C-reactive protein >3 mg/L is not associated with SCD or fast VT/VF, however, is a strong predictor of HF mortality. Biomarkers combined with clinical markers allow an excellent risk stratification of mortality at 2 years.

No abstract

Recent findings suggest that inflammation plays a key role in atherosclerosis from the earliest stage of lesion initiation, to the ultimate complication of thrombosis. In patients who died because of acute coronary syndromes (ACS), coronary atherosclerotic plaques are characterized by the presence of macrophages, and to a lesser extent T-lymphocytes, at the immediate site of either plaque rupture or superficial erosion. The rupture-related inflammatory cells are activated, indicating ongoing inflammation. ACS patients are also characterized by activated circulating lymphocytes, monocytes and neutrophils, and by increased concentrations of proinflammatory cytokines and of the highly sensitive acute phase reactant C-reactive protein. Interestingly, an unusual subset of T cells, CD4+ CD28null T cells, involved in vascular complication of rheumatoid arthritis because of their functional profile predisposing for vascular injury, are expanded in the peripheral blood and infiltrate the coronary lesions of ACS patients. The presence of activated T lymphocytes implies antigenic stimulation, but the nature of such antigen(s) remains to be investigated. Several autoantigens expressed in the atherosclerotic plaque, including oxidized LDL and heat shock proteins, and infectious agents are able to elicit an immune response. The inflammatory component is not localized to the 'culprit' plaque, but it is diffused to the entire coronary vascular bed, and involves also the myocardium.

In recent years a growing body of evidence has emphasized the role of C-reactive protein (CRP) as a marker of future cardiovascular events. CRP is a pentameric molecule widely utilized as a marker of infections and inflammation. The evidence that inflammation plays an important role in the pathogenesis of coronary artery disease and in plaque destabilization has lead to use of CRP as a marker of cardiovascular disease as well. First described as a component of the inflammatory pathway in acute coronary syndromes, CRP has been consistently found to be associated with the risk of future events in no-ST elevation acute coronary syndromes, independently of other risk factors, including troponine. Subsequently CRP has been described as a powerful marker of risk of future events in large populations of apparently healthy subjects. So far there is very little doubt that CRP represents a reliable marker of cardiovascular events, but some issues remain unanswered such as why CRP is a good marker of cardiovascular events and whether or not a better inflammatory marker exists. It must be stressed that CRP, because of its analytical and biological properties and the large amount of available data, is the only inflammatory marker accepted for clinical use.

The CAMI GUIDE study will assess the predictive role of CRP in SCD in patients with previous MI undergoing ICD implantation. Its results will improve risk stratification, thereby enabling better-tailored and more cost-effective therapies to be undertaken in those patients whose need is greatest.