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Coagulation abnormalities and cardiovascular disease
1Department of Medicine, Oregon Health Sciences University, Portland 97201-3098, USA. delought@ohsu.edu
Insights
Genetic defects causing excessive venous thrombosis are common. However, links between common genetic variations in key clotting factors and heart disease risk remain unclear, despite their role in thrombosis.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Genetics
Background:
- Excessive venous thrombosis is linked to genetic defects in 60-80% of patients.
- Increased plasma levels of fibrinogen and PAI-1 correlate with myocardial infarction risk.
- Common polymorphisms in coagulation factors (Factor VIII, PAI-1, fibrinogen) have an ambiguous association with ischemic cardiac disease.
Purpose of the Study:
- To clarify the association between common genetic polymorphisms of coagulation proteins and ischemic heart disease.
- To investigate the role of venous hypercoagulable states in coronary ischemic syndrome.
- To explore pathogenic polymorphisms in platelet receptors and lipoprotein mediation in coagulation.
Main Methods:
- Review of existing literature on genetic defects and thrombosis.
- Analysis of studies investigating polymorphisms in Factor VIII, PAI-1, and fibrinogen.
- Examination of research on platelet receptors and lipoproteins in coagulation processes.
Main Results:
- While genetic defects are prevalent in thrombosis, their link to ischemic heart disease is not definitively established.
- Two common venous hypercoagulable states lack convincing evidence implicating them in ischemic heart disease.
- Lipoproteins are identified as potential mediators in coagulation processes.
Conclusions:
- The relationship between common coagulation protein polymorphisms and ischemic heart disease requires further investigation.
- Current evidence does not strongly support the role of common venous hypercoagulable states in ischemic heart disease.
- Further research into platelet receptor polymorphisms and lipoprotein involvement is warranted.
Abstract:
In patients with excessive venous thrombosis, genetic defects predisposing to thrombosis can be found in 60-80%. Increased plasma levels of coagulation proteins such as fibrinogen and plasminogen activator inhibitor-1 (PAI-1) are associated with an increased risk of myocardial infarction. However, despite the presence of polymorphisms that regulate plasma levels of factor VIII, PAI-1, and fibrinogen the association between common polymorphisms of these coagulation protein and ischemic cardiac disease remains ambiguous. Up to 10% of the population have defects that predispose them to excessive venous thrombosis. In spite of the essential role of thrombosis in coronary ischemic syndrome, no convincing evidence has implicated the two most common venous hypercoagulable states in ischemic heart disease. Pathogenic polymorphisms in the platelet fibrinogen and collagen receptors remains an area of intense research interest. Finally, it has been shown that lipoproteins can act as mediators of coagulation processes.