© 2001 American Heart Association, Inc.
Editorial |
Is Visceral Adiposity the "Enemy Within"?
From the University of Vermont College of Medicine, Colchester.
Correspondence to Dr Russell P. Tracy, University of Vermont, Departments of Pathology and Biochemistry, 55A South Park Dr, Colchester, VT 05446.
Key Words: obesity • inflammation • cardiovascular disease
Recently, 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 Virchow2 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.
Focusing 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
without10 11 12 13
(M. Cushman, 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,
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