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Mild hyperhomocysteinemia and hemostatic factors in patients with arterial vascular diseases
G Freyburger1, S Labrouche, G Sassoust
1Laboratoire d'Hématologie, Hôpital Pellegrin, Bordeaux, France.
Insights
Mild hyperhomocysteinemia is linked to premature arterial disease. Elevated homocysteine levels, particularly after methionine loading, correlate with more pronounced alterations in blood clotting and fibrinolytic parameters.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Metabolic Disorders
Background:
- Mild hyperhomocysteinemia, from genetic or environmental factors, is a known risk factor for premature arterial disease.
- Arterial diseases include peripheral arterial occlusion, thrombotic stroke, and myocardial infarction.
- Hyperhomocysteinemia can be identified by elevated fasting homocysteine or increased levels after methionine loading.
Purpose of the Study:
- To investigate hemostatic parameters in patients with premature arterial disease.
- To determine if hyperhomocysteinemia influences specific hemostatic alterations in these patients.
Main Methods:
- Studied 88 patients with premature arterial disease (mean age 43 ± 11 years).
- Assessed hemostatic parameters, comparing them between hyperhomocysteinemic and non-hyperhomocysteinemic patients.
- Analyzed alterations based on fasting homocysteine and post-methionine load homocysteine levels.
Main Results:
- Confirmed known hemostatic alterations in vascular patients compared to controls.
- Patients with elevated fasting homocysteine showed greater alterations in factors VIIIc, von Willebrand, and thrombin-antithrombin complexes.
- Patients with elevated post-methionine load homocysteine exhibited more pronounced changes in fibrinolytic parameters.
Conclusions:
- Hyperhomocysteinemia is associated with distinct hemostatic and fibrinolytic alterations in patients with premature arterial disease.
- The pattern of hemostatic changes differs depending on whether fasting or post-methionine load homocysteine levels are elevated.
- These findings highlight the importance of homocysteine levels in understanding the pathophysiology of arterial disease.
Abstract:
Mild hyperhomocysteinemia, due to genetic or to environmental factors, is now recognized as a risk factor for premature arterial disease, including peripheral arterial occlusion, thrombotic stroke and myocardial infarction. It is defined by either an increased level of fasting homocysteine or by an increased level after loading with methionine, which is more frequently altered than the former. We studied the hemostatic parameters in 88 patients with premature arterial disease (mean age 43 +/- 11 years). We confirmed previously known hemostatic alterations described in vascular patients when compared to controls, but found that, among patients, some of these parameters were more altered in hyperhomocysteinemic patients. When fasting homocysteine was increased, higher alterations were found in factors VIIIc, von Willebrand and thombin-antithrombin complexes were more elevated. When post-methionine load homocysteine was increased, alterations in fibrinolytic parameters were more pronounced.