Editorial [Hot Topic: Modifying Coronary Risk Factors: C-Reactive Protein,Haemostatic Factors and Cardiovascular Risk (Executive Editor: Aurelio Leone)]

There has been conflicting debate about the relationship among those parameters which are generally involved in cardiovascular events such as C-Reactive Protein, haemostatic factors and other major cardiovascular risk factors. The debate seems to be a result for establishing the exact mechanisms of cardiovascular damage, that is believed to be due to either a direct action on coagulation/fibrinolysis cascade components either a consequence of interaction between haemostatic factors, inflammatory factors and the other cardiovascular risk factors. Cardiovascular damage expresses itself mainly as thromboembolic damage because of structural and biochemical components of coagulation/fibrinolysis cascade involved. Clot formation and lysis involve a large series of structures at different levels: vascular level, cellular level, and plasmatic level. Physiologically, the whole mechanism is directed to stop haemorrhage and keep vessel lumen patency. Damage at any of these levels may cause alterations potentially harmful against cardiovascular system. After a vasoconstriction following a stimulus of different types, endothelium is the first structure involved in coagulation/ fibrinolysis cascade. If the endothelium is intact, physiological stimulation not only causes vessel vasodilation, but also protects the vessel wall against the development of atherosclerosis and thrombotic vascular events. On the contrary, in presence of endothelial damage and/or dysfunction a series of occurrences produced by biochemical factors activates platelets (cellular level) that increase their secretion, adhesiveness, and aggregation initiating those processes that, in case of pathological response, may lead to thrombi formation. Plasmatic factors (plasmatic level) mainly fibrinogen and fibrin, together a reduced activity of plasminogen activators, impair further the phenomenon. The interference with other cardiovascular risk factors increases heavily the appearance of cardiovascular events by a complex series of chemical, biological, and inflammatory mechanisms, the exact action of which has yet to be clarified. However, CReactive Protein and haemostatic system alterations play a fundamental part in causing cardiovascular events. The paper of Carolyn Smith from London [1] underlines the role of ADMA as a mediator of cardiovascular disorders as well as its relationship with C-reactive protein. The complex interaction between C-reactive protein with the vascular endothelium is widely discussed by Claudio Ferri and Coworkers [2] from the University of L'Aquila, Italy. Human atherosclerosis is characterized by a multifactorial etiology, but endothelial dysfunction has a significant role in determining the appearance of atherosclerotic alterations. Among haemostatic factors, three papers [3-5] discuss the role of fibrinogen as a predictor of vascular disease, the interference of smoking with coagulation-fibrinolysis cascade, and the mechanisms by which platelets may be related to cardiovascular risk as well as those measures able to prevent cardiovascular damage. Moreover, the new role played by platelets in atherothrombosis is widely discussed by Weyrich and Coworkers [6]. The relationship between C-reactive protein and hypertension [7] is discussed by Virdis and Coworkers of Pisa, Italy. Nowdays, there is no clear evidence of a strong link between those two factors. An emerging role to explain many hypotheses of cardiovascular risk seems to be due to the knowledge of the circulating endothelial progenitor cells. The paper of Balbarini and Co-workers [8] clarifies the physiologic characteristics of the circulating endothelial progenitor cells as well as their relationship with cardiovascular risk. Finally, an overview of the relevant biology and pharmacology of COX 2 in atherosclerosis [9] is assessed in the paper of Iezzi and Coworkers from Chieti and L'Aquila, Italy. The articles in this issue provide a current summary to how understand the mechanisms and interactions of the main cardiovascular risk factors with C-Reactive Protein and some haemostatic system components, analysing the newest knowledges yet under study. Therefore, I believe that the present issue can up to date researchers, physicians, and also students on the state of art of a subject that is continuously in growth.......