Pathogenetic and Immunological Paradigm of Atherosclerotic Plaque

Conclusions

Inflammation plays a key role in atherosclerosis. A number of different biomarkers of inflammation are measurable in blood. These include cytokines, chemokines, soluble adhesion molecules, and acute-phase reactants. The first three of these groups of molecules are not routinely available in clinical laboratories. In contrast, however, C-reactive protein is readily measurable, and numerous clinical studies have demonstrated its usefulness as a marker of atherosclerotic risk [12, 13]. Other independent predictive risk factors of cardiovascular events are: myeloperoxidase, serum CD40L (sCD40L), adiponectin, and vWF.

Given its pro-inflammatory properties, myeloperoxidase, produced by the activated PMNs, could be utilised as a marker and mediator of vascular inflammation, confirming the importance of activated PMNs in the physiopathology of the acute coronary syndrome.

The different combinations of immunocompetent cells (macrophage-monocytes and T lymphocytes), of the vascular wall cells, of atheronecrotic material, and of fibrous material regulated by cytokines and growth factors produced by the same cells, allow us to say that every plaque is different from the next. This combination is responsible for the clinical manifestations of coronary atherosclerosis that affect only 5–10% of the individuals who have these lesions.

This hypothesised physiopathological and pathogenetic paradigm is a useful reference point for therapeutic strategies and prevention.