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At least 1,225 records · Page 68Linked to original sources
PubMed2003

Influence of systemic inflammation on efficiency of antiplatelet therapy in PAOD patients.

Recently it was shown that inflammation adversely influences results obtained from the platelet function analyzer system, PFA-100, hypothesizing that inflammation could confound interpretation of platelet function results. We investigated the clinical relevance of these results in patients with peripheral arterial occlusive disease (PAOD), with and without signs of systemic inflammation. In 98 PAOD patients, all treated with acetyl-salicylic acid (ASA), we obtained PFA-100 values upon stimulation with epinephrine. C-reactive protein (CRP) values were investigated as indicator for systemic inflammation. Mean CRP levels were elevated in 23 patients (23%). There was no difference of mean PFA-100 results between patients with elevated CRP levels and those without. Our results indicate that the effect of ASA on platelet aggregation, as measured by the PFA-100, is not relevantly influenced in PAOD patients with elevated CRP.

Arterial Occlusive Diseases↗
PubMed1999

The platelet function analyzer (PFA-100) may not be suitable for monitoring the therapeutic efficiency of von willebrand concentrate in type III von willebrand disease.

We describe a type-III von Willebrand patient who was admitted to the hospital with severe deformity and functional deficit of the left knee joint due to recurrent hemarthrosis. Orthopedic intervention was necessary. To prevent bleeding episodes, von Willebrand factor (vWF) replacement therapy was given during and after surgery. APTT, plasma FVIII activity (FVIIIc), vWF antigen (vWF Ag), and vWF ristocetin cofactor (vWF Rco) were measured. Primary hemostasis was monitored using the PFA-100. This "Platelet Function Analyzer" is designed to measure platelet adhesion and aggregation capacities. Whole blood is aspirated through a capillary and is forced to flow through the central hole of a membrane coated with collagen and epinephrine (COL/EPI) or ADP (COL/ADP) as platelet activators. Irreversible platelet aggregation results in the formation of a stable platelet plug, closing the central hole. The result is expressed as "closure time" (CT), i.e., time necessary to stop the blood flow, and is a measure of platelet hemostasis capacity. Laboratory investigations during substitution therapy revealed no shortening of closure times with both COL/EPI and COL/ADP cartridges despite normalization of plasma vWF Ag, vWF Rco, and FVIIIc levels. These observations suggest that intraplatelet vWF, which is totally absent in type-III von Willebrand disease, plays an important function in the adhesion of platelets to the collagen-coated membrane of the PFA-100 system, simulating an injured vessel wall. Consequently, we conclude that the PFA-100 may not be suitable for monitoring the therapeutic efficacy of von Willebrand concentrate in type-III von Willebrand patients during substitution therapy.

Adult↗
PubMed2001

Type 2B von Willebrand's disease due to Val1316Met mutation. Heterogeneity in the same sibship.

An analysis was conducted in four members of the same family, two of whom had a history of severe bleeding associated with type 2B von Willebrand's disease (VWD) which, although found to be due to the same mutation, nevertheless exhibited different phenotype patterns in the two subjects involved. Von Willebrand's factor (VWF) multimers were assayed with high- and low-resolution sodium dodecyl sulfate (SDS) agarose gels. The patients were studied before and after intravenous administration of desmopressin (DDAVP) at doses of 0.4 microg/kg body weight. Automatic sequencing techniques were used to analyze VWF gene exon 28. The propositus presented with mild basal thrombocytopenia with ristocetin-induced platelet aggregation (RIPA) at low concentrations of ristocetin. He had a very prolonged bleeding time (BT), and his plasma VWF was found to be lacking in large and intermediate multimers. Thrombocytopenia was observed to intensify transiently after the administration of DDAVP. The propositus' mother, in contrast, presented reduced RIPA while in a basal state, with only partial loss of the high molecular weight VWF multimers. Although she had a very prolonged BT, her platelet count was borderline. Transient correction of BT and a decrease in the platelet count were observed after administration of DDAVP and RIPA was observed at low concentrations of ristocetin. Exon 28 sequencing revealed a G4196A-->Val1316Met mutation in both patients. No other abnormality was detected within this exon. Val1316Met has been reported in type 2B VWD. In conclusion, in the family presented here, the phenotype pattern in one patient was typical of type 2B VWD, whereas the pattern in his mother was closer to type 2A VWD. After administration of DDAVP, however, a type 2B phenotype could be clearly attributed to both, indicating that this drug can be a useful tool for elucidating ambiguous phenotypes.

Adult↗
PubMed1998

[Long term effects of 50 mg acetylsalicylic acid alone and in combination with dipyridamole on platelet function after coronary bypass surgery].

In a prospective randomized trial in 42 patients undergoing coronary artery bypass surgery, we analyzed the long term platelet inhibiting effects of 50 mg acetylsalicylic acid (ASA) by itself and in combination with dipyridamole (2 x 200 mg), in comparison with phenprocoumon. Three and six months therapy led to significant inhibition of maximum aggregation induced by collagen 1 microgram/ml in platelet rich plasma (PRP) by more than 50% (p < or = 0.05). In PRP stimulated with 5 micrograms/ml collagen maximum inhibition amounted to nearly 20% (n.s.). The groups treated with ASA/ASA + dipyridamole showed an ADP threshold concentration 2.5 times higher than the group treated with phenprocoumon (p < or = 0.05). After stimulation with collagen 1 microgram/ml and 5 micrograms/ml thromboxane B2 synthesis in vitro in both groups treated with ASA was reduced to 1% of the base line values (p < or = 0.01). Inhibition of aggregation in whole blood appeared evident, but was not statistically significant due to considerable fluctuation of measurement. An additional effect of dipyridamole was not detectable. In conclusion, treatment with 50 mg ADA/d results in a lasting, effective inhibition of aggregation of platelets in patients with coronary artery bypass surgery. There is no synergistic effect of additional dose of 400 mg dipyridamole/d.

Anticoagulants↗
PubMed2003

Aspirin non-responder status in patients with recurrent cerebral ischemic attacks.

BACKGROUND: Antiplatelet agents such as acetylsalicylic acid (aspirin) reduce the relative risk for cerebrovascular events in patients with cardiovascular or cerebrovascular disorders by approximately 23 %. Recent observations raise the possibility that aspirin resistance may contribute to the failure of aspirin treatment in a significant proportion of patients (aspirin non-responders). To evaluate the clinical relevance of aspirin non-responder status, we analysed platelet functions in symptomatic and asymptomatic patients treated with aspirin for secondary prevention of cardiovascular and cerebrovascular events. METHODS: A total of 53 patients on 100 mg aspirin daily for secondary prevention (mean treatment duration > 60 months) were included. Patients were categorized as asymptomatic if they were free of cerebrovascular incidents for at least 24 months (n = 18). Symptomatic patients had suffered ischemic strokes or transient ischemic attacks within the previous 3 days (n = 35). Platelet function was assessed using the PFA-100 system that allows for quantitative assessment of platelet function, reporting platelet aggregatability as the time required to close a small aperture in a biologically active membrane. RESULTS: Collagen/epinephrine closure times were significantly shorter in symptomatic patients than in asymptomatic patients (p < 0.01). Individual closing times were normal in 12 of 35 symptomatic patients (34 % non-responders) whereas all asymptomatic patients had prolonged closure times. CONCLUSIONS: Aspirin non-responder status may contribute to failure of aspirin therapy in the secondary prevention of cerebrovascular incidents in as much as 30-40 % of patients. Quantitative assessment of platelet functions may provide a means to predict aspirin treatment failure in individual patients and to re-direct therapeutic strategies.

Aged↗
PubMed2005

Platelet aggregates in various stages of diabetic retinopathy: evaluation using the particle-counting light-scattering method.

AIMS: To investigate the possible correlation between platelet aggregation and the severity of diabetic retinopathy using the light-scattering method. METHODS: Using a light-scattering platelet aggregometer, we measured spontaneous platelet aggregation in 86 diabetics with retinopathy of varying severity and 30 healthy volunteers (controls). Platelet aggregates were classified as small, medium, and large according to their light intensity; patients were grouped based on the severity of retinopathy. In each patient group, we recorded for 10 min the total light intensities emitted by each aggregate size in the area under the curve (AUC). Then, we compared the AUC of each level of retinopathy severity with the controls and determined the correlation between the AUC of each aggregate size and each severity level. RESULTS: Of the 86 diabetics, 22 had no apparent retinopathy (NAR), 13 had mild nonproliferative diabetic retinopathy (NPDR), 17 had moderate NPDR, 12 had severe NPDR, and 22 had proliferative diabetic retinopathy (PDR). While the NAR group manifested significantly more small aggregates than the controls (20.5 x 10(6) versus 8.3 x 10(6) a.u., p=0.024), none of the other groups showed a significant increase in aggregates of any size. In the AUC of large aggregates, there was a weak-positive correlation with the severity of retinopathy (r=0.255, p=0.018); in the AUC of small and medium aggregates, there was no correlation. CONCLUSION: Although we did not find a significant correlation between platelet aggregation and the severity of diabetic retinopathy, our pilot study did detect some tendencies. Further studies on larger populations are underway to determine whether these tendencies are real.

Aged↗
PubMed2006

Meta-analysis of antiplatelet therapy for IgA nephropathy.

BACKGROUND: Antiplatelet agents have been widely used in the management of immunoglobulin A (IgA) nephropathy in the Japanese population. To systematically evaluate the effects of antiplatelet agents for IgA nephropathy, we conducted a meta-analysis of the published studies. METHODS: Data sources consisted of MEDLINE, EMBASE, the Cochrane Library, Ityu-shi (Japanese medical database), and bibliographies from the studies. The quality of the studies was evaluated from the intention to treat analysis and allocation concealment, as well as by the Jadad method. Meta-analyses were performed on the outcomes of proteinuria and renal function. RESULTS: Seven articles met the predetermined inclusion criteria. The use of antiplatelet agents showed statistically significant effects on proteinuria and renal function. The pooled risk ratio for proteinuria was 0.61 (95% confidence intervals (CI) 0.39-0.94) and for renal function it was 0.74 (95% CI 0.63-0.87). CONCLUSIONS: Antiplatelet agents resulted in reduced proteinuria and protected renal function in patients with IgA nephropathy. However, studies of high-quality design were rare, and most studies assessed surrogate outcomes. More properly designed studies are needed to reach a definitive assessment of this matter.

Dilazep↗
PubMed2005

Correction of changes in ADP-induced platelet aggregation with vasopressin analogue desglycinamide-arginine-vasopressin.

We studied the effect of vasopressin analogue desglycinamide-arginine-vasopressin on changes in platelet hemostasis produced by intragastric administration of Ticlid or clopidogrel (inhibitors of ADP-induced platelet aggregation). Intranasal administration of the peptide under conditions of hemorrhagic diathesis produced a hemostatic effect and normalized some parameters of blood coagulation.

Adenosine Diphosphate↗
PubMed1982

In vivo platelet aggregation and plasma catecholamines in acute myocardial infarction.

In vivo platelet aggregation assessed with the Filtragometer and potential correlates were compared among (1) patients with acute myocardial infarction (AMI), (2) normal controls, (3) patients with acute chest pain in whom AMI was eventually ruled out (ROMI), and (4) chronic outpatients (Cardiac Clinic group) with a history of myocardial infarction and/or angina pectoris. The measure was independent of sex, age, platelet count, immediate food intake, serum cholesterol, and triglyceride levels. The AMI group showed higher in vivo platelet aggregation than any of the other three groups (p less than 0.01). Least in vivo aggregation was seen in the normal group. Despite lack of correlation with the platelet aggregation measure, plasma epinephrine and norepinephrine showed statistically significant differences between the AMI and each of the other three groups. Our data support an association between platelet function and AMI, although not necessarily a cause and effect relationship.

Cholesterol↗
PubMed1980

Platelet function studies in coronary artery disease. VII. Effect of aspirin and tachycardia stress on aortic and coronary venous blood.

The effects of orally administered aspirin (650 mg) on platelet aggregation patterns and counts in aortic and coronary venous blood were evaluated in patients with coronary artery disease. Studies were conducted at rest and during the stress of tachycardia. Before administration of aspirin, platelet aggregation and counts were lower (p less than 0.01) in coronary venous blood than in aortic blood. The stress of tachycardia resulted in increased (p less than 0.01) platelet aggregation only in coronary venous blood. After administration of aspirin, differences in platelet aggregation and counts between coronary venous and aortic blood at rest were eliminated, and the tachycardia-associated increase in coronary venous blood platelet aggregation was significantly reduced. These observations suggest that aspirin influences and abolishes the changes that occur in blood platelet function as platelets traverse the atherosclerotic myocardial vascular bed. The absence of an increase in platelet aggregation during the stress of tachycardia after administration of aspirin may have important pathophysiologic and therapeutic implications.

Adult↗
PubMed1980

Platelet function studies in coronary heart disease. IX. Increased platelet prostaglandin generation and abnormal platelet sensitivity to prostacyclin and endoperoxide analog in angina pectoris.

Platelet prostaglandin generation (malondialdehyde production) and platelet sensitivity to prostacyclin (a vasodilator and platelet aggregation inhibitor) and to epoxymethanodienoic acid (EMA) (a vasoconstrictor and platelet aggregation stimulant endoperoxide analog) were studied in patients with angina pectoris and in control subjects. Platelet malondialdehyde production was higher in patients than in control subjects (mean +/- standard error of the mean 2.50 +/- 0.30 versus 1.70 +/- 0.13 nmol/10(9) platelets, p < 0.02). Platelets from patients were significantly less sensitive to prostacyclin's antiaggregatory effects than were those from control subjects (amount of prostacyclin required for 50 percent platelet aggregation inhibition 1.90 +/- 0.35 versus 0.68 +/- 0.05 ng, p < 0.02). Furthermore, less EMA was required to induce 50 percent platelet aggregation in patients with angina pectoris than in the normal subjects (133 +/- 8 versus 194 +/- 16 ng, p < 0.001). These observations suggest that increased platelet prostaglandin generation and abnormal platelet sensitivity to prostacyclin and endoperoxide analog in certain patients with coronary artery disease are important potential mechanisms in the pathogenesis of myocardial ischemia.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1981

Role of blood platelets and prostaglandins in coronary artery disease.

In the last decade, several studies evaluating blood platelet function in patients with coronary heart disease have been reported. Although several platelet function abnormalities such as enhanced platelet aggregation, decreased platelet survival and increase in platelet release reaction in the stable condition and during stress in patients with myocardial ischemia have been recognized, the mechanism of these abnormalities is just beginning to be understood. Discovery of certain platelet and endothelium-generated prostaglandins has provided some information as to the possible mechanism of platelet dysfunction. Abnormalities of prostaglandin production and platelet sensitivity to various prostaglandins may have an important bearing on the enhanced platelet aggregation in vivo, genesis of atherosclerosis and probably precipitation of acute ischemic events. Since the discovery of these prostaglandins, the precise mode of action of several commonly used platelet-active drugs has been clarified. Development of new drugs acting at selective steps in the prostaglandin pathways may provide some exciting novel therapeutic procedures in patients with coronary heart disease.

Acute Disease↗
PubMed1990

Effects of nitroglycerin at therapeutic doses on platelet aggregation in unstable angina pectoris and acute myocardial infarction.

The platelet aggregation response to adenosine diphosphate (ADP) and to thrombin was quantified in 10 patients, 5 with unstable angina pectoris and 5 with acute myocardial infarction, before, during and after a 45-minute infusion of nitroglycerin. An impedance aggregometer allowing rapid bedside studies in whole blood was used. The reproducibility of the methods was documented to be within 10%. Doses of nitroglycerin were titrated for a 10 mm Hg decrease in mean arterial blood pressure with mean doses being 1.2 +/- 0.2 (standard error of the mean) micrograms/kg/min. Nitroglycerin decreased the area under the aggregation curve induced by ADP from 43 +/- 3.6 to 30 +/- 6.3 cm2 (p = 0.007) and by thrombin from 8.9 +/- 1.7 to 4.1 +/- 0.9 cm2 (p = 0.003). Peak responses to ADP were decreased from 13.3 +/- 1 to 9.1 +/- 1.7 ohms (p = 0.005) and to thrombin from 9.3 +/- 2 to 5.0 +/- 1.2 ohms (p = 0.003). All patients had greater than or equal to 50% inhibition with 1 agent or the other and the inhibition was greater than 50% with each of the 2 aggregating agents in 6 patients. Analyses performed on blood withdrawn 15 minutes after the discontinuation of nitroglycerin showed a return to baseline before nitroglycerin results. When analyses were delayed and performed on blood preserved at room temperature for 30 minutes, no effect of nitroglycerin could be detected. Thus, bedside platelet aggregation studies document a significant and reversible effect of nitroglycerin at therapeutic doses on platelet function.

Adenosine Diphosphate↗
PubMed1994

Platelet activation in stable coronary artery disease.

To elucidate the role of physical activity in the pathogenesis of acute ischemic syndromes in patients with coronary artery disease (CAD), we hypothesized that platelet activation occurs when coronary blood flow velocity and shear stress increase across an atherosclerotic vascular bed. We measured platelet aggregation by using angiologic catheterization to obtain simultaneous samples of whole blood from the coronary sinus and the aorta while at rest, 2 minutes after the onset of rapid atrial pacing, and 10 minutes after termination of pacing. Of 82 consecutive patients included in our study, 36 had stenosis of the left coronary artery, 12 had stenosis of the right coronary artery only, and 34 had no evidence of CAD. Samples taken at rest revealed no arteriovenous difference in platelet aggregation between patients with CAD and those without CAD. In patients with significant stenosis (> or = 50%) of the left coronary artery, atrial pacing caused platelet aggregation to increase in samples from the coronary sinus (64 +/- 9% increase; p < 0.01) but not in blood from the aorta (2 +/- 8% decrease; difference not significant). This increase was transient, with aggregation returning almost to resting values 10 minutes after pacing ended. Atrial pacing elicited no change in platelet aggregation in samples from either the coronary sinus or aorta of patients with nonsignificant stenosis (< 50%) of the left coronary artery, patients with significant stenosis of the right coronary artery only, and patients free of CAD. Thus, under resting conditions, no evidence of platelet activation across the coronary bed was seen regardless of CAD status.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Flow Velocity↗
PubMed1980

Acquired dysfunction due to the circulation of "exhausted" platelets.

An acquired platelet functional defect was found to be present in eight patients who presented with various clinical conditions--three with renal allograft rejection, three with the hemolytic uremic syndrome or thrombotic thrombocytopenic purpura, one with acute consumption coagulopathy due to an incompatible transfusion and one with systemic lupus erythematosus. They showed defective platelet aggregation and reduced levels of adenine nucleotides and serotonin with abnormal uptake and storage of the amine. The bleeding time was more prolonged than predicted from the platelet count. These abnormalities were strikingly similar to those occurring in patients with congenital storage pool deficiency. The acquired defect is thought to be related to the presence in the circulation of "exhausted" platelets following their in vivo exposure to inducers of the release reaction such as damaged endothelium, thrombin and immune complexes. The bleeding tendency of the underlying diseases might be aggravated by the impairment of platelet function.

Adenosine Diphosphate↗