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Type 2 diabetes mellitus and atherosclerosis are complex and progressive conditions that share several common antecedents. Recent data suggest that inflammation may play a central role in the origins and complications of cardiovascular disease and, possibly, type 2 diabetes mellitus. C-reactive protein and plasminogen activator inhibitor-1 are circulating markers of low-grade inflammation, thrombosis, and vascular injury. Together with homocysteine, they have been associated with the underlying inflammatory processes and are considered to be "nontraditional" risk factors of atherosclerosis. The role of their measurement in clinical practice remains unclear. In this article, we review the available evidence demonstrating a link between inflammation, cardiovascular disease, and diabetes. We discuss how therapeutic agents used for both cardiovascular disease and diabetes modulate the inflammatory responses and possibly attenuate the complications of these two chronic disorders that cause significant morbidity and mortality.

Until recently, atherosclerosis was thought to be a passive process of lipid deposition in the arterial wall, followed by progressive occlusion of the lumen, and finally plaque rupture and thrombosis. Recent data suggest the contrary-atherosclerosis is a dynamic process developing over many years, characterized by active uptake of lipids and smooth muscle proliferation, "molding" of plaque, and subject to the influence of many environmental and genetic factors. Central to these processes, both at initiation and propagation, are factors associated with inflammation. Insulin resistance (IR), the underlying cause of type 2 diabetes mellitus (DM), is also associated with elevated levels of inflammatory factors, such as C reactive protein (CRP), plasminogen activator inhibitor-1 (PAI-1), and fibrinogen. Recent studies indicate that these same factors precede and predict DM. These findings have led to the notion that the strong association of IR/DM with cardiovascular disease (CVD) may be through inflammation pathways. In this article, we review what is known about the association of inflammation with IR and atherosclerosis. We show that many of the same inflammatory factors associated with IR are present in atherosclerosis. We also discuss the underlying determinants of inflammation in these conditions.

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