Ateroskleroza je sustavna bolest koja dovodi do bolesti koronarnih, karotidnih i perifernih arterija. Vodeći je uzrok smrti u razvijenim zemljama. Patofiziologija ateroskleroze ovisi o brojnim urođenim i stečenim čimbenicima. Ključno uporište za nastanak ateroskleroze je gubitak normalne funkcije endotela. Klinička istraživanja dala su brojne dokaze da snižavanje koncentracije lipida može dovesti do korisnih kvalitativnih promjena u atarosklerotskom plaku i povoljno utjecati na kliničko očitovanje bolesti. U aterosklerotskim promijenjenim krvnim žilama česti su kalcifikati koje je moguće radiološki dijagnosticirati, a služe kao pokazatelj težine i ishoda ishemijske bolesti srca. U bolesnika s kroničnim zatajenjem srca, a posebno onih koji su na dijalizi, kalcifikati u koronarnim arterijama čest su nalaz. Najčešće se dovode u vezu s dobi, trajanjem dijalize i dislipidemijom. Liječenjem bolesnika sa zatajenjem bubrega uz pomoć statina i sevelamera moguće je usporiti godišnju progresiju kalcificiranja koronarnih arterija s 30 % na 6 %. Prema podacima iz nekih istraživanja smanjenje koncentracije LDL kolesterola < 2,59 mmol/l može zaustaviti proces odlaganja kalcija ili čak dovesti do njegove regresije. Dodatna istraživanja pokazala su da smanjenje koncentracije LDL kolesterola uz istovremeno povećanje koncentracije HDL kolesterola mogu povoljno utjecati na smanjenje debljine intime i medije karotidnih arterija, kao i na smanjenje veličine plaka u koronarnim arterijama., Atherosclerosis is a systemic disease that is the leading cause of death in the developed world and leads to coronary artery, carotid artery, and peripheral arterial atherosclerotic syndromes. The pathophysiology of atherosclerosis is known to be dependent on multiple hereditary and environmental factors. Loss of normal endothelial function is a fundamental step in the atherosclerotic disease process. A consistent body of evidence from large clinical trails suggests that qualitative changes in plaques contribute importantly to the striking reduction in clinical events produced by lipid lowering. Calcium mineral deposits that frequently accompany atherosclerosis are readily quantifiable radiographically, serve as a surrogate marker for the disease, and predict a higher risk of myocardial infarction and death. Coronary artery calcification is a common observation in chronic kidney disease and end-stage renal disease and is mainly related to age, duration on dialysis, and dyslipidemia. The annual progression of coronary artery calcification can be reduced from 30 % to 6 % with LDL cholesterol reduction caused by statins and possibly sevelamer. At treated LDL cholesterol levels somewhere below 2.59 mmol/l, several sources of data suggest that the anatomic burden of coronary artery disease, including coronary artery calcification, regresses. Additional supportive studies indicate that carotid intima media thickness and the volume of coronary atheroma can also be reduced by LDL cholesterol reduction in concert with elevation of HDL cholesterol.