Low high-density lipoprotein cholesterol as the possible risk factor for stroke.

Recent evidence suggests that lower HDL-cholesterol (HDL-C) may worsen the atherosclerotic process by promoting inflammation and progression from subclinical lesion to clinical event. Carotid intima-media thickness (CIMT) is recognized as a marker of early atherosclerosis and used to predict future vascular events. Among the common lipid parameters, LDL has strongest relation with carotid plaque. Cumulative effect of achieving optimal levels of LDL-C, HDL-C, triglycerides and blood pressure is a reduced risk of recurrent stroke and major cardiovascular events. The protective effect of higher HDL-C is maintained at low levels of LDL-C. Studies have demonstrated a trend toward a higher risk of stroke with lower HDL-C and support HDL-C as an important modifiable stroke risk factor. In patients with recent stroke or transient ischemic attack and no coronary heart disease, only lower baseline HDL-C predicted the risk of recurrent stroke. Substantial amount of residual cardiovascular risk remains in patients treated with statins due to elevated triglycerides and low HDL-C, even when LDL-C is well controlled. Niacin promotes significant increase in HDL-C and reduces cardiovascular risk. By combining niacin with the LDL-lowering therapy of statins, the progression of atherosclerosis is slowed down and residual cardiovascular and risk of stroke is reduced. Non-pharmacological control of serum lipids includes regular physical activity and modification in daily diet. In primary prevention, when HDL-C is below the average and other risk factors are present, a statin added to non-pharmacological therapy is appropriate choice. Fibrate therapy may be appropriate in men with manifest coronary disease with isolated low HDL-C. If HDL-C remains low, with or without high triglyceride levels, a fibrate or niacin may be added.