Positive Health Online

Abstract

FRICCHIONE and colleagues, Brigham and Womens Hospital, Division of Psychiatry, Boston, Massachussetts USA review (60 references) the role of the macrophage in the pathology of coronary artery disease (CAD), in which the central interaction of macrophage, endothelial and smooth muscle cell is considered in the context of hyperlipidaemia. The macrophage appears to be at the start of a chain of events starting with elevated low density lipoprotein (LDL). Stress, especially in those people with a core hostility, may be associated with higher catecholamine levels as well as higher serum lipid levels which will be processed by macrophage and endothelial cells to oxidised LDL. Oxidised LDL molecules will contribute to atherosclerotic plaque, a side effect of which may be a diminished vasodilatory response to the nitric oxide (NO) produced by macrophages and endothelium. In fact, paradoxical vasoconstriction occurs in atherosclerosis in response to neurotransmitters including serotonin and acetylcholine which under normal conditions produce vasodilation. There is also evidence that macrophages and endothelial cells can both regulate NO production via a specific mu-3 morphine receptor, which can be blocked by naloxone, which may explain the clinical effectiveness of morphine and nitroglycerin in patients with CAD. The authors state that more research is needed to elucidate the neuroimmunologic basis for atherosclerosis which could lead to prospects for better treatment and management in the future.

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References

Fricchione GL et al. Neuroimmunologic implications in coronary artery disease. Adv Neuroimmunol 6(2): 131-42. 1996.