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The recently published study by Kovanen et al¹ and the editorial accompanying the study² reopen an important question for the area of clinical and fundamental research concerning the role of inflammatory events in the initiation and progression of the atherosclerotic lesion. Despite the clinical and experimental data accumulated during the last 2 decades, the importance of the inflammatory events in atherogenesis is still underestimated.

Several pieces of information could be added to the data presented in the above-mentioned articles.^1-2 The role of the complement system in the pathogenesis of atherosclerosis has been documented by clinical and experimental studies. The complement system, a complex of enzymes and regulators, has multiple biological effects in circulation and in tissues inducing opsonization, chemoattraction of leukocytes, cell lysis, and cell activation and rescue from apoptosis.³ In previous studies we have demonstrated a complex relationship between the circulating immunoglobulins deposited as immune complexes in the arterial . . . [Full Text of this Article]

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Arch Intern Med. 1999;159(19):2364-2365.
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