In cardiovascular disease pathogenesis, key roles are played by hypercoagulation disorders mainly associated with platelet activation, aggregation processes, and endothelial dysfunction. Current research is studying new molecular species that might interfere with both previously known and new biochemical pathways, leading to the activation and aggregation of platelets, and growing evidence suggests close links between inflammation and thrombosis. It has been suggested that, in cardiovascular disease, circulating pentameric C-reactive protein (CRP) can dissociate into the monomeric form on activated platelets and the surface of circulating microvesicles, and this could potentially accelerate thrombogenesis and link platelet hemostatic processes with the immune response. Increased microvesicles level has confirmed the link between microvesicles and the inflammatory process in diseases with a strong inflammatory reaction. The treatment of coronary artery disease is partly based on properly selected pharmacotherapy. Despite the significant progress that has recently been made in recognizing and combatting abnormal response to oral antiplatelet agents, it is still unknown why some patients who receive dual antiplatelet therapy do not benefit from expected therapeutic effects. Part of the antithrombotic action that antiplatelet agents exert in different clinical settings may be explained by a modulation in the generation of platelet-derived microvesicles bound monomeric CRP. It is suggested that markers of inflammation, such as monomeric CRP or platelet-derived microvesicles, may provide markers of disease activity or response to treatment and may be used in the prognosis of the course of various diseases. This paper aims to provide an overview of the relationship between the monomeric form of C-reactive protein, associated with membrane microvesicles, higher platelet activation, and the possible association with lower antiplatelet response.