Detection of Circulating Platelet Aggregates in Thromboembolic Disease

Summary: The method of Wu and Hoak in det rmining circulating platelet aggregates in vivo was used.In different cardiac and vascular states, a low aggregation index is found: aorto-iliac occlusion (Leriche syndrome)- 38 csses(index X ± SD 0.52 ± 0.05 in comparison with normal subjects 0.91 ± 0.05); valvular diseasses (0.40±0.006); during extracorporeeal circulation - 14 cases (0.5±0.02l); thrombophlebitia-25 casea(0.84±0.065).After an antiaggaagation treatment (Dipiridamol) in 12 cases of aortoiliac occlusion the value of the aggregation index normalised(0.84±0.065) Experimenntlllly, 10 rabbits were perfused wi th thrombin soution (2 u./body woight k.); the lower values of the aggreeation index (0.91±0.085 brfore Emd 0.43±0.035 after the thromhin perfuaion) prove the fidelity of the method.The simplicity of the technique, the reproducti bili ty in experimental conditions and the normalisation of the valuwa after treatment prove the practical value in determining the circulating platelet aggregates.

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Detection of Circulating Platelet Aggregates in Thrombo-Embolic Disease

10.1055/s-0038-1665806 ◽

1979 ◽

Author(s):

Marie Scrobohaci ◽

Teodora Petrilă ◽

M. Constantinescu ◽

Magdolnra Stadler ◽

Doina Mihšilă ◽

...

Keyword(s):

Body Weight ◽

Normal Subjects ◽

Experimental Conditions ◽

Aggregation Index ◽

Leriche Syndrome ◽

Circulating Platelet Aggregates ◽

Valvular Diseases ◽

Platelet Aggregates ◽

Iliac Occlusion

SummaryThe method of Wu and Hoak in determining circulating platelet aggregates in vivo was used.In different cardiac and vascular states, a low aggregation index is found: aorto-iliac occlusion(Leriche syndrome)- 38 cases(index X ± SD 0.52 ±0.05 in comparison with normal subjects 0.91± 0.05):valvular diseases - 24 cases (0.40±0.006); during extracorporeeal circulation- 14 cases(0. 5±0.021) ; thrombophlebitis-25 cases(0.84±0.065).After an antiaggregation treatment(Dipiridamol) in 12 cases of aorto - iliac ocdusion the value of the aggregation index normalised(0.84±0.065) Experimentally, lo rabbits were perfused with thrombin so ution(2 u./body weight k.);the lower values of the aggregation index(0.91±0.085 before and 0.43±0.035 after the thrombin perfusion) prove the fidelity of the method.The simplicity of the technique, the reproductibility in experimental conditions and the normalisation of the values after treatment prove the practical value in determining the circulating platelet aggregates.

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Do patients with thromboembolic disease have circulating platelet aggregates?

Blood ◽

10.1182/blood.v64.1.205.bloodjournal641205 ◽

1984 ◽

Vol 64 (1) ◽

pp. 205-209 ◽

Cited By ~ 1

Author(s):

FH Kohanna ◽

MH Smith ◽

EW Salzman

Keyword(s):

Platelet Rich Plasma ◽

Venous Blood ◽

Adenosine Diphosphate ◽

Normal Subjects ◽

Thromboembolic Disease ◽

Circulating Platelet Aggregates ◽

Platelet Aggregates ◽

Lower Ratio

Reports of circulating platelet aggregates (ie, microemboli) in thromboembolism and other vascular disorders are based on a method (Wu and Hoak , 1974) in which venous blood is collected via scalp vein needle and tubing into either formaldehyde, which fixes aggregates, or EDTA, which disperses them. The ratio of platelet counts in platelet- rich plasma (PRP) from the two blood samples after centrifugation is interpreted as a measure of platelet aggregates in the circulation in vivo. We compared this standard Wu and Hoak technique with a modified one, in which blood was drawn directly into a syringe, and with a third method that avoided centrifugation by counting single platelets in whole blood. Both modified techniques could detect aggregates generated in vitro with adenosine diphosphate (ADP). In 12 normal subjects, the three methods were equivalent, but in 37 patients with thromboembolic disorders, the standard Wu and Hoak method gave a lower ratio than the other methods. Similar results were found in a subset of eight patients with myocardial infarction. Heparin treatment of patients did not influence the results. The data suggest that formation of platelet aggregates occurred during venipuncture. Platelets may be hyperactive in patients with thromboembolic disease and may form aggregates in vitro during collection, but the concept of chronic microembolism in such patients should be reassessed.

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Do patients with thromboembolic disease have circulating platelet aggregates?

Blood ◽

10.1182/blood.v64.1.205.205 ◽

1984 ◽

Vol 64 (1) ◽

pp. 205-209 ◽

Cited By ~ 15

Author(s):

FH Kohanna ◽

MH Smith ◽

EW Salzman

Keyword(s):

Platelet Rich Plasma ◽

Venous Blood ◽

Adenosine Diphosphate ◽

Normal Subjects ◽

Thromboembolic Disease ◽

Circulating Platelet Aggregates ◽

Platelet Aggregates ◽

Lower Ratio

Abstract Reports of circulating platelet aggregates (ie, microemboli) in thromboembolism and other vascular disorders are based on a method (Wu and Hoak , 1974) in which venous blood is collected via scalp vein needle and tubing into either formaldehyde, which fixes aggregates, or EDTA, which disperses them. The ratio of platelet counts in platelet- rich plasma (PRP) from the two blood samples after centrifugation is interpreted as a measure of platelet aggregates in the circulation in vivo. We compared this standard Wu and Hoak technique with a modified one, in which blood was drawn directly into a syringe, and with a third method that avoided centrifugation by counting single platelets in whole blood. Both modified techniques could detect aggregates generated in vitro with adenosine diphosphate (ADP). In 12 normal subjects, the three methods were equivalent, but in 37 patients with thromboembolic disorders, the standard Wu and Hoak method gave a lower ratio than the other methods. Similar results were found in a subset of eight patients with myocardial infarction. Heparin treatment of patients did not influence the results. The data suggest that formation of platelet aggregates occurred during venipuncture. Platelets may be hyperactive in patients with thromboembolic disease and may form aggregates in vitro during collection, but the concept of chronic microembolism in such patients should be reassessed.

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Experimental Study of a platelet Antiaggregating Agent - Application to Ticlopidine

10.1055/s-0039-1680818 ◽

1977 ◽

Author(s):

J.F. Stoltz ◽

M. Verry ◽

B. Farge

Keyword(s):

Arterial Disease ◽

Biochemical Properties ◽

Control Group ◽

Group Index ◽

Aggregation Index ◽

Circulating Platelet Aggregates ◽

Platelet Aggregates ◽

Definition Of ◽

Induced Aggregation

The authors consider the various methods suitable for in vivo study of the anti-aggregating properties of a new drug - Ticlopidine :- study of photometric ADP-induced aggregation and screen filtration pressure in vivo in the rabbit treated per os for 5 days with doses of 25 and 50 mg/kg/d. This gave average inhibitions of 30% and 45% respectively.- study of circulating platelet aggregates using the method of Wu and Hoak after continuous infusion of ADP or of thrombin. The principle of the method involves definition of an aggregation index : the ratio between the platelet counts in the two specimens (EDTA + formol 1 % + EDTA alone).The average results showed : control group index 0.9 -after infusion of ADP 0.57- after infusion of ADP under the influence of Ticlopidine (50 and 100 mg/kg/d) 0.66 to 0.78.- the mechanism of action of the drug was studied using crossed aggregation experiments and by the study of interference with ionised or ionisable groups of the platelet membrane (isotope method, electrophoresis in liquid phase).In parallel with these experiments, studies in vivo in the rabbit and in patients (obliterative arterial disease, Raynaud’s syndrome) are in progress : interference with membrane groups, rheological properties (viscosity, rouleau formation, erythrocyte deformability) and biochemical properties (erythrocyte glycolysis enzymes).

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In Vivo Platelet Activation Following Myocardial Infarction and Acute Coronary Ischaemia

Thrombosis and Haemostasis ◽

10.1055/s-0038-1657241 ◽

1982 ◽

Vol 48 (02) ◽

pp. 133-135 ◽

Cited By ~ 30

Author(s):

A Hughes ◽

S Daunt ◽

G Vass ◽

J Wickes

Keyword(s):

Myocardial Infarction ◽

Chest Pain ◽

Acute Chest Pain ◽

Normal Subjects ◽

Specific Protein ◽

Control Group ◽

Platelet Activity ◽

Circulating Platelet Aggregates ◽

Platelet Aggregates

SummaryForty-seven patients presenting with acute chest pain had in vivo platelet activity assessed by measuring plasma levels of the platelet-specific protein beta thromboglobulin (BTG), and by screening for the presence of circulating platelet aggregates. Nineteen patients with transmural myocardial infarction (MI), 21 patients with acute coronary ischaemia (CI), and 7 patients with non-cardiac chest pain (NCCP) were investigated in a serial study and compared with a normal control group. The means of all BTG determinations in the MI (34, ± SD = 21-57) and CI (33, ± SD = 19-57) groups were significantly higher than those in the NCCP group (24, ± SD = 17-34; p Ã0.01) and normal subjects (22,5, ± SD = 14-37; p Ã0.001). There was no difference in BTG between those with MI or CI, nor between the NCCP group and normal subjects. Raised numbers of circulating platelet aggregates could not be detected in either MI or CI. The mean BTG levels in both MI and CI patients were significantly raised, compared to normal subjects, on the first day of admission to hospital and remained so on each of the subsequent nine days. Neither heparin plus warfarin nor sulphinpyrazone had any significant effect in lowering BTG levels. 15/40 patients (37.5%) following MI and CI had repeatedly raised BTG levels throughout the study period, and it is suggested that these patients represent an “at risk” group that may benefit from anti-platelet therapy in secondary prevention studies.

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The Induction of Platelet Aggregates in Healthy Subjects by Venousocclusion

10.1055/s-0039-1682681 ◽

1977 ◽

Author(s):

D.A. F. Chamone ◽

J. Vermylen

Keyword(s):

Healthy Subjects ◽

Light Transmission ◽

Diastolic Pressure ◽

Platelet Rich Plasma ◽

In Vivo Evaluation ◽

Modified Method ◽

Circulating Platelet Aggregates ◽

Platelet Aggregates ◽

Set Up

Circulating platelet aggregates have been observed in various clinical conditions (Wu and Hoak, Lancet, 1974, ii, 924). Using a slightly modified method, we have found that platelet aggregates can be induced in vivo in healthy subjects.Nine volunteers (7 males, 2 females, age 23-38 years) were studied. Blood was drawn from an antecubital vein of one arm immediately before and of the other arm after twenty minutes of occlusion midway between systolic and diastolic pressure. The ratio of the platelet count in platelet-rich plasma (PRP) obtained from blood collected on forma lin-EDTA to that from blood collected on EDTA only was 0.934 + 0.028 (mean ± S.E .) before and 0.768 ± 0.033 after occlusion (p < 0.001 ). Spontaneous aggregation in PRP, measured as percent increase in light transmission during 10 minutes of stirring in the a gg re gome ter, was 4 .20 ± 1.17 before and 3 .80 + I .69 after occlusion (p > 0 .1).This system may help elucidate some of the mechanisms involved in the generation of circulating platelet aggregates. It may also constitute a simple set-up for the in vivo evaluation of drugs affecting platelet function.

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Prevention of in vivo Platelet Aggregation by Indobufen in Angina Patients during Exercise

Journal of International Medical Research ◽

10.1177/030006058100900205 ◽

1981 ◽

Vol 9 (2) ◽

pp. 113-119 ◽

Cited By ~ 1

Author(s):

E M Pogliani ◽

R Fantasia ◽

C Perini ◽

G Corvi

Keyword(s):

Platelet Aggregation ◽

Bicycle Ergometer ◽

Crossover Design ◽

Double Blind ◽

Before And After ◽

Circulating Platelet Aggregates ◽

Platelet Aggregates ◽

Induced Aggregation ◽

Platelet Functions

Platelet aggregation induced by 3 concentrations of ADP and collagen was assessed in thirty patients with stable angina, before and after exercise with a bicycle ergometer. The patients received a single oral 200 mg dose of indobufen and placebo according to a crossover design in double-blind conditions. Platelet sensitivity to both aggregating agents increased when exercise was carried out after placebo, whereas indobufen markedly inhibited ADP- and collagen-induced aggregation. Circulating platelet aggregates increased in some patients during exercise after placebo but not after indobufen. These results suggest that effort may be an important factor in activation of platelet functions and that the use of drugs blocking the arachidonate pathway and the release reaction may be appropriate in patients with angina.

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Platelet Activation in Psoriasis

Thrombosis and Haemostasis ◽

10.1055/s-0038-1661271 ◽

1985 ◽

Vol 53 (02) ◽

pp. 195-197 ◽

Cited By ~ 30

Author(s):

Mauro Berrettini ◽

Pasquale Parise ◽

Vincenzo Costantini ◽

Serena Grasselli ◽

Giuseppe G Nenci

Keyword(s):

Platelet Activation ◽

Vascular Diseases ◽

Study Groups ◽

Epidemiological Studies ◽

Regeneration Time ◽

Control Subjects ◽

Thrombotic Complications ◽

Circulating Platelet Aggregates ◽

Platelet Aggregates

SummaryRecent epidemiological studies have suggested that psoriasis represents a risk factor for thrombotic vascular diseases. In order to evaluate the possible role of hemostatic changes in the development of thrombotic episodes in psoriasis, some parameters of the hemostatic “balance” were investigated in 22 male psoriatic patients and compared to those of 22 male control subjects. Incidence of known risk factors for vascular diseases (diabetes, hypertension, smoking, dyslipidemia) was comparable in the two study groups. There were no statistically significant differences in platelet count, circulating platelet aggregates, platelet production of malondialdehyde (MDA), total plasma anti thrombin and fibrinolytic activities. In patients with psoriasis the incidence of spontaneous platelet hyperaggregability and plasma levels of β-thromboglobulin were significantly higher than in control subjects. Platelet regeneration time, measured as MDA recovery after aspirin ingestion, was significantly shorter in psoriatic patients. These data suggest that an in vivo platelet activation occurs in patients with psoriasis and could contribute to the development of thrombotic complications. The release of mitogenic and inflammatory substances by activated platelets may play a role in the histogenesis of psoriatic lesions.

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Circulating Platelet Aggregates Indicative of in Vivo Platelet Activation in Pulmonary Hypertension

Angiology ◽

10.1177/000331979304400905 ◽

1993 ◽

Vol 44 (9) ◽

pp. 701-706 ◽

Cited By ~ 25

Author(s):

Antonio Augusto Lopes ◽

Nair Yukie Maeda ◽

Ana Almeida ◽

Rui Jaeger ◽

Munir Ebaid ◽

...

Keyword(s):

Pulmonary Hypertension ◽

Platelet Activation ◽

Circulating Platelet Aggregates ◽

Platelet Aggregates

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Thrombocytosis And Platelet Activation In Alcoholics During Alcohol Withdrawal

10.1055/s-0038-1652724 ◽

1981 ◽

Author(s):

R A Hutton ◽

R Fink ◽

D T Wilson ◽

D H Marjot

Keyword(s):

Alcohol Withdrawal ◽

Statistical Significance ◽

Normal Subjects ◽

Treated Group ◽

Thrombotic Risk ◽

Normal Limits ◽

Alcohol Detoxification ◽

Thrombotic Complications ◽

Circulating Platelet Aggregates ◽

Platelet Aggregates

In order to further investigate the basis of the increased thrombotic risk reported in association with acute alcohol withdrawal, we have carried out platelet studies in a group of alcoholics admitted to a formal alcohol detoxification programme.All patients were alcoholaemic on admission but had taken no other platelet inhibiting medications for at least two weeks. Platelet counts, platelet aggregabi1ity, plasma betathromboglobulin (BTG) assays,platelet nucleotide levels and circulating platelet aggregates were measured sequentially over a 4-6 week period.On admission, platelet aggregabi1ity was impaired, compared to normal controls, particularly using ADP or adrenaline as agonists, but all other platelet studies were within normal limits.Compared to normal subjects, the treated group showed a statistically significant mean increase in platelet count, the level of circulating platelet aggregates, the plasma BTG level and in the aggregation response to ADP and adrenaline. There was also a small increase in the aggregation observed with collagen and Ristocetin and in the platelet nucleotide levels but these did not reach conventional statistical significance.The changes were not associated with any clinically overt thrombotic complications during the period of study,but may contribute to the increased incidence of thrombosis reported by others.

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