[Coagulation and fibrinolytic activation in lacunar infarct patients].

Lacunar infarcts are related to occlusion of penetrating arteries. Lipohyalinosis affects the smaller arteries 40-200 microns in diameter, and atherosclerosis involves larger arteries 200-850 microns in diameter. We hypothesized that the processes of thrombus formation might be different among these two kinds of lacuner infarcts, including those caused by lipohyalinosis and atherosclerosis. We studied acute coagulation and fibrinolytic activation in lacunar infarct patients which were divided into two groups according to their size: smaller lacunar group and larger lacunar group. Then we divided lacunar infarct patients into two groups in terms of the progression of motor deficits: those who showed the progression and those did not. And coagulation and fibrinolytic activation were compared each other. One hundred and twenty four patients were enrolled in this study, including 34 control subjects, 39 patients with smaller lacune (3 mm-10 mm in diameter), 28 patients with large lacune (10 mm-20 mm), and 23 patients with atherothrombotic infarcts confirmed by angiography. The levels of TAT activity in large lacune and atherothrombotic infarcts were significantly higher than those in control subjects (p = 0.009, p < 0.0001, respectively), whereas those in small lacune were not. Also, the levels of D-dimer activity in large lacune and atherothrombotic infarcts were significantly higher than those in control subjects (p = 0.0003, p < 0.0001, respectively), whereas those in small lacune were not. The progression of motor deficits were more frequently recognized in large lacune than in small lacune: three patients out of 39 small lacune patients and 22 patients out of 28 large lacune patients (difference was significant, p = 0.001). The level of TAT activity in patients who showed progression of motor deficits was significantly higher than that in those who did not (p = 0.0002), whereas the difference of the levels of D-dimer activity in two groups did not reach significant differencial levels. The process of thrombin and fibrin formation in large lacunar infarcts which are related to microatheroma and atheroscrelosis appears to be different from that in small lacunar infarcts. Antiplatelet and anticoagulation therapy should be tailored to large lacunar infarct patients.