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The Influence of the Proteins of the Contact Activation System on Thrombus Formation Under Different Flow-conditions in Blood
This study is currently Recruiting
August 2011 By Maastricht University Medical Center
First Recieved on April 12, 2010
Last Updated on August 25, 2011
Rationale: Cardiovascular diseases are important causes of morbidity and mortality in the
industrialized world. Clinical studies indicate an important role for the proteins of the
contact activation system (coagulation factor XII (FXII), FXI, prekallikrein and high
molecular weight kininogen (HMWK)) on the risk of cardiovascular disease. There is
substantial evidence from mouse studies that FXII and FXI participate in the formation and
stability of thrombi and in vitro studies showed that collagen is able to activate FXII and
hereby stimulate thrombin formation and potentiate the formation of platelet-fibrin thrombi.
The investigators want to determine the role of the proteins of the contact activation
system in platelet mediated thrombus formation in human blood.
Objective: The investigators will study the effects of the proteins of the contact
activation system on platelet mediated thrombus formation, embolization and degradation on
collagen in a perfusion flow model.
Study design: Blood will be collected from human volunteers via a venipuncture in the
forearm. Each volunteer will donate maximally four times 30 ml of blood over a period of two
days. This blood is used in perfusion flow experiments: blood flows over a coverslip covered
with collagen in a flow chamber. The investigators will vary several conditions such as the
concentration of the proteins and the shear rate. For perfusion flow experiments, the
investigators need fresh whole blood because platelets are viable for four hours. After this
time, new blood is needed.
Study population: For this study the investigators need blood from human volunteers with a
coagulation defect in one of the proteins of the contact activation system, e.g. FXII, FXI,
prekallikrein or HMWK and controls without any coagulation defects.
Main study parameters/endpoints: The investigators main study endpoint is the ex vivo
formation of platelet-mediated thrombi on collagen in a perfusion flow model. The
investigators hypothesize that thrombi formed from blood of patients deficient in FXII or
FXI are less stable than those formed from blood from controls.
||Time Perspective: Cross-Sectional
Resources/Links provided by NLM:
|Study Start Date:
|Estimated Primary Completion Date:
|Factor XII deficiency:|
Patients deficient in coagulation factor XII
|Factor XI Deficiency:|
Patients deficient in coagulation factor XI
Patients deficient in prekallikrein
Patients deficient in high molecular weight kininogen (HMWK)
|Ages Eligible for Study:||18 Years|
|Genders Eligible for Study:||Both|
|Accepts Healthy Volunteers:||Accepts Healthy Volunteers|
- Patient group:
- Age: ? 18 years
- Deficiency in factor XII, factor XI, prekallikrein or high molecular weight
- Control group:
- Age: ? 18 years
- (Other) Coagulation defects
- Symptoms of active disease
- The use of antiplatelet drugs
- The use of aspirin/ascal
- Investigator: Hugo Ten Cate, MD, PhD - Principal Investigator - Maastricht University Medical Centre