"Has it ever struck you that there's a thin man inside every fat man, just as they say there's a statue inside every block of stone?" George Orwell, Coming Up For Air (1939) R ecently, data from diverse areas of investigation have come together to implicate chronic low-level inflammation as an important pathogenetic factor in atherosclerotic cardiovascular disease (CVD). As recently summarized by Ross, 1 studies in cell biology, animal models, clinical research, and epidemiology have been remarkably consistent in validating the early work of Virchow 2 and others, suggesting that atherosclerotic lesions are essentially an inflammatory response. In clinical research and epidemiology, 2 inflammation blood markers in particular, fibrinogen and C-reactive protein (CRP), have been used. Many studies have confirmed that these markers predict future cardiovascular events independently of more traditional cardiovascular risk factors, such as plasma lipid levels. [3][4][5] Because of this, several investigators have suggested that CRP might prove useful in clinical practice, 6,7 whereas others have favored fibrinogen. 8,9 Although there are important details to work out before either of these markers enters the clinical domain, this interest provides a clear and compelling imperative for understanding how inflammation integrates into both normal physiology and atherothrombotic pathophysiology.
See p 961 and 968Focusing on CRP, population-based research efforts have revealed that in general, women have slightly higher values than men, blacks have higher values than whites, and those with clinical CVD have higher values than those without [10][11][12][13] et al, manuscript in preparation). In those without clinical CVD, metabolic variables consistently correlated with CRP include body mass index (BMI), glucose tolerance status/diabetes status, and level of coagulation activation. In addition, depending on the population being studied, other correlates of CRP may include smoking status, plasma lipids (especially HDL cholesterol), hypertension, evidence of chronic infection, and measures of subclinical atherosclerotic disease, such as ankle-brachial blood pressure index (ABI).