Increased Plasma Fibrinogen and Platelet-Aggregates in Type II Hyperlipoproteinaemia

1979 ◽  
Author(s):  
J.L.H.C. Third ◽  
G.D.O. Lowe ◽  
M.M. Drummond ◽  
W.F. Bremner ◽  
T.D.V. Lawrie ◽  
...  
Keyword(s):  
Plasma Lipids ◽  
Young Patients ◽  
Adult Life ◽  
Arterial Disease ◽  
Arterial Injury ◽  
Plasma Fibrinogen ◽  
Type Ii ◽  
Platelet Aggregate ◽  
Circulating Platelet Aggregates ◽  
Platelet Aggregates

Plasma-fibrinogen and circulating platelet-aggregates (method of Wu and Hoak1) were measured in 21 patients with Type II hyperlipoproteinaeima and 21 matched control subjects. Patients with hyperlipoproteinaemia had increased levels of fibrinogen (3.5 g/l ± SEM 0.2 vs. 2.5 g/l±0.1, p(0.01) and platelet-aggregates (platelet aggregate ratio 0.71 vs. 0.65, p(0.01). Young patients with hyperlipoproteinaemia had prematurely high fibrinogen levels, and the normal fibrinogen rise durina adult life was abolished. There were no significant correlations between fibrinogen, platelet-aggregates, and plasma lipids (cholesterol, cholesterol fractions, or triglyceride). High librinogen and platelet-aggregate levels may play a part in the development of the premature arterial disease associated with Type II hyperlipoproteinaemia, or may be markers of arterial injury. 1Wu, K.K., Hoak, J.C.Lancet, 1974, ii, 924.

Increased Plasma Fibrinogen and Platelet-Aggregates in Type II Hyperlipoproteinaemia

1979 ◽  
Vol 42 (05) ◽  
pp. 1503-1507 ◽  
Author(s):  
G D O Lowe ◽  
Maureen M Drummond ◽  
Jane L H C Third ◽  
W F Bremner ◽  
C D Forbes ◽  
...  
Keyword(s):  
Plasma Lipids ◽  
Young Patients ◽  
Adult Life ◽  
Arterial Disease ◽  
Arterial Injury ◽  
Plasma Fibrinogen ◽  
Type Ii ◽  
Familial Type ◽  
Platelet Aggregate ◽  
Platelet Aggregates

SummaryPlasma fibrinogen and platelet-aggregates (method of Wu and Hoak) were measured in 21 patients with familial Type II hyperlipoproteinaemia and 21 matched control subjects. Patients with hyperlipoproteinaemia had increased levels of fibrinogen and platelet- aggregates (p<0.01). Young patients with hyperlipoproteinaemia had prematurely high fibrinogen levels, and the normal rise in fibrinogen during adult life was abolished. There were no statistically significant correlations within the patient group between fibrinogen, platelet-aggregates, and plasma lipids. High fibrinogen and platelet-aggregate levels may play a part in the development of the premature arterial disease associated with Type II hyperlipoproteinaemia, or may be markers of arterial injury.

Increased Plasma Fibrinogen and Circulating Platelet-Aggregates in Type II Hyperlipoproteinaemia

1979 ◽  
Vol 56 (3) ◽  
pp. 21P-21P ◽  
Author(s):  
G. D. O. Lowe ◽  
M. M. Reavey ◽  
J. L. H. C. Third ◽  
W. F. Bremner ◽  
C. D. Forbes ◽  
...  
Keyword(s):  
Plasma Fibrinogen ◽  
Type Ii ◽  
Circulating Platelet Aggregates ◽  
Platelet Aggregates

scholarly journals The landscape of circulating platelet aggregates in COVID-19

2021 ◽  
Author(s):  
Yuqi Zhou ◽  
Masako Nishikawa ◽  
Hiroshi Kanno ◽  
Tinghui Xiao ◽  
Takuma Suzuki ◽  
...  
Keyword(s):  
Large Scale ◽  
Multiorgan Failure ◽  
Young Patients ◽  
Clinical Feature ◽  
Platelet Activity ◽  
Multiple Organs ◽  
Characteristic Clinical Feature ◽  
Circulating Platelet Aggregates ◽  
Platelet Aggregates ◽  
D Dimer

A characteristic clinical feature of COVID-19 is the frequent occurrence of thrombotic events. Furthermore, many cases of multiorgan failure are thrombotic in nature. Since the outbreak of COVID-19, D-dimer testing has been used extensively to evaluate COVID-19-associated thrombosis, but does not provide a complete view of the disease because it probes blood coagulation, but not platelet activity. Due to this limitation, D-dimer testing fails to account for thrombotic events which occur despite low D-dimer levels, such as sudden stroke in young patients and autopsy-identified widespread microthrombi in multiple organs. Here we report the landscape of circulating platelet aggregates in COVID-19 obtained by large-scale single-cell image-based profiling and temporal monitoring of the blood of COVID-19 patients (n = 110). Surprisingly, our analysis shows the anomalous presence of excessive platelet aggregates in nearly 90% of all COVID-19 patients, including those who were not clinically diagnosed with thrombosis and those with low D-dimer levels (less than 1 ug/mL). Additionally, results indicate a strong link between the concentration of platelet aggregates and the severity and mortality of COVID-19. Finally, high-dimensional analysis and comparison with other diseases reveal that COVID-19 behaves as a product of thrombosis (localized) and infectious diseases (systemic), as a cause of systemic thrombosis.

PLATELET AGGREGATE-ASSOCIATED FIBRIN FORMATION AS A FUNCTION OF AGGREGATE SIZE AND HEPARIN CONCENTRATION

1987 ◽  
Author(s):  
L J Wurzinger ◽  
K Herbst ◽  
H Schmid-Schonbein
Keyword(s):  
Whole Blood ◽  
Aggregate Size ◽  
Arterial Disease ◽  
Amidolytic Activity ◽  
Protein Assay ◽  
Heparin Concentration ◽  
Platelet Aggregate ◽  
Minimum Number ◽  
Platelet Aggregates

The in vitro observation that fibrin forms withina few minutes in the crevices and niches inside and on the surface of platelet aggregates (PA), preparedfrom heparinized (5 U/ml) blood is consistent with the doubtful efficiency of heparin in the treatment of occlusive arterial disease (Thrcmb. Haemost. 46: 666,1981). Release of heparin- neutralizing proteins into limited and largely disclosed plasma compartments between aggregated platelets was held responsible for this remarkable phenomenon. However, the minimum number of aggregated platelets necessary to overcome the heparin inhibition remained undetermined then.PRP prepared from whole blood ant^coagulated with 0.5, 1 and 5 U/ml of mucosal heparin (Liquemin ), was aggregated with 10 or 100 pM ADP for 2 min at 37°C. Single PAs of various dimensions were withdrawn, washed, and incubated with a chromogenic substrate (S-2238, Kabi AB) to measure their thrombin content. Subsequently the number of platelets contained in the PA was evaluated by assaying the protein content of the aggregates. Microscopic PAs, their mass being toosmall to be determined precisely by a protein assay, were isolated with a filter technique, their extension was documented on photomicrographs for later calculation of aggregate volume and platelet content, before they were incubated with S-2238. Aggregates toosmall to develop detectable amidolytic activity, were checked microscopically for fibrin formed.S 2238 amidolytic activity (thrombin) in heparinizedPRP samples evolved as a linear function of the logarithm of PA mass. For a given heparin concentration (in whole blood) the following lowerthreshold platelet numbers of aggregates were found sufficient to allow the formation of detectable quantities of thrombin:These results suggest a fatal role platelet aggregates of minute dimensions may well play as a nidus of coagulation in fully heparinized blood.

Correlation Between Migraine and Circulating Platelet Aggregates

Cephalalgia ◽  
1985 ◽  
Vol 5 (2_suppl) ◽  
pp. 87-88 ◽  
Author(s):  
Carla Buttinelli ◽  
Maria Pia Lazzaro ◽  
Gian Luigi Lenzi ◽  
Stefano Paolucci ◽  
Massimiliano Prencipe
Keyword(s):  
Normal Range ◽  
Control Subjects ◽  
Platelet Aggregate ◽  
Complicated Migraine ◽  
Circulating Platelet Aggregates ◽  
Platelet Aggregates ◽  
The Mean

We studied platelet aggregates, by Wu and Hoak's technique, in 73 patients (49 F and 24 M), aged 14-61 (mean age 50.4 ± 12.2) with migraine. Platelet aggregates were expressed as Platelet Aggregate Ratio (PAR). We consider as pathological PAR values lower than 86. Mean PAR value of migraine patients (78.3 ± 8.68 SD) was significantly lower ( p < 0.001) than that of 90 control subjects (95.4 ± 6.15 SD). Normal PAR values were found only in 27.4% of the migraine patients. The patients were divided according to the interval from the last attack: 17 patients were studied in the 1st week (PAR = 73.76 ± 7.6 SD; 5.8% of the values in the normal range), 15 in the 2nd week (76.6 ± 7.02 SD; 13.3% of the values in the normal range) and 41 between 15th and 30th day (80.78 ± 8.78 SD; 29.6% of the patients in the normal range). The mean PAR value of the patients studied during the first week was significantly lower ( p < 0.01) than that of the patients studied between 15th and 30th day. No significant differences were found between the patients with classical, common and complicated migraine.

scholarly journals Prevention by Suloctidil of Spontaneous Platelet Aggregates in Rats

1977 ◽  
Author(s):  
R. N. Saunders ◽  
T. S. Burns ◽  
M. R. Stelzer
Keyword(s):  
Cerebrovascular Disease ◽  
Platelet Rich Plasma ◽  
Male Rats ◽  
Prevention Activity ◽  
Platelet Aggregate ◽  
Circulating Platelet Aggregates ◽  
Platelet Aggregates ◽  
5 Ht Uptake ◽  
Rat Platelets

Atherosclerosis and cerebrovascular disease have been reported by Wexler and True (Circ. Res. 12: 659,1963) to-occur in retired breeder rats but not in virgin rats of the same age. We have discovered that retired breeder (RB) male rats have spontaneous circulating platelet aggregates (CPA) as determined by the method of Wu and Hoak (Lancet 2: 924, 1974). These CPA respond to therapy with clinically proven antiplatelet drugs. Suloctidil (S) [l-(4-isopropyl-thiophenyl)-2-n-octylamino propanol, Continential Pharma, Brussels] administered for 8 days at 100 mg/kg i. g. showed a significant reduction in CPA from 0.76+0.05 (S.E.M.) to 0.92 + 0.03 (where 1.0 indicates no CPA). In these same rats, the endogenous platelet 5-HT level was significantly (P<0.01) lowered to 0.88+0.04 (S. E.M.) μg/10 9 platelets compared to control values of 1.66+0.08 μg/10 9platelets. Plasma 5-HT levels were not altered. In vitro rat platelet 5-HT uptake is inhibited 50% by S at 6.4 χ 10 -6M in platelet-rich plasma. In rat platelets with labeled 5-HT pools, 5 min incubation with S at 10 -5M resulted in significantly (P<0.01) greater release at 10, 20 and 30 sec after the addition of 2U/ml of thrombin. This suggests that S may decrease uptake as well as increase release of platelet 5-HT. The reduction of endogenous platelet 5-HT levels by S may be related to its observed platelet aggregate prevention activity.

scholarly journals Experimental Study of a platelet Antiaggregating Agent - Application to Ticlopidine

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).

Circulating Platelet Aggregates in Normal Pregnancy and Rpeeclampsia

1979 ◽  
Author(s):  
I. Rákóczi ◽  
F. Tallián ◽  
I. Cseh ◽  
I. Gáti
Keyword(s):  
Pregnant Women ◽  
Platelet Activation ◽  
Normal Pregnancy ◽  
Third Trimester ◽  
The Third ◽  
Platelet Aggregate ◽  
Circulating Platelet Aggregates ◽  
Platelet Aggregates ◽  
The Mean

Circulating platelet aggregates have been observed in various thromboembolic states. It is known that severe preeclamsia is associated with features of intravascular coagulation. To evaluate the role of platelets in this disorder we have determined circulating platelet aggregates in 10 patients with severe preeclampsia, in 30 patients in the third trimester of uncomplicated pregnancies and in 35 healthy nonpregnant volunteers. Platelet aggregate ratio /P.A.R./ was measured by a modification of a method described by Wu and Hoak, The mean P.A.R. of severe preeclamptic patients /0.732 ± 0,063 SEM/ was significantly lower than that of the uncomplicated pregnant women /0,860 ± 0,052 SEM/ and of the nonpregnant volunteers /0.880 ± 0,061 SEM/.The results indicate that severe preeclamptic patients have increased levels of circulating platelet aggregates and platelet activation is a feature of preeclampsia.

scholarly journals The landscape of circulating platelet aggregates in COVID-19

2021 ◽  
Author(s):  
Keisuke Goda ◽  
Yuqi Zhou ◽  
Masako Nishikawa ◽  
Hiroshi Kanno ◽  
Ting-Hui Xiao ◽  
...  
Keyword(s):  
Large Scale ◽  
Multiorgan Failure ◽  
Young Patients ◽  
Clinical Feature ◽  
Platelet Activity ◽  
Multiple Organs ◽  
Characteristic Clinical Feature ◽  
Circulating Platelet Aggregates ◽  
Platelet Aggregates ◽  
D Dimer

Abstract A characteristic clinical feature of COVID-19 is the frequent occurrence of thrombotic events. Furthermore, many cases of multiorgan failure are thrombotic in nature. Since the outbreak of COVID-19, D-dimer testing has been used extensively to evaluate COVID-19-associated thrombosis, but does not provide a complete view of the disease because it probes blood coagulation, but not platelet activity. Due to this limitation, D-dimer testing fails to account for thrombotic events which occur despite low D-dimer levels, such as sudden stroke in young patients and autopsy-identified widespread microthrombi in multiple organs. Here we report the landscape of circulating platelet aggregates in COVID-19 obtained by large-scale single-cell image-based profiling and temporal monitoring of the blood of COVID-19 patients (n = 110). Surprisingly, our analysis shows the anomalous presence of excessive platelet aggregates in nearly 90% of all COVID-19 patients, including those who were not clinically diagnosed with thrombosis and those with low D-dimer levels (≤1 µg/mL). Additionally, results indicate a strong link between the concentration of platelet aggregates and the severity and mortality of COVID-19. Finally, high-dimensional analysis and comparison with other diseases reveal that COVID-19 behaves as a product of thrombosis (localized) and infectious diseases (systemic), as a cause of systemic thrombosis.

A Modification of the Wu and Hoak Method for the Determination of Platelet Aggregates and Platelet Adhesion

1985 ◽  
Vol 53 (03) ◽  
pp. 381-385 ◽  
Author(s):  
Sudhir K Bowry ◽  
Colin R M Prentice ◽  
J M Courtney
Keyword(s):  
Platelet Adhesion ◽  
Platelet Rich Plasma ◽  
Blood Collection ◽  
Buffer System ◽  
Modified Method ◽  
Healthy Donors ◽  
Platelet Aggregate ◽  
Circulating Platelet Aggregates ◽  
Platelet Aggregates

SummaryThe Wu and Hoak method for determining circulating platelet aggregates has poor reproducibility; problems have been reported with the composition of the buffer systems, haemolysis, the effects of blood collection technique and a divergence of the platelet aggregate ratio in blood for healthy donors from the theoretical value of 1. Our investigations suggest that the original technique is highly operator-dependent, especially the collection of blood and the method of counting platelets after centrifugation. We describe an improved modification of the Wu and Hoak technique; a new buffer system has been developed and the proportion of blood in the buffered EDTA and buffered EDTA- formalin solutions has been altered to obtain platelet rich plasma. The platelet aggregate ratio (PAR) by this modified method for healthy donors in two different studies was 0.97 ± 0.02 and 0.98 ± 0.01 respectively. Finally, the principle of Wu and Hoak was used to measure accurately platelet adhesion, without the role of platelet-platelet interactions (aggregation). Platelet adhesion and aggregation were then used to evaluate the thrombogenicity of various artificial surfaces, including silicone rubber and polytetra- fluoroethylene (PTFE) vascular grafts.

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