Related Experiment Video

Updated: May 30, 2026

Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay
13:08

Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay

Published on: September 9, 2012

Factor VII Activating Protease Polymorphism (G534E) Is Associated with Increased Risk for Stroke and Mortality

Stella Trompet1, Douwe Pons, Sandip M Kanse

  • 1Department of Cardiology, Leiden University Medical Center, C5-P, P.O. Box 9600, 2300 RC Leiden, The Netherlands.

Stroke Research and Treatment
|July 27, 2011
PubMed

Insights

The FSAP-Marburg I polymorphism increases stroke risk and all-cause mortality but may reduce restenosis risk. This genetic variant influences cardiovascular disease outcomes, impacting plaque stability and hemostasis.

Area of Science:

  • Genetics and Cardiovascular Disease
  • Molecular Biology and Vascular Health

Background:

  • The FSAP-Marburg I polymorphism (1704G>A) is linked to reduced FSAP activity and carotid stenosis complications.
  • Understanding genetic influences on cardiovascular disease is crucial for risk stratification and treatment.

Purpose of the Study:

  • To investigate the impact of FSAP-Marburg I and Marburg II polymorphisms on cardiovascular outcomes.
  • To analyze these genetic variants in large, independent elderly and interventional study populations.

Main Methods:

  • Genotyping of Marburg I and II polymorphisms in the HABP2 gene (encoding FSAP).
  • Analysis of data from the PROSPER study (n=5804, elderly at risk) and the GENDER study (n=3104, post-PCI).

Main Results:

  • In PROSPER, Marburg I was associated with increased stroke risk (HR: 1.60) and mortality (HR: 1.33).
  • In GENDER, Marburg I carriers showed a trend towards lower restenosis risk (HR: 0.59).
  • Marburg II polymorphism exhibited similar, but less pronounced, associations.

Conclusions:

  • Marburg I polymorphism may increase stroke risk via effects on smooth muscle cells and matrix metalloproteinases, affecting plaque stability.
  • A potential protective effect against restenosis might stem from reduced zymogen activation, influencing hemostasis and matrix remodeling.

More Related Videos

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation04:37

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation

Published on: May 23, 2025

Tail Vein Transection Bleeding Model in Fully Anesthetized Hemophilia A Mice08:13

Tail Vein Transection Bleeding Model in Fully Anesthetized Hemophilia A Mice

Published on: September 30, 2021

Related Concept Videos

Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu01:29

Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu

Genetic variations significantly influence drug response through pharmacokinetics, receptor interactions, and biologic milieu modifications. Pharmacokinetic alterations impact drug metabolism and clearance, affecting efficacy and toxicity. Variants in drug-metabolizing enzymes, such as CYP2C9 and CYP2C19, alter drug activation and elimination. For example, CYP2C9 loss-of-function variants require lower warfarin doses to prevent excessive bleeding, while CYP2C19 variants reduce clopidogrel...
Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

Anticoagulant Drugs: Low-Molecular-Weight Heparins

Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
Extrinsic and Intrinsic Pathways of Hemostasis01:20

Extrinsic and Intrinsic Pathways of Hemostasis

Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which forms a...
Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
Pharmacogenetics of Drug Metabolism: Overview01:27

Pharmacogenetics of Drug Metabolism: Overview

Genetic polymorphism in drug metabolism is crucial to the inter-individual variability observed in drug responses. Drug metabolism primarily involves the chemical modification of drugs and other xenobiotics to enhance their elimination by increasing their polarity. Two main classes of enzymes mediate this biotransformation process: Phase I enzymes, primarily cytochrome P450s, catalyze oxidation and reduction reactions, while other enzymes, such as esterases, mediate hydrolysis, and Phase II...
Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants01:18

Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants

Oral anticoagulants are vital tools in preventing and treating blood clotting disorders. This diverse class of medications can be categorized as vitamin K antagonists, exemplified by warfarin, and direct thrombin inhibitors (DTIs), such as dabigatran, as well as factor Xa inhibitors, including rivaroxaban.
Warfarin, a prominent vitamin K antagonist family member, exerts its effect by inhibiting the enzyme VKORC1 (vitamin K epoxide reductase complex 1). By hindering this enzyme, warfarin...