Impact of Dyslipidemia on Ischemic Stroke

Abstract

High cholesterol and lipids, especially low-density lipoprotein cholesterol (LDL-C) in the blood are associated with a higher risk of vascular events including stroke and myocardial infarction. In addition to therapeutic lifestyle changes, treatment with an HMG coenzyme-A reductase inhibitor (statin) medication is recommended for the primary prevention of ischemic stroke in patients estimated to have a high risk for cardiovascular events. Aggressive reduction of low-density lipoprotein cholesterol is likely to yield greater benefit than more modest reductions. Epidemiological evidence has suggested that high-density lipoprotein cholesterol (HDL-C) levels are inversely correlated with stroke risk. Nevertheless, direct evidence for the clinical benefit of elevating HDL-C is scarce, because the efficacy of lipid-modifying drugs that raise HDL-C levels had not been directly assessed in large-scale clinical trials in stroke patients.

Triglyceride (TG) level is high in many clinical situations and has influenced adverse cardiovascular diseases. Despite managing LDL-C adequately, residual risks still remain. Therefore, we must closely observe TGs for patients who are at high risk of atherosclerotic cardiovascular disease (ASCVD). Postprandial TGs could be a reasonable marker of average lipid concentration since people consume food on a daily basis and non-fasting hours are longer than fasting hours. A recent clinical trial proved that lowering TGs has positive effects on cardiovascular disease.

Lipoprotein(a) (Lp(a)) is an LDL-like particle and has an apolipoprotein(a) (apo (a)) bound to apolipoprotein B100 (apo 100). Increased levels of Lp(a) are associated with ASCVD and calcified aortic valve disease. Unfortunately, there is no approved effective Lp(a) lowering therapy as of today. Ongoing clinical trials for lowering Lp(a) are promising.