ABSTRACT
Together, laboratory and clinical data have provided substantial evidence supporting a fundamental role of inflammation in atherothrombosis (I). Laboratory researchers have identified macrophages, T-Iymphocytes, and their biochemical messengers as key participants in the initiation, progression, and destabilization of atherosclerotic vascular disease (2). These pathobiological insights have directed the attention of clinical investigators to inflammatory markers as potential novel indicators of underlying atherosclerosis and cardiovascular risk. These efforts have produced a consistent body of epidemiological data demonstrating an association between clinical evidence of inflammation and increased risk of atherothrombosis (3). Moreover, the expansion in our understanding of atherogenesis has prompted reevaluation of the therapeutic mechanisms for several established pharmacological interventions, and pointed in new directions for the prevention and treatment of atherosclerotic vascular disease (2).
