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Rationale. In contrast to coronary heart disease (CHD), the role of plasma lipid abnormalities in ischemic cerebrovascular disease (ICVD) is still controversial, presumably because ICVD is etiopathogenetically more heterogeneous than CHD indeed, only ischemic events related to atherothrombotic occlusion of a large precerebral vessel (large vessel disease, LVD) or to perforating artery occlusion (lacunar stroke or small vessel disease (SVD) represent homogeneous etiopathogenetic ICVD subtypes. Aim and design. To elucidate the role of plasma lipid abnormalities in ICVD, we evaluated the fasting plasma lipid profile in 356 consecutive stroke (or transient ischemic attack, TIA) patients in whom clinical and instrumental findings were congruous with LVD or SVD. Univariate analysis was performed by Student s t or 2 tests. Multivariate analysis was performed by ANOVA test corrected for age, sex, smoking habits, hypertension and diabetes, as defined in NECP Panel II. Results. We studied 119 (33.4%) subjects with an etiopathogenetic diagnosis of LVD and 83 (23.3%) with a diagnosis of SVD. Mean age, sex ratio, smoking habits, diabetes and hypertension prevalence did not differ between the two groups. Moreover, no significant differences in total and HDL cholesterol, LDL cholesterol, tryglicerides, HDL2 and HDL3 subfractions, or apoA1 and apoB were evident. Lp(a) was the unique lipid parameter that significantly differed between the two groups in fact, its levels were significantly higher in LVD patients than in SVD (3.071.20 and 2.551.07, after logarithmic transformation). Conclusions. In our series, Lp(a) is the only lipid parameter that differs between LVD and SVD. It may be hypothesized that high Lp(a) levels may promote arterial thromboembolism on large atheromatous plaques by suppressing local fibrinolysis with a subsequent procoagulant state. Further studies are mandatory to elucidate the etiopathogenic role of Lp(a) in ICVD.