Alterations in LDL and HDL after an ischemic stroke associated with carotid atherosclerosis are reversed after 1 year

Approximately, 20% of ischemic strokes are attributed to the presence of atherosclerosis. Lipoproteins play a crucial role in the development of atherosclerosis, with LDL promoting atherogenesis and HDL inhibiting it. Therefore, both their concentrations and their biological properties are decisive factors in atherosclerotic processes. In this study, we examined the qualitative properties of lipoproteins in ischemic stroke patients with carotid atherosclerosis. Lipoproteins were isolated from the blood of healthy controls (n = 27) and patients with carotid atherosclerosis (n = 64) at 7 days and 1 year postischemic stroke. Compared to controls, patients' LDL 7 days poststroke showed increased levels of apoC-III, triacylglycerol, and ceramide, along with decreased cholesterol and phospholipid content. LDL from patients induced more inflammation in macrophages than did LDL from controls. HDL isolated from patients 7 days after stroke showed alterations in the apolipoprotein cargo, with reduced levels of apoA-I and increased levels of apoA-II, and apoC-III compared to controls. Patients' HDL also showed a higher electronegative charge than that of controls and partially lost its ability to counteract the modification of LDL and the inflammatory effects of modified LDL. One year after stroke onset, the composition of patients' LDL and HDL resembled those of the controls. In parallel, LDL and HDL gained positive charge, LDL became less prone to oxidation and aggregation, and HDL regained protective properties. In conclusion, LDL and HDL in ischemic stroke patients with carotid atherosclerosis exhibited alterations in composition and function, which were partially reversed 1 year after stroke.