ABSTRACT
Atherosclerosis and its complications contribute to a large percentage of morbidity and mortality in older people. Cardiovascular disease is the leading worldwide cause of morbidity and death.1 However, our understanding of the pathogenetic mechanisms underlying atherosclerosis and its complications remain incomplete, since more than half of patients with atherosclerosis do not show classical risk factors, such as hypercholesterolemia, hypertension, smoking history, diabetes, obesity, or sedentary life style.1,2
On the other hand, atherosclerosis, formerly considered a lipid storage disease, is now known to involve an ongoing inflammatory response. Recent advances in basic science have established a fundamental role for innate immunity and inflammation in mediating all stages of this disease from initiation through progression and, ultimately, to the thrombotic complications. Clinical studies have shown that the emerging biology of inflammation in atherosclerosis applies directly to human patients. Elevation of markers of inflammation predicts outcomes of patients with acute coronary syndromes, independently of myocardial damage. In addition, low-grade chronic inflammation, as indicated by levels of the inflammatory marker reactive C protein (CRP) and pro-inflammatory cytokines, prospectively defines risk of atherosclerotic complications, thus adding to prognostic information provided by traditional risk factors. In fact, levels of CRP or IL-6 have been suggested to be significant predictive risk factors for future development of cardiovascular events.2-4
Furthermore, increased levels of serum IL-1b have been associated with high risk of congestive heart failure and angina pectoris5 and altered levels of IL-1b have been implicated in chronic inflammation related to high blood pressure.6
