**Author details**

**5. Summary**

86 Atherosclerosis - Yesterday, Today and Tomorrow

sclerotic plaque [41].

site effects [75].

are clinical studies [35].

Progress within understanding the causes of the described disorders and the mechanisms leading to the formation of a blood clot opens up new therapeutic possibilities now and in the future to prevent acute cardiovascular incidents. The importance of the anti-inflammatory activity of statins as shown in many studies proving their clinical efficacy has already been mentioned. Similar importance has been demonstrated for other forms of therapy to lower LDL cholesterol with the help of ezetimibe or evolocumab. Controlling inflammation with patient behavior and statin drugs administration reveals other mechanisms leading to destabilization of atherosclerotic plaques. It cannot be ruled out that statins act on different levels of ongoing inflammation. In patients with HIV, there exist demonstrated beneficial effects of rosuvastatin, which reduced the presentation of PD-1 receptor on the surface of naïve-CD8+ [41]. It cannot be ruled out that it may be an indirect effect of its activity, by lowering levels of LDL cholesterol. Similar effects, including other pathways, leading to increased production of IL-2 and the intensification of differentiate naïve-CD8+ lymphocytes in the direction of Treg can restore the immunological balance and prevent destabilization of inflammatory athero-

Understanding of the immunological mechanisms, vulnerability of atherosclerotic plaque creates the chance to obtain antibodies against antigens involved in this process. The multitude of these antigens operating at different stages of development is currently an important difficulty. There exist attempts to gain effective antibodies against oxy-LDL, the key antigen for activation of inflammation and atherosclerosis. Research is directed into the efficacy and safety of antibodies directed against interleukins active in generating plaque instability. Some hopes are in the direction of tocilizumab, that is, IL-6 antagonist. The disadvantage to the trials that use anti-inflammatory medications is due to accompanying increase in metabolic disorders of the lipid fraction which can negatively affect the progression of atherosclerotic lesion [34]. In the last published results of CANTOS study, it has been shown to reduce the risk of several percent in recurrent cardiovascular events after the monoclonal antibody—canakinumab application, which is the antagonist of IL-1β, and reduce the level of highly sensitive C-reactive protein without affecting the level of cholesterol. The result of this study was considered inflammatory confirmation theory of atherosclerosis and a new perspective in its treatment [73, 74]. An interesting suggestion for therapy is in trying to influence the MMP family. Some of them, like MMPs-8; 10; 12; 13, are the enzymes responsible for the destruction of the fibrous cap as well as plaque rupture, its stabilization and reconstruction. MMPs are an interesting target for therapy of acute coronary syndromes; however, their general inhibition may lead to oppo-

Strong anti-inflammatory and anti-atherogenic effects have apoA-I, which is a protein component of high-density lipoprotein HDL. HDL is responsible for the reverse transport of cholesterol contained in the atherosclerotic plaque into the bloodstream. Change in aspect ratio of apoB/apoA-I can change the course of the atherosclerotic process. Significant in this regard Ewelina Dziedzic<sup>1</sup> , Michał Machowski2 , Małgorzata Oleszczak-Kostyra<sup>1</sup> and Marek J. Dąbrowski<sup>1</sup> \*

\*Address all correspondence to: marekda@bielanski.med.pl

1 Cardiology Clinic of Physiotherapy Division of the 2nd Faculty of Medicine, Medical University of Warsaw, Poland

2 Cardiology Department in Bielanski Hospital, Warsaw, Poland
