PubMed2000
In the past decades it has become apparent that inflammation plays a role in atherogenesis and rapid coronary artery disease progression. Active, or vulnerable, atheromatous plaques are responsible for acute coronary events and contain high concentrations of inflammatory cells as well as molecules involved in the inflammatory process, such as cytokines, adhesion molecules and growth factors. From a clinical perspective, early detection of these plaques may prevent the occurrence of serious coronary events. Unfortunately, current diagnostic techniques -i.e. angiography- do not allow the characterization of events taking place in the arterial wall. Therefore, these diagnostic tools cannot identify vulnerable plaques. Recent studies have suggested that markers of systemic inflammation may help in the detection of high risk patients. Although the role of inflammation in the pathogenesis of atherosclerosis is established, it is not known what triggers inflammation in this context. Infectious agents such as viruses and Gram negative bacteria -i.e. Chlamydia pneumoniae- have been postulated to play a role. Several mechanisms, involving inflammation and immunological processes, have been suggested to explain how chronic infections may cause atherosclerosis. Small pilot studies have also been carried out which suggest a causal role of infection in coronary artery disease. These results, however, await confirmation by other large, currently ongoing, studies. The infectious hypothesis of atherosclerosis is still a matter of debate; however, this theory has contributed to the rapid advance of our knowledge regarding the pathogenesis of coronary artery disease in the past few years. Moreover, the notion that coronary artery disease can be considered to be an inflammatory condition in its own right has opened new and challenging avenues for research.