vs 11% with an iliac artery reference, respectively. Increases in graft radioactivity correlated with increases in both plasma β-thromboglobulin and platelet factor 4 at 3 months (r = 0.6 to 0.9; p < 0.05 to 0.001 depending on the imaging technique used). At 6 months, differences did not persist. In fact, technetium subtraction techniques suggested less Dacron conduit reactivity. It is speculated that differences in platelet accumulation and activation associated with different graft substrates may prove clinically important.

Lack of influence of low-dose acetylsalicylic acid (100 mg daily) on platelet survival time, β-thromboglobulin and platelet factor 4 in patients with peripheral arterial occlusive disease

In this study we investigated the influence of low-dose (100 mg daily) acetylsalicylic acid (ASA) on 111-In-platelet survival time (PST) and on plasma levels of β-thromboglobulin (β-TG) and platelet factor 4 (PF 4) in 30 patients (median age: 60 years) with arteriographically proven peripheral arterial occlusive disease in a chronic stable phase. We observed no significant changes of PST during therapy with ASA (weighted mean: 169.8 → 166 [median] hours; multiple hit: 168.3 → 170.6 hours), and also the plasma levels of B-TG (median: 31.8 → 32.3 ng/ml) and of PF 4 (3.6 → 3.9 ng/ml) remained unchanged.

Evaluation of platelet function in pregnancy comparative studies in non-smokers and smokers

We have evaluated the possible role of platelet functional abnormalities as a contributory cause of thrombosis during pregnancy and to the increased fetal mortality and morbidity among women who smoke. Fifty-three pregnant women were enrolled and evaluated on two separate prenatal visits held between the 20th and 36th week of pregnancy and, when possible, post partum. Smoking status was evaluated by personal statement and alveolar carbon monoxide levels. Women in the smoking group deliberately avoided cigarettes for at least, 20 minutes before sampling. Plasma levels of β-thromboglobulin, thromboxane B 2, and 6-Keto PGF 1a were evaluated. A significant increase in 6-Keto PGF 1α was noted among smoking women as pregnancy advanced. 6-Keto PGF 1α levels decreased among non-smoking women while β-thromboglobulin increased significantly between the 20th and 33rd week of pregnancy in non-smokers. Platelet aggregation, both in platelet rich plasma and in whole blood (by impedance aggregometry), was evaluated by five different parameters and four different aggregating agents. Significant differences between the non-smoking and smoking pregnant women were noted for selected age cohorts and aggregating agents. An increase in platelet reactivity among smokers was observed in whole blood by impedance aggregometry with adenosine diphosphate and in two age cohorts using platelet rich plasma. In two groups in which aggregation was significantly accelerated among non-smokers, epinephrine was used as the aggregating agent.

Influence of acetylsalicylic acid (1.0 g/day) on platelet survival time, β-thromboglobulin and platelet factor 4 in patients with peripheral arterial occlusive disease

In this study we investigated the influence of acetylsalicylic acid (ASA) 1.0 g/day on 111-In-platelet survival time (PST) and on plasma levels of β-thromboglobulin (β-TG) and platelet factor 4 (PF 4) in 37 patients (median age: 63.4 years) with arteriographically proven peripheral arterial occlusive disease (PAOD) in a chronic stable phase. We found a slight but significant increase of PST during therapy with ASA (weighted mean (WM): 184.3 → 193.2 [median]hours, p < 0.05; multiple hit (MH): 182.4 → 192.8 hours, p<0.005) for the total group of patients. Concerning the influence of risk factors of PAOD on PST during ASA-therapy, there was a significant increase of PST only in the nondiabetics (WM: 180.3 → 204.6 hours p<0.01; MH: 176.8 → 195.3 hours, p<0.01). There was a negative correlation between the baseline values of PST and their increase following ASA therapy (WM: r = - 0.63; p<0.0001; MH: r = - 0.61, p<0.0001). The pretreatment levels of β-TG - but not PF 4 - were significantly (p<0.001) elevated compared to healthy controls. Therapy with ASA caused a significant decrease in the plasma levels of β-TG (median: 30.4 → 26.6 ng/ml, p<0.001) and PF 4 (2.95 2.2 ng/ml, p<0.01).