Key result
Plasma lipoprotein profiles showed increased total cholesterol, VLDL, and LDL in patients with cortical infarction, whereas patients with lacunar infarction presented a normal profile.
Why the study?
Are specific plasma lipoprotein profiles associated with different subtypes of ischemic stroke (cortical vs lacunar) and TIA?
Case-Control (n=103)
Are specific plasma lipoprotein profiles associated with different subtypes of ischemic stroke (cortical vs lacunar) and TIA?
Plasma lipoprotein abnormalities are associated with cortical infarction but not lacunar infarction, suggesting that lipid-related risk factors differ based on the mechanism of ischemic stroke.
Lipid abnormalities were associated with cortical but not lacunar infarction; leaves open subtype-specific prevention strategies pending prospective validation.
We investigated the relation of plasma lipids to the risk for cortical infarction with (22 cases) or without (38 cases) cardiac arrhythmias, for lacunar infarction (28 cases) and transient ischaemic attacks (TAI) (15 cases). In the group of cortical infarction with or without cardiac arrhythmias, we observed a maximum increase of total cholesterol, of very low density lipoprotein (VLDL) and low density lipoprotein (LDL), triglycerides, total Apolipoprotein (Apo) B, LDL-Apo B and Apo-A1. On the contrary, we observed a decrease of total ApoE, HDL-ApoE, a distribution of LDL in a single layer and the presence of LDL of small weight. TAI is different from the former group by a low level of HDL and the lack of abnormalities of Apo-A1, and on the distribution and the weight of LDL. Finally, lacunar infarction presents a normal plasma lipoprotein profile. These data suggest that previously demonstrated differences in LDL-cholesterol levels between patients with ischaemic stroke and control subjects may apply to patients with cortical but not lacunar infarction. The presence or not of a cardiac arrhythmia doesn't give a special lipoprotein profile, and TAI has no changes on the distribution and the weight of LDL. Therefore, separation of ischaemic strokes into types based on mechanism as large vessel atherosclerosis versus small vessel atherosclerosis may help clarify lipid-related risk factors in cerebrovascular disease.
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Giroud et al. (1992) conducted a case-control in Ischaemic stroke and transient ischaemic attacks (n=103). Plasma lipoproteins vs. Control subjects was evaluated on Plasma lipid and lipoprotein profiles. Plasma lipoprotein profiles showed increased total cholesterol, VLDL, and LDL in patients with cortical infarction, whereas patients with lacunar infarction presented a normal profile.
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