Jong-Ho Park1, Bruce Ovbiagele2. 1. Department of Neurology, Myongji Hospital, Hanyang University College of Medicine. 2. Department of Neurology, University of California.
Abstract
AIMS: Low-density lipoprotein (LDL)-lowering statin therapy is an established secondary stroke prevention strategy. However, the differential impact of key non-LDL levels on recurrent stroke risk, while on lipid-modifying therapy (LT), remains unclear. METHODS: We analyzed the dataset of a multicenter trial involving 3640 recent (<4 months) noncardioembolic stroke patients followed for 2 years. Participants were categorized into four groups of presumed improving lipid profile: level 0, no LT prescribed; level I, LT use with low high-density lipoprotein cholesterol (HDL-C) (<40 mg/dL for men; <50 mg/dL for women); level II, LT use with high HDL-C (≥ 40 mg/dL and ≥ 50 mg/dL, respectively); and level III, level II with low triglycerides (<150 mg/dL). Independent associations of LT category with stroke, major vascular events (MVEs; stroke/coronary heart disease/vascular death), and all-cause death were assessed. RESULTS: LTs were mostly statins (>95%). The unadjusted recurrent stroke rate declined with LT category level (9.2% for level 0; 8.4% for level I; 7.5% for level II; and 5.7% for level III). Compared with level 0, the adjusted hazard ratio of stroke for level I was 0.78 (95% confidence interval (CI), 0.59-1.03), level II 0.80 (0.54-1.18), and level III 0.63 (0.43-0.91). Multivariable analyses of MVEs and all-cause death followed a similar pattern of declining risk with higher LT category level. CONCLUSIONS: Compared with the nonuse of LT, there may be a hierarchy of residual vascular risk after stroke by non-LDL type and target, while on LT. Particularly, stroke patients with low HDL-C levels on LT may benefit from additional therapeutic strategies to improve their outcomes.
RCT Entities:
AIMS: Low-density lipoprotein (LDL)-lowering statin therapy is an established secondary stroke prevention strategy. However, the differential impact of key non-LDL levels on recurrent stroke risk, while on lipid-modifying therapy (LT), remains unclear. METHODS: We analyzed the dataset of a multicenter trial involving 3640 recent (<4 months) noncardioembolic strokepatients followed for 2 years. Participants were categorized into four groups of presumed improving lipid profile: level 0, no LT prescribed; level I, LT use with low high-density lipoprotein cholesterol (HDL-C) (<40 mg/dL for men; <50 mg/dL for women); level II, LT use with high HDL-C (≥ 40 mg/dL and ≥ 50 mg/dL, respectively); and level III, level II with low triglycerides (<150 mg/dL). Independent associations of LT category with stroke, major vascular events (MVEs; stroke/coronary heart disease/vascular death), and all-cause death were assessed. RESULTS: LTs were mostly statins (>95%). The unadjusted recurrent stroke rate declined with LT category level (9.2% for level 0; 8.4% for level I; 7.5% for level II; and 5.7% for level III). Compared with level 0, the adjusted hazard ratio of stroke for level I was 0.78 (95% confidence interval (CI), 0.59-1.03), level II 0.80 (0.54-1.18), and level III 0.63 (0.43-0.91). Multivariable analyses of MVEs and all-cause death followed a similar pattern of declining risk with higher LT category level. CONCLUSIONS: Compared with the nonuse of LT, there may be a hierarchy of residual vascular risk after stroke by non-LDL type and target, while on LT. Particularly, strokepatients with low HDL-C levels on LT may benefit from additional therapeutic strategies to improve their outcomes.
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