Revisting the role of lipids in ischemic stroke

Introduction: A Large meta-analysis from 20031 showed no reduced stroke risk when cholesterol was lowered. This may be due to the inability to stratify cholesterol components to stroke subtypes, or because stroke may have been caused by non-atherosclerotic mechanisms. Conversely, results from statin intervention trials demonstrate a consistent reduction in the ischaemic stroke rate. Eleven years later, statins are more widely used for primary and secondary prevention of cerebrovascular events. We hypothesize that certain ischaemic stroke subtypes like atherosclerotic strokes or lacunar infarcts (caused by an occlusion of small-diameter arteries) are related to lipids. Objectives: To examine fasting lipid profiles of patients admitted with acute ischaemic stroke and to analyse if lipid profiles vary between stroke subtypes (Bamford classification). Materials and methods: We retrospectively evaluated all consecutive acute stroke admissions from January to March 2014 (n=190) and classified them according to the Bamford classification. Haemorrhagic and total anterior circulation ischemic (TACI) strokes were excluded due to a large number of cardio-embolic strokes in the later sub-group. For the remaining 73 patients fasting lipids were analysed within 48 hours of admission. Results: Table 1: There was no significant difference between stroke sub-groups, LDL-C values were higher in 20031,2 and HDL was lower when compared to our recent data. TC: total cholesterol, LDL-C low density lipid cholesterol, HDL-C: high density lipid cholesterol; all measurements in mmol/L. Lacunar (LACI), partial anterior circulation (PACI) , posterior circulation strokes (POCI). We were unable to demonstrate statistically significant differences between stroke sub-groups. However, an interesting finding was that our results show that patients presenting in 2014 had lower TC and LDL-C and higher mean HDL levels as compared to the pre-2003 patients included in the metaanalysis. This is likely due to increasing statin use. Discussion: There was a trend that LDL-C and TC, were higher in the ischaemic stroke subgroups LACI and POCI (which are more likely to have lipid-related mechanisms), as compared to PACI, which may be contaminated by cardioembolic aetiology strokes. Limitations of our study are the relatively small sample size and the lack of inclusion of confounding variables ( e.g. TOAST criteria, diabetes, smoking) into the statistical analysis. Conclusion: Lipid pathophysiology may play a characteristic role in certain stroke subtypes (LACI and POCI). Future studies should stratify between stroke subtypes and include important co-variables. References: Bowmen TS, Sesso HD, Ma J, et al. Cholesterol and the Risk of Ischemic Stroke. Stroke. 2003; 34: 2930-2934. 1 Shahar E, Chambless LE, et al. Plasma Lipid Profile and Incident Ischemic Stroke: The Atherosclerosis Risk in Communitites (ARIC) Study. Stroke. 2003; 34: 623-631