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PubMedDate not supplied

Mean platelet volume as an indicator of platelet activation: methodological issues.

BACKGROUND: Mean platelet volume (MPV) is increased in patients at high risk for athero-thrombotic diseases. Thus, an elevated MPV may be a risk marker for platelet activation. METHODS: Healthy subjects with normal triglyceride (TG) levels (90+/-6 mg/dl; n = 40) or mild hypertriglyceridemia (161+/-79 mg/dl; n = 32) were studied. MPV was measured in fasting blood samples before and after stimulation with collagen (10 micro g/ml), and exposure to 4 or 37 degrees C. Samples from the normotriglyceridemic subjects were tested again 4 h after consuming a high-fat drink. RESULTS: Collagen and exposure to 4 degrees C increased MPV, whereas incubation at 37 degrees C lowered MPV regardless of TG level. There was no significant difference in unstimulated MPV between the fasting and the fed states in the normotriglyceridemic subjects (both 7.2+/-0.1 fl; mean+/-SEM), nor between the latter group and hypertriglyceridemic subjects (7.0+/-0.1 fl). There was a significant negative relation between MPV and fasting TG level. CONCLUSIONS: This study suggests that MPV response to low-dose collagen may be a useful indicator of platelet propensity to activation. Further studies are warranted to correlate MPV with classical platelet aggregation tests and with the use of platelet-active drugs.

Adult↗
PubMed2004

Dextran 40 reduces in vitro platelet aggregation in peripheral arterial disease.

Dextran 40 has been used to prevent post-operative thrombosis. However, its antithrombotic and antiplatelet effects in peripheral arterial disease (PAD) are poorly understood. We studied the in vitro effects of Dextran 40 on platelet function in control subjects and PAD patients using whole blood methods. Platelet function was assessed in 20 control subjects and 20 PAD patients. Spontaneous platelet aggregation (SPA) and agonist-induced platelet aggregation in response to increasing concentrations of Dextran 40 in vitro were measured by whole blood aggregometry. Flow cytometric measurements of platelet P-selectin, GpIIb/IIIa, GpIb and PAC-1 binding were also performed. There was no difference in SPA or ADP-induced aggregation in control patients with Dextran 40 in vitro. However, Dextran 40 inhibited collagen-induced aggregation in control patients (P < 0.05, Friedman test). In PAD patients, SPA and ADP (1 microM)-induced aggregation were significantly reduced by Dextran 40 in vitro (P < 0.001, Friedman test). In PAD patients, collagen-induced platelet aggregation (1 and 5 microg/ml) was significantly reduced by Dextran 40 in vitro (P < 0.01, Friedman test). GpIIb/IIIa, PAC-1 and P-selectin expression were significantly reduced in whole blood samples from PAD patients following incubation with Dextran 40 (P < 0.05, Wilcoxon rank test) but not in samples from control patients. Dextran 40 reduces spontaneous and agonist-induced platelet aggregation as well as the surface expression of markers of platelet activation in PAD patients. This antiplatelet effect may be of benefit to patients undergoing vascular surgical procedures where thrombosis is a significant risk.

Adenosine Diphosphate↗
PubMed2003

Platelet characteristics associated with coronary artery disease.

BACKGROUND/OBJECTIVE: To test the hypothesis that circulating platelets display evidence of interactions with atherogenesis, platelet capacity to express P-selectin and propensity for spontaneous microaggregation in vitro were measured in samples from normal donors (N), patients with asymptomatic advanced coronary calcification (CC) or acute coronary syndromes (AC). To measure the effect of angioplasty on platelet function, samples obtained before, 30 min after and 24 h after angioplasty were compared. PATIENTS/METHODS: Platelet P-selectin was measured after maximal stimulation with thrombin. Microaggregation was measured as a platelet count deficit in citrate-anticoagulated platelet-rich plasma (PRP) relative to EDTA-anticoagulated blood. RESULTS: P-selectin expression was significantly lower for platelets from patients with either AC or CC compared to normals. In addition, platelets from AC and CC patients have a significantly greater propensity to form microaggregates in citrate anticoagulant. After angioplasty, the PRP-platelet count decreased transiently. CONCLUSION: Both acute unstable and chronic stable coronary disease are associated with an increased share of platelets unable to express P-selectin and an increased share of platelets that microaggregate in citrate anticoagulant. The genesis of these platelet characteristics is not fully explained by focal acute arterial injury and may reflect exposure to systemic atherosclerosis or the atherogenic process.

Angioplasty↗
PubMed1995

Platelet ultrastructural and functional studies in myelodysplasia.

We studied the platelets of 8 patients with myelodysplasia aged 49-77 years, using both ultrastructural and functional techniques. Five of the 8 patients were classified as having refractory anaemia, and 3 as refractory anaemia with excess of blasts (RAEB). Electron microscopically, the myelodysplastic patients had in addition to normal ones, platelets containing significantly less alpha-granules. In part of these hypogranular platelets, the dense tubular system was abundant, but in contrast with normal platelets, it was not dispersed between the other organelles, nor did it form a membrane complex with the open cannalicular system. From a functional point of view, collagen-induced shape change was the most frequently disturbed parameter: there was a total loss of collagen-induced shape change in 5 patients. In 2 patients, there was a complete lack of response to collagen in platelet-rich plasma (both shape change and aggregation); in one of them, there was also a total loss of adenosine triphosphate secretion in response to all inducers tested. After 4 years of follow-up, 5 patients had died, of whom 3 were RAEB patients. An initial complete absence of collagen-induced shape change was found in these 5 patients, while in the 3 patients who were still alive at the end of the follow-up period, collagen-induced shape change was normal in 2 and slightly diminished in one.

Aged↗
PubMed2003

Evaluation of a rat model of preeclampsia for HELLP syndrome characteristics.

OBJECTIVE: To determine whether a rat model of preeclampsia includes features consistent with HELLP (hemolysis, elevated liver enzymes, low platelets) syndrome. METHODS: Preeclampsia was induced experimentally in timed-pregnant Sprague-Dawley rats using the reduced uterine perfusion pressure (RUPP) model. On day 14 of gestation, silver clips were placed around the aorta below the renal arteries and on the left and right uterine arcade at the ovarian artery. All animals were chronically instrumented to determine conscious blood pressure and to obtain blood samples for analysis of complete blood count, platelet count, liver function tests, uric acid, creatinine, and albumin. Blood samples were collected and animals sacrificed on day 19 of gestation, at which time placental and pup weight were obtained. A control group was analyzed similarly. Statistical analysis was performed with the Student t test. RESULTS: The RUPP model animals (n = 8), when compared with the normotensive controls (n = 9), did not show a statistically significant difference in hemoglobin, platelets, liver function tests, uric acid, creatinine, or albumin, although the mean arterial pressure was higher (mean +/- SD 131.9 +/- 17.1 mmHg versus 104.0 +/- 14.0 mmHg, respectively; P = .003) and pup number was lower (RUPP 6.6 +/- 2.4 versus control 13.8 +/- 2.3, P < .001). CONCLUSION: Although decreased uteroplacental perfusion induces changes similar to symptoms of preeclampsia, the RUPP rat model does not appear to express features of HELLP syndrome.

Animals↗
PubMed2004

Platelet reactivity in response to mental stress in syndrome X and in stable or unstable coronary artery disease.

INTRODUCTION: Previous studies showed differences in platelet reactivity in response to exercise in patients with syndrome X (SX) and those with obstructive coronary artery disease (CAD). In this study, we investigated whether similar differences could be detectable in response to a mental stressful stimulus. MATERIALS AND METHODS: We studied 30 SX patients (60+/-8 years, 8 men), 20 patients with stable angina and angiographically documented CAD (SA, 66+/-8 years, 14 men), and 11 patients with unstable angina (UA, 67+/-8 years, 6 men). A control group of 22 healthy controls (50+/-7 years, 5 men) was also studied. All subjects underwent a mathematical mental stress test (MST) consisting of rapid consecutive subtractions of number 7 for a period of 5 min. A venous blood sample was collected at baseline and immediately after MST. Platelet reactivity was measured on flowing blood as time necessary to occlude a ring coated with collagen-adenosine diphosphate (ADP; closure time, CT), using the platelet function analyzer (PFA-100) system. RESULTS: At rest, CT was lower in UA patients (87+/-19 s) compared to controls (109+/-24 s, p=0.02) and SA patients (105+/-37 s, p=0.055), and also tended to be lower in SX patients (96+/-18 s) compared to controls (p=0.07). The CT response to MST differed significantly among groups (p=0.0009). At peak MST, CT did not change in controls (110+/-27 s, p=0.88), whereas it decreased in SA patients (96+/-29 s, p=0.003) and tended to decrease in UA patients (82+/-15 s, p=0.25). In contrast, a significant increase in CT with MST was shown in SX patients (103+/-21 s, p=0.007). CONCLUSIONS: Platelet reactivity is increased by MST in patients with CAD, whereas it paradoxically decreases in SX patients, which may constitute a protective effect against stress-induced events in these patients.

Aged↗
PubMed2005

von Willebrand disease R1374C: type 2A or 2M? A challenge to the revised classification. High frequency in the northwest of Spain (Galicia).

Patients initially diagnosed with type 1 von Willebrand disease (VWD) have been reclassified as type 2 after a more exhaustive analysis in several studies. Our study's objectives were (1) to reanalyze patients that were previously diagnosed as type 1 to achieve a more accurate diagnosis and (2) to compare the von Willebrand factor (VWF) ristocetin cofactor assay (VWF:RCo) and the VWF collagen binding assay (VWF:CB) in order to evaluate the possibility of replacing the former assay with the latter in the diagnosis of VWD. Twenty-one patients from two large unrelated families and 104 normal controls were studied. VWF:Ag, VWF:RCo, FVIII coagulant activity (FVIII:C), bleeding time (BT), PFA(100), and multimeric analysis of VWF were tested. Genetic analysis by sequencing exon 28 on the VWF gene was also carried out. Patients presented lower levels of VWF:Ag and VWF:RCo, a dissociation between VWF:RCo/VWF:Ag, and the presence of all sizes of multimers in plasma VWF. The results for VWF:CB varied depending on the type of collagen used. The genetic analysis showed that the mutation R1374C is responsible for type 2M VWD. A high frequency of the R1374C mutation is observed in northwestern Spain (Galicia). Some types of 2M VWD are misdiagnosed as type 1 VWD. The VWF:CB (with type I collagen) assay was unable to discriminate defective platelet binding of the R1374C VWF. This confirms that VWF:CB cannot substitute for VWF:RCo, and both should be tested when diagnosing VWD.

Blood Coagulation Tests↗
PubMed1999

[Preeclampsia not (yet) predictable from the blood platelet count].

Platelet activation plays an important role in the pathogenesis of pre-eclampsia as demonstrated by reduced platelet count, increased mean platelet volume and elevated plasma concentrations of beta-thromboglobulin and platelet factor 4 in pre-eclamptic patients. Thrombocytopenia precedes the onset of clinical symptoms of pre-eclampsia. Possibly an enhanced activation state of the platelets in the circulation is present some time before the onset of pre-eclampsia: platelet activation might then be used to predict pre-eclampsia. Flow cytometry is considered the most sensitive technique at this moment to measure the activation of platelets. Fluorescent-labelled antibodies are used to detect antigens that appear on the platelet surface or change their conformation upon activation. During the first and second trimester of pregnancy pre-eclamptic patients have an increased expression of some antigens on the surface of their platelets, such as CD63. There is no reliable platelet test yet to predict the onset of pre-eclampsia.

Adult↗
PubMed2003

A rapid, automated flow cytometric method to measure activated degranulated platelets by density determination.

Platelet activation is reported to correlate with acute coronary syndromes. A platelet analysis method on the ADVIA 120 Hematology System provides rapid analysis of platelet density, reported as mean platelet component (MPC) concentration, utilizes routine hematology specimens, requires no pre-treatment, and thirty seconds to generate results. Sub-populations of platelets separated by density gradients showed excellent correlation with the ADVIA 120 MPC parameter (r = 0.997). Platelet activation induced by thrombin treatment resulted in a shift of platelets into the lowest density fraction (d</=1.068 g/mL) with a corresponding reduction in MPC from 24.7 to 20.6 g/dL, N = 4 subjects (p < 0.004). There was also excellent correlation between expression of CD62P measured by fluorescence flow cytometry and the ADVIA 120 Hematology System MPC values (r = 0.85). These results indicate that the ADVIA 120 MPC parameter may be a useful new test for assessing activated platelets and platelet density.

Automation↗
PubMed1995

Laboratory assessment of von Willebrand factor. Use of different assays can influence the diagnosis of von Willebrand's disease, dependent on differing sensitivity to sample preparation and differential recognition of high molecular weight VWF forms.

Three separate laboratory assays for von Willebrand Factor (VWF), a standard "antigen" (antisera-ELISA-based) assay (VWF:Ag), a standard ristocetin-dependent-platelet-agglutination procedure (VWF:RCof), and an ELISA-based collagen-VWF binding assay (VWF:CBA), have been evaluated for their ability to detect alterations in VWF levels following differential processing of blood for testing, and specifically in (1) serum compared to plasma and (2) filtered plasma compared to nonfiltered plasma. Although all assays tended to detect some change, sensitivity of detection varied between assays, with the VWF:CBA most consistently able to detect large decreases in VWF levels in serum and filtered plasma. The authors propose that the increased sensitivity of the VWF:CBA assay to VWF depleted in these circumstances is that this assay selectively detects higher molecular weight forms (ie, those known to be more functionally relevant), and that assay results reflect the preferential incorporation of these forms in in the platelet-fibrin-gel during the clotting process, and onto the filter matrix during filtration. To confirm this, multimer analysis was performed and showed a reduction in high molecular weight forms of VWF in these cases. Finally, direct evidence that the VWF:CBA assay preferentially detects high molecular weight forms of VWF was obtained following fractionation of normal plasma VWF (separation according to molecular weight using size exclusion matrix; confirmed by specific multimer analysis) and assessment of eluted VWF. Using a standard VWF:Ag assay, detection of eluted VWF was unrelated to molecular size. In contrast, the VWF:CBA showed selective detection, and was able to preferentially discriminate high and intermediate forms of VWF from low molecular weight forms. The findings are of particular relevance to diagnostic pathology laboratories because filtered plasma or serum can be inappropriately (and unknowingly) provided for the clinically queried diagnosis of von Willebrand's disease (VWD). As outlined in this report, these samples can yield VWF results that closely mimic those of a Type 2A or Type 2B VWD individual, and thus, VWD may be incorrectly diagnosed.

Blood↗
PubMed2005

[Thrombocytosis and essential thrombocythemia in childhood].

Thrombocytosis is frequently observed in pediatric patients. Among them the secondary thrombocytosis are the most frequent and result from several causes. The rarely primary thrombocytosis can be either constitutive (and often familial) or acquired (essential thrombocythemia). The purpose of this article is to give diagnostic orientation and to suggest which biological tests should be performed.

Bleeding Time↗
PubMed2004

Clopidogrel (Plavix) and cardiac surgical patients: implications for platelet function monitoring and postoperative bleeding.

The use of clopidogrel (Plavix), an inhibitor of adenosine diphosphate (ADP)-induced platelet aggregation, has been proven to reduce ischemic events in cardiovascular patients, but little information is available for optimal monitoring of platelet function in patients receiving the drug preoperatively. In the first part of the study we compared different testing modalities (thrombelastography (TEG), platelet aggregometry, and whole blood aggregation) to assess platelet ADP receptor inhibition. Because clopidogrel is a pro-drug, we used an in vitro model of ADP inhibition with 5'-p-fluorosulfonylbenzoyladenosine (FSBA). FSBA at final concentration of 80 microM completely inhibited platelet aggregation but had no effect on TEG maximum amplitude (MA). In the second part of the study, antiplatelet effects of clopidogrel were clinically assessed and correlated to postoperative bleeding in 18 coronary bypass surgery patients. Preoperative TEG results were normal or hypercoagulable in clopidogrel-treated patients, although platelet aggregation responses to ADP were inhibited. Clopidogrel-treated patients who underwent cardiopulmonary bypass had a high incidence (84.6%) of platelet transfusion therapy due to increased chest tube drainage. In conclusion, we have demonstrated that normal preoperative TEG-MA does not preclude clopidogrel-induced ADP receptor blockade; however, TEG can be a reliable monitor for CPB-induced platelet dysfunction related to GPIIb/IIIa. For monitoring clopidogrel, it is necessary to perform more specific platelet function tests (aggregometry or platelet count ratio) using ADP as an activator.

Adenosine↗
PubMed1989

The laboratory diagnosis of lupus anticoagulants.

With the well-documented association of lupus anticoagulants with thrombotic disease and recurrent spontaneous abortion, the laboratory approach to diagnosing these inhibitors is more critical now. To this end, we examined plasma samples from 21 patients who initially presented with a prolonged prothrombin time or activated partial thromboplastin time or both for the presence of lupus anticoagulants. We used a battery of coagulation tests, including both immediate and two-hour mixing studies, a platelet neutralization procedure, a tissue thromboplastin inhibition test, and dilute Russell viper venom times. Two patients (10%) had only a prolonged prothrombin time, seven (33%) had only a prolonged activated partial thromboplastin time, and in 12 (57%) both were abnormal. In 15 patients, inhibition was evident on immediate assay of equal-volume mixture studies of patient plasma and normal pooled plasma, but in three additional patients it was evident only after a two-hour incubation. Fifteen of 18 samples showed correction of the abnormal screening study when platelets were used as a source of phospholipid. Both the tissue thromboplastin inhibition test and dilute Russell viper venom times were sensitive assays, being abnormal in 20 of 21 and 13 of 14 samples, respectively. In four patients, discordance of studies necessitated specific coagulation factor levels being measured to confirm the presence of the inhibitor. Because of the variable effect of the inhibitors on all currently available assay procedures, we would suggest that any evaluation will require a laboratory to have a battery of tests available before such an inhibitor can be excluded.

Adolescent↗
PubMed1997

Platelet aggregation in response to collagen and thrombin reliably detects the ingestion of low-dose aspirin.

The exposure of blood donors to aspirin is not reliably excluded by pharmacokinetic measurements due to the irreversible effects of aspirin which persist even after elimination of aspirin and its metabolites from plasma. Tests of platelet functions do overcome this deficit, but are usually limited by substantial inter-individual variability of parameters of platelet function. We have evaluated platelet aggregation ex vivo in 20 aspirin-treated (100 mg single oral dose/day) patients in comparison with a control group of 20 aspirin-free donors. The results demonstrate a significant reduction in the collagen(2.5 micrograms/ml)-induced platelet aggregation by aspirin treatment, whereas thrombin(50 mumol/l TRAP-6)-induced platelet aggregation was not affected at all. Assessment of collagen-induced platelet aggregation relative to platelet responses of the same subject elicited either by thrombin or by a combination of collagen and thrombin does substantially improve the reliability of functional assays of aspirin.

Administration, Oral↗
PubMed2000

Effects of beraprost and cilostazol and renal function on serum thrombomodulin levels in diabetic patients.

Serum thrombomodulin (TM) levels were determined in diabetic patients, and the effects of diabetic complications and renal function on TM were studied. Serum TM levels increased in diabetics, and patients with diabetic nephropathy tended to manifest higher levels of TM. There was a significant correlation between TM and serum creatinine levels. In addition, there was a significant elevation in serum TM levels in diabetics over time (1 year to 1 year 8 months), and the changes were particularly evident in patients who had a higher TM level from before the observation period. Furthermore, when patients were treated with an antiplatelet agent--beraprost (CAS 88475-69-8) or cilostazol (CAS 73963-72-1)--a significant reduction in TM levels was observed after 3 months. It is suggested that TM could be used as index to assess the development of clinical complications in diabetics and that anti-platelet agents have potential usefulness in delaying the aggravation of diabetic complications.

Cilostazol↗
PubMed1999

Quantitative and qualitative platelet disorders.

Platelet disorders are common during childhood. Those conditions that are clinically significant are generally diagnosed with ease. Qualitative platelet disorders rarely cause clinical problems. The armamentarium of diagnostic tests, although limited, is usually satisfactory to allow for accurate diagnosis and effective treatment of those children with platelet disorders who are at risk of hemorrhage.

Blood Platelet Disorders↗
PubMed2006

Point of care testing of aspirin resistance in patients with vascular disease.

INTRODUCTION: The reported range in rates of aspirin resistance (5.5-60%) may reflect difficulties in studying platelet function and the variety of tests used. This study used a platelet function analyzer (PFA-100) to prospectively document aspirin resistance in a cohort of patients with arterial disease. METHODS: Patients with internal carotid artery (ICA) stenosis or intermittent claudication (IC) were recruited. Exclusion criteria were contraindications to aspirin, prescription of other medication with known antiplatelet effects or known platelet abnormalities. After prescription of 100 mg aspirin/day for 2 weeks an uncuffed venous blood sample was taken and analysed with the PFA-100. Aspirin resistance was defined as closure time (CT) less than the upper limit of normal (158 s collagen/epinephrine agonist; 118 s collagen/adenosine diphosphate (ADP) agonist). RESULTS: Thirty-three patients with IC and 12 patients with ICA stenosis were recruited (n = 45). Median (range) age was 74 years (49-85) and the male to female ratio was 1.5:1. The median (range) CT was >300 (85 to >300) s with collagen/epinephrine and 100 (52 to >300) s with collagen/ADP agonist. Twelve patients (27%) in the collagen/epinephrine group had normal CT despite treatment with 100 mg aspirin, indicating resistance. Of the 33 patients with collagen/epinephrine CT prolonged by aspirin, 10 patients also had prolonged collagen/ADP CT, suggesting excessive platelet inhibition. CONCLUSION: A significant proportion of patients taking aspirin do not show laboratory evidence of platelet inhibition and may not be protected from atherothrombotic events. The PFA-100 appears to be a useful tool to screen for both aspirin resistance and excessive aspirin mediated platelet inhibition.

Aged↗