Summary
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 Wille- brand and thombin-antithrombin
complexes were more elevated. When post-methionine load homocysteine was increased,
alterations in fibrinolytic parameters were more pronounced.
