Biofilms, Lipoprotein Aggregates, Homocysteine, and Arterial Plaque Rupture

The finding that bacteria form biofilms within the majority ofcarotid arterial plaques is a further demonstration of the im-portant role played by microorganisms in the etiology of athero-sclerotic vascular disease (1). Many investigators believe that the first step in atherogenesis is the creation of atherosclerotic plaques and that infection by microorganisms is a secondary phenome-non. In contrast, we believe that microbial infection is an essential component of the atherogenic process. More than a dozen research groups have demonstrated that lipoproteins participate in the innate immune system by binding and inactivating microorganisms and their toxic products by forming circulating complexes (2–4). The size of these complexes may increase in cases of hyperhomocysteinemia, because homo-cysteine reacts with and causes aggregation of low-density lipo-protein (LDL). Autoantibodies may be created against homocys-teinylated LDL, further enhancing the aggregation process. I