Serum lipids and stroke.

Serum lipids and lipoproteins are strongly related to coronary atherosclerosis but their association with cerebrovascular atherosclerosis is far less clear and consistent, though lipid levels have been related to carotid artery atherosclerosis, in anumber of studies having angiographic or ultrasonographic evidences of atheromas of common carotid bifurcation and internal carotid artery. In these studies there appears to be an impressive correlation of increased low density lipoprotein (LDL) and reduced high density lipoprotein (HDL) to the atherosclerosis. Lipoprotein (a), Apoproteins (apo B and apo AI), and HDL sub fractions (HDL2 and HDL3) are emerging better indicators of cranial atherosclerosis than conventional serum lipid levels. Varying levels of serum cholesterol are responsible for deferring vascular pathologies of underlying stroke. With levels of total serum cholesterol below 160 mg/dL there is a greater proclivity for intracerebral hemorrhage, whereas elevated levels predispose to large vessel at herothrombosis. There is no definite proof that cholesterol reduction by diet or drug will reduce the incidence of stroke. Total cholesterol decreases after myocardial infarction and similarly, stroke is also accompanied by variable alterations in serum lipids levels, hence, post-stroke measurement of serum lipids may not be a true representative of the individual's risk. Anunanswered query is, the time when blood should be sampled for the lipid and lipoprotein estimation following stroke? This is difficult to state categorically. Some favor that it should be done immediately after the stroke but others argue that it should be performed after the patient's condition is stabilized (approximately 3 months after the stroke). Treatment with diet and or drugs may be required in a hyperlipidemic patient to lesson the risk of coronary heart disease (CHD) and possibly even subsequent stroke.