However, a wide variety of activities, such as innate immunity, coagulation, and others, fall under the term inflammation. Each of these activities plays an important role in our response to trauma and/or environmental challenge: coagulation and fibrinolysis in restricting blood loss and in wound repair; complement activation and T-cell differentiation as part of innate and adaptive immunity; endothelial cell, neutrophil, and monocyte activation in immunity and wound repair; antioxidation in response to oxidative challenge; and others. In addition, variances in the genes responsible for the overall regulation of this system may play important roles in disease susceptibility; eg, IL-6 and tumor necrosis factor (TNF)-a genes. Finally, other environmental factors (eg, diet, smoking, etc)- and the volume of inflammation-mediating tissue (eg, visceral fat) also appear to be important. It is clear, therefore, that the relationship of inflammation to atherosclerosis is complex and much additional research will be needed before we can truly understand these processes and their relationships to health and disease. other
A number of inflammatory markers have been shown to predict future CVD events, all with a certain degree of similarity. For example, ceruloplasmin—the major copper-transporting protein in plasma— had similar risk prediction to CRP in the Monitoring Trends and Determinants in Cardiovascular Disease-Augsburg cohort. In the Cardiovascular Health Study, fibrinogen, factor VIII, and CRP each independently predicted future CVD events with similar relative risks. Also, in the Iowa 65+ Rural Health Study, both CRP and IL-6 predicted future fatal CVD events, again with similar risk prediction. These similarities, however, do not necessarily mean that one marker can be directly substituted for another.