here has been a surge of interest in the role of inflammation in causation of atherosclerosis and acute coronary syndromes. This interest is spurred both by pathological studies showing that ruptured coronary plaques manifest inflammatory characteristics 1 and by the demonstration that inflammatory biomarkers in the plasma correlate with risk for acute coronary syndromes. 2,3 Among the biomarkers that correlate with acute coronary syndromes, the most robust is C-reactive protein (CRP). 4 The liver is known to respond to high levels of cytokines in the circulation with an increased production of CRP. A recent report by the American Heart Association/Centers for Disease Control and Prevention (AHA/CDC) 4 indicated that CRP measurements may provide incremental information for global risk assessment for coronary heart disease beyond that obtained from established risk factors. These measurements can be made at the discretion of physicians, provided that established risk factors are given priority in global risk assessment.
See p 150Another recent observation of significance is that elevated CRP levels associate with the metabolic syndrome. The latter is a syndrome in which several metabolic risk factors cosegregate in one person. Risk factors of the metabolic syndrome include atherogenic dyslipidemia (raised triglycerides, elevated apolipoprotein B, small LDL particles, and low HDL cholesterol), elevated blood pressure, insulin resistance (Ϯglucose intolerance), a proinflammatory state, and a prothrombotic state. 5 Several studies 6 -8 add support to the concept that a proinflammatory state is one component of the metabolic syndrome. Ridker et al 9 have confirmed that elevated CRP associates strongly with metabolic syndrome risk factors; moreover, these workers 9 reported that high CRP levels impart risk for major coronary events beyond that imparted by the other metabolic risk factors. The reasons for a link between inflammation and metabolic syndrome are not fully understood. One explanation may be that adipose tissue in obese persons with the metabolic syndrome releases increased amounts of cytokines into the circulation 10 ; this in turn accounts for a greater production of CRP by the liver. Another possibility is that insulin resistance per se is responsible for a higher production of cytokines. 11 Regardless of mechanism, the finding that patients with metabolic syndrome exhibit characteristics of a proinflammatory state provides a new and exciting connection between inflammation and metabolic processes. This connection promises to yield new insights into pathways whereby the metabolic syndrome leads to atherosclerosis and acute coronary syndromes. Undoubtedly, the connections between inflammation and metabolism are complex and present a challenge for new research.One area of this association is explored by Erlinger et al 12 in the present issue of Circulation. These authors examined the effects of a therapeutic dietary pattern named Dietary Approaches to Stop Hypertension (DASH) on plasma lipids and lipoprote...