‘Silent’ Cerebral Infarction Is Associated With Hypercoagulability, Endothelial Cell Damage, and High Lp(a) Levels in Elderly Japanese

Abstract

Abstract “Silent” lacunar stroke, often found in the elderly, has been proposed as a predisposing condition for clinically overt stroke. However, the risk factors related to this condition have not been studied thoroughly. We conducted brain magnetic resonance imaging and measured the levels of fibrinogen, molecular markers of coagulation activation [prothrombin fragment 1+2 (F1+2)] and endothelial cell damage [von Willebrand factor (vWF) and thrombomodulin], and lipid profiles including lipoprotein (a) [Lp(a)] in 178 asymptomatic, high-risk, Japanese subjects aged 44 to 93 years. We also studied 32 symptomatic patients with lacunar stroke (symptomatic lacunar group). The prevalence of silent lacunar stroke increased with age up to 85 years but decreased with age in those 85 years old and older. Of the 160 elderly subjects (≥60 years) 84 (53%) had ≥1 lacunar infarcts (silent lacunar group) and the remaining 76 were considered as the nonlacunar group. Fibrinogen and F1+2 levels in the silent lacunar group were significantly higher than those in the nonlacunar group ( P <.01). Mean Lp(a) levels and the prevalence of subjects with an Lp(a) level >30 mg/dL were significantly higher in the symptomatic lacunar group than the nonlacunar group ( P <.05), whereas these levels in the silent lacunar group were intermediate to those of the other two groups. When we further classified the silent lacunar group into three subgroups based on the number of lacunes (few lacunes, 1 or 2; moderate number of lacunes, 3 or 4; and numerous lacunes, ≥5), levels of Lp(a), F1+2, vWF, and thrombomodulin were significantly higher and Lp(a) levels >30 mg/dL more common in the numerous-lacune than in the few-lacune subgroup. We conclude that silent lacunar stroke is often found in asymptomatic, high-risk, elderly Japanese patients and that silent multiple lacunar stroke is associated with hypercoagulability, endothelial cell damage, and high Lp(a) levels.