Platelet Hyperreactivity: Report of a Case with Catastrophic Arterial Thrombosis in a Child

2012 ◽  
Vol 18 (4) ◽  
pp. 22-26
Author(s):  
Elizabeth F. Plocharczyk ◽  
Sarah H. O'Brien ◽  
Jill L. Crumbacher ◽  
Samir B. Kahwash
Keyword(s):  
Arterial Thrombosis

The present state of aspirin and clopidogrel resistance

2009 ◽  
Vol 29 (03) ◽  
pp. 285-290 ◽  
Author(s):  
K. E. Guyer
Keyword(s):  
Diagnostic Tests ◽  
Arterial Thrombosis ◽  
Cardiovascular Events ◽  
Treatment Success ◽  
Antiplatelet Agents ◽  
Antiplatelet Drug ◽  
Coronary Syndrome ◽  
Testing Method ◽  
Pharmacological Response ◽  
Platelet Physiology

SummaryAntiplatelet therapy has demonstrated significant clinical benefit in the treatment of acute coronary syndrome. However, as with any treatment strategy it has been unable to prevent all cardiovascular events. This is far from surprising when considering the complexity of arterial thrombosis and more specifically platelet physiology. This lack of treatment success has provoked the introduction of various diagnostic tests and testing platforms with the intent of guiding and optimizing clinical treatment. Such tests have resulted in the generation of clinical data that suggest suboptimal response to antiplatelet agents such as aspirin and clopidogrel.In the case of both aspirin and clopidogrel, this suboptimal response has been termed resistance. Drug resistance would imply a lack of pharmacological response that has not been specifically investigated in many of the clinical studies performed to date. Rather, the term resistance has been used to describe various facets of platelet activation and aggregation relative to the testing method. Many of these measured parameters are not addressed in the therapeutic intent of the antiplatelet drug in question.

Severe Arterial Cerebral Thrombosis in a Patient with Protein S Deficiency (Moderately Reduced Total and Markedly Reduced Free Protein S): A Family Study

1989 ◽  
Vol 61 (01) ◽  
pp. 144-147 ◽  
Author(s):  
A Girolami ◽  
P Simioni ◽  
A R Lazzaro ◽  
I Cordiano
Keyword(s):  
Arterial Thrombosis ◽  
Protein C ◽  
Protein S ◽  
Protein S Deficiency ◽  
Protein C Deficiency ◽  
Free Protein ◽  
Her Family ◽  
S Deficiency ◽  
Increased Risk ◽  
Patient Reported

SummaryDeficiency of protein S has been associated with an increased risk of thrombotic disease as already shown for protein C deficiency. Deficiencies of any of these two proteins predispose to venous thrombosis but have been only rarely associated with arterial thrombosis.In this study we describe a case of severe cerebral arterial thrombosis in a 44-year old woman with protein S deficiency. The defect was characterized by moderately reduced levels of total and markedly reduced levels of free protein S. C4b-bp level was normal. Protein C, AT III and routine coagulation tests were within the normal limits.In her family two other members showed the same defect. All the affected members had venous thrombotic manifestations, two of them at a relatively young age. No other risk factors for thrombotic episodes were present in the family members. The patient reported was treated with ASA and dipyridamole and so far there were no relapses.

Effects of Antithrombotic Drugs in a Rat Model of Aspirin-Insensitive Arterial Thrombosis

1993 ◽  
Vol 69 (05) ◽  
pp. 509-514 ◽  
Author(s):  
W A Schumacher ◽  
T E Steinbacher ◽  
C L Heran ◽  
J R Megill ◽  
S K Durham
Keyword(s):  
Arterial Thrombosis ◽  
Light And Electron Microscopy ◽  
Platelet Activating Factor ◽  
Thrombin Inhibitor ◽  
Experimental Conditions ◽  
Once Daily ◽  
Thromboxane Receptor ◽  
Vessel Patency ◽  
Electrolytic Injury ◽  
Thromboxane Receptor Antagonist

SummaryThese studies describe experimental conditions where aspirin is less effective than other antiplatelet and anticoagulant drugs in inhibiting acute arterial thrombosis. External electrolytic injury of the rat carotid artery was used to induce occlusive thrombi in 97% of vehicle-treated rats. Thrombi were revealed by light and electron microscopy to be comprised primarily of platelets enmeshed in a fibrin network. The thrombin inhibitor D-phenylalanyl-L-prolyl-L-arginyl chloromethy ketone (PPACK; 6 mg/kg, i. v.) decreased thrombus weight by 90%. Aspirin alone (1, 10 and 30 mg/kg, i. v.), dipyridamole alone (5 mg/kg i. v.) and aspirin (1 and 10 mg/kg, i. v.) in combination with dipyridamole (5 mg/kg, i. v.) did not inhibit thrombosis. The platelet-activating factor (PAF) antagonist, WEB 2086, (1 mg/kg i. v.) was also ineffective. Other drugs had intermediate activity. Thrombi were decreased 56% by the thromboxane receptor antagonist, BMS 180,291, either alone (5.8 mg/kg i.v.) or in combination with aspirin (10 mg/kg, i.v.). Heparin (900 U/kg, i.v.), warfarin (0.25 mg/kg, p.o. once daily for 3 days) and ticlopidine (200 mg/ kg, p.o. once daily for 3 days) reduced thrombus weight by 63, 73 and 43% respectively. Reductions in thrombus weight were always associated with improvements in either average blood flow or vessel patency.

Arterial Thrombosis and Protein S Deficiency

1989 ◽  
Vol 62 (03) ◽  
pp. 1040-1040 ◽  
Author(s):  
P Sié ◽  
B Boneu ◽  
R Biermé ◽  
M L Wiesel ◽  
L Grunebaum ◽  
...  
Keyword(s):  
Arterial Thrombosis ◽  
Protein S ◽  
Protein S Deficiency ◽  
S Deficiency

The Modification of Experimental Occlusive Arterial Thrombosis in the Rat by Malayan Pit Viper Venom

1968 ◽  
Vol 19 (01/02) ◽  
pp. 242-247 ◽  
Author(s):  
K. E Chan
Keyword(s):  
Arterial Thrombosis ◽  
Thrombus Formation ◽  
Arterial Occlusion ◽  
Control Group ◽  
Antithrombotic Effect ◽  
Daily Dose

SummaryThe effect of Malayan pit viper (Ancistrodon rhodostoma) venom on the fate of experimental arterial thrombosis was studied in rats. A suitable daily dose of venom (500 μg) was used to induce hypofibrinogenaemia in the treated rats for the greater part of each of three consecutive post-operative days.The treated animals showed a statistically significant overall reduction in the incidence of both red thrombus formation and thrombotic arterial occlusion when compared to a control group. This antithrombotic effect of the venom could be observed in the 7-day period following the cessation of the treatment.

Depression of Collateral Blood Flow Following Arterial Thrombosis

1977 ◽  
Vol 38 (04) ◽  
pp. 0850-0862 ◽  
Author(s):  
Robert G. Schaub ◽  
Ronald Sande ◽  
Kenneth M. Meyers
Keyword(s):  
Blood Flow ◽  
Arterial Thrombosis ◽  
Hind Limb ◽  
Therapeutic Interventions ◽  
Collateral Blood Flow ◽  
Serotonin Antagonist ◽  
Limb Perfusion ◽  
Clinical Consequences ◽  
Collateral Vessels ◽  
Iliac Bifurcation

SummaryPermanent ligation of the feline aorta at the iliac bifurcation is followed by rapid opening of pre-existing collateral blood vessels. However, if ligation is combined with formation of a clot, these protective collateral vessels do not function. This study was undertaken to determine if drugs which alter serotonin function can improve collateral blood flow after arterial thrombosis. Permanent ligations were placed at the iliac bifurcation, circumflex iliac and sixth lumbar arteries in all cats. A clot was produced in the aorta of 27 cats by injection of 0.1 ml of thromboplastin. Ligated clot-occluded cats were untreated (10); had blood serotonin depleted using a single dose of reserpine (0.1 mg/kg i. m.) followed by para-chlorophenylanine (p-CPA) (100 mg/kg orally) every 3 days (9) ; or were treated prior to surgery with a serotonin antagonist cinanserin HC1 (4 mg/kg i. v.) (8). Control cats (18) were acutely ligated. 9 of these cats were untreated, 5 were cinanserin HC1-treated, and 4 were reserpine/p-CPA-treated. Extent of collateral development was assessed by aortograms 3 days after occlusion and by neurologic rating. Aortograms of acutely ligated cats indicated a significant collateral blood flow around the segment of ligated aorta, while ligated clot-occluded cats had a severely depressed hind-limb perfusion. Reserpine/p-CPA-treated ligation clot-occluded cats had aortograms similar to acutely ligated cats. The cinanserin HC1-treated ligation clot-occluded cats had aortograms which indicated hind-limb perfusion was not as adequate as the acutely ligated cats. However, the perfusion of these animals was improved over untreated ligation clot-occluded cats. Neurologic rating correlated with aortograms. These results suggest: 1) the clinical consequences of arterial thrombosis cannot be entirely attributed to mechanical occlusion of an artery, but may be due to depression of protective collateral blood flow induced by thrombosis, 2) serotonin is an important factor in this depression of collateral blood flow, and 3) isolation of the factors responsible for collateral inhibition could permit the development of therapeutic interventions.

The Effects of Acute Smoking on Platelet Behaviour, Fibrinolysis and Haemorheology in Habitual Smokers

1984 ◽  
Vol 51 (01) ◽  
pp. 006-008 ◽  
Author(s):  
J J F Belch ◽  
B M McArdle ◽  
P Burns ◽  
G D O Lowe ◽  
C D Forbes
Keyword(s):  
Platelet Aggregation ◽  
Factor Viii ◽  
Plasminogen Activator ◽  
Arterial Thrombosis ◽  
Plasma Viscosity ◽  
Red Cell ◽  
Cell Deformability ◽  
Red Cell Deformability ◽  
Cigarette Smokers ◽  
Smoking Group

SummaryThere is an increased frequency of arterial thrombosis in cigarette smokers. The changes in blood coagulation seen in these subjects have been studied by many workers but results have not always been in agreement. We wished to study the effects of acute .smoking on platelet behaviour, fibrinolysis and haemorheology in ten habitual smokers, and to compare these results with nonsmoking controls. Results show that the smoking group had higher plasma fibrinogen (p <0.04), lower plasminogen (p <0.02) and plasminogen activator (p <0.05), and higher plasma viscosity (p <0.003). The changes seen in cigarette smokers after smoking three cigarettes were an increase in the rate of platelet aggregation to ADP (p <0.02), an increase in α2M, (p <0.02), and factor VIII RAG (p <0.05). Plasma viscosity was decreased (p <0.02) as was red cell deformability (p >0.02).We confirm an increased tendency to hypercoagulability in smokers compared to controls which becomes more pronounced immediately after smoking three cigarettes.

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