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Atherosclerosis 2012-Aug

Plasma fasting and nonfasting triglycerides and high-density lipoprotein cholesterol in atherosclerotic stroke: different profiles according to low-density lipoprotein cholesterol.

يمكن للمستخدمين المسجلين فقط ترجمة المقالات
الدخول التسجيل فى الموقع
يتم حفظ الارتباط في الحافظة
Suk Jae Kim
Yun Gyoung Park
Ji Hyun Kim
Yun Kyung Han
Hong Keun Cho
Oh Young Bang

الكلمات الدالة

نبذة مختصرة

Although low-density lipoprotein cholesterol (LDL-C) is the main lipid target for cardiovascular risk reduction, recent studies suggest that other lipid indicies are also associated with vascular events. We hypothesized that the association of triglycerides (TG) and high-density lipoprotein cholesterol (HDL-C) with atherosclerotic stroke (AS) differs depending on LDL-C levels. Data prospectively collected on subjects admitted with acute ischemic stroke to a university medical center were analyzed. We divided the patients into AS and non-atherosclerotic stroke (NAS) groups and independent association of lipid parameters and genetic influences of apolipoprotein A5 (ApoA5) polymorphisms with AS were evaluated. Of 268 patients, 160 (59.7%) were classified with AS and 108 (40.3%) were classified with NAS. Vascular risk factors were more prevalent in AS patients than in those with NAS; additionally, AS patients' anthropometric indexes and laboratory findings showed that they were prone to atherosclerosis. AS was independently associated with fasting TG (OR per 10 mg/dL increase, 1.38; 95% CI, 1.16-1.64; OR for highest vs. lowest tertile, 12.85; 95% CI, 3.31-49.85), HDL-C (OR per 10 mg/dL increase, 0.61; 95% CI, 0.42-0.88; OR for lowest vs. highest tertile, 4.28; 95% CI, 1.16-15.86), and nonfasting TG (OR per 10 10 mg/dL increase, 1.25; 95% CI, 1.11-1.42; OR for highest vs. lowest tertile, 8.20; 95% CI, 1.98-33.88) only among patients with LDL <100 mg/dL. No interaction was observed between fasting and nonfasting TG and ApoA5 polymorphisms. In conclusion, fasting and nonfasting TG and HDL-C were associated with AS only when patients had low levels of LDL-C. Non-LDL-C may have an additional role in addition to the LDL-C levels in AS development.

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