Are They in Collusion to Accelerate Atherogenesis?
From the Center of Vascular Biology, Cornell University, New York, NY. Correspondence to David P. Hajjar, Center of Vascular Biology, Cornell University, 1300 York Ave, New York, NY 10021. E-mail dphajjar@mail.med.cornell.edu Key Words: Editorials lipoproteins atherosclerosis infection inflammation Recent epidemiological studies have documented an increased incidence of some forms of coronary artery disease (CAD) in patients who have chronic infections and inflammatory disorders. Chlamydia pneumonia1 2 3 and herpes viruses4 5 6 have been implicated in the pathogenesis of CAD on the basis of their detection in human atherosclerotic plaques and epidemiological evidence of a higher incidence of CAD in patients infected with these agents. In this regard, many investigative reports have focused on the proatherosclerotic effects of infectious agents on vascular cells in tissue culture and how they may affect the biology of the arterial wall. The panoply of changes induced include those that