Introduction: Remnant cholesterol, comprising triglycerides(TG)-rich lipoproteins, accumulates in intimal foam cells and causes atherosclerosis. Fasting TG is reported to be associated with atherosclerotic stroke, but relationships between non-fasting TG (NFTG) and ischemic stroke subtypes are unknown. Recently NFTG was found to produce endothelial dysfunction. This study aimed to elucidate the association of fasting and NFTG with ischemic stroke subtypes, especially large-artery atherosclerosis (LAA) and small vessel occlusion (SVO).
Methods: Using a prospective multicenter stroke registry (Clinical Research Center for Stroke - 5th division), we identified acute ischemic stroke patients, hospitalized within 48 hours of onset, and whose fasting and non-fasting TG values were available. We measured lipid profiles in each individual twice; at presentation and after overnight fasting. Initial TG were regarded as NFTG when measured within 8 hours from last mealtime.
Results: Total 3,170 patients were analyzed. Stroke subtypes were categorized as LAA (37.9%), SVO (18.7%) and non-LAA and non-SVO (43.4%). Lipid levels according stroke subtypes are presented in Table. Lipid levels were divided by quartiles and the highest quartile was compared to others. In multinomial analyses compared to non-LAA and non-SVO group, fasting TG was associated with LAA (adjusted ORs 1.33 [95% CIs 1.09 - 1.62]) and SVO (1.61 [1.27 - 2.04]). NFTG was associated not with LAA (1.05 [0.87 - 1.28]), but with SVO (1.36 [1.08 - 1.71]). With respect to other lipid levels, fasting and non-fasting LDL were associated with both LAA (1.57 [1.29 - 1.90], fasting; 1.89 [1.56 - 2.29], non-fasting) and SVO (1.40 [1.11 - 1.77], fasting; 1.74 [1.38 - 2.19], non-fasting).
Conclusions: This study may be the first one to demonstrate an association between non-fasting TG and SVO. It should be explored further on mechanisms of differential effect of fasting and non-fasting TG on ischemic stroke subtypes.