NEUROIMMUNOLOGIC IMPLICATIONS IN CORONARY-ARTERY DISEASE

In this review, the role of the macrophage in the pathophysiology of c oronary artery disease (CAD) is examined. The central interaction of m acrophage, endothelial cell and smooth muscle cell in the context of h yperlipidemia is considered. The macrophage appears to be at the begin ning of a chain of events that starts with elevated low density lipopr otein (LDL). Stress, particularly in those with a core hostility, may be associated not only with higher catecholamine levels but also with higher serum lipid levels, These lipids will in turn be processed to o xidized LDL by macrophage and endothelial cells. Oxidized LDL molecule s will contribute to atherosclerotic plaquing. A side effect of such p laque formation may be a diminished vasodilatory response to the nitri c oxide (NO) produced by macrophages and endothelium. Indeed, paradoxi cal vasoconstriction occurs in atherosclerosis in response to neurotra nsmitters such as serotonin and acetylcholine, which under normal circ umstances cause vasodilation. There also is evidence that both macroph ages and endothelial cells can regulate NO production through a specif ic mu 3 morphine receptor, an effect that can be blocked by naloxone. The clinical effectiveness of morphine and nitroglycerin in CAD patien ts may relate to these mechanisms. More research will be needed to elu cidate the neuroimmunologic basis for atherosclerosis with prospects f or better treatment and management in future. Copyright (C) 1996 Elsev ier Science Ltd