C-reactive protein (CRP) belongs to the family of pentraxins and as such consists of five identical non-covalently linked subunits. Recent evidence links CRP to the pathogenesis of atherosclerosis. We recently identified a dissociation mechanism on activated platelets that leads to a conformational change from the circulating native, pentameric CRP (pCRP) to its monomeric subunits (mCRP). This dissociation changes the proinflammatory profile of the protein and might be of causal relevance in the pathogenesis of atherosclerosis. Here, we review our results in the light of the recent literature with emphasis on the role of activated platelets, of different CRP isoforms, and of the CRP dissociation process in atherosclerotic plaque formation.