%0 Journal Article
%T Lipoprotein(a) Is the Best Single Marker in Assessing Unstable Angina Pectoris
%A Vidosava B. Djordjevi£¿
%A Vladan £¿osi£¿
%A Ivana Stojanovi£¿
%A Slavica Kundali£¿
%A Lilika Zvezdanovi£¿
%A Marina Deljanin-Ili£¿
%A Predrag Vlahovi£¿
%A Lidija Popovi£¿
%J Cardiology Research and Practice
%D 2011
%I Hindawi Publishing Corporation
%R 10.4061/2011/175363
%X This study evaluated whether statin therapy changed a diagnostic validity of lipid and inflammatory markers in ischemic heart disease (IHD) patients. Levels of lipids, lipoproteins, apolipoproteins, inflammatory markers, and atherogenic indexes were determined in 49 apparently healthy men and women, 82 patients having stable angina pectoris (SAP), 80 patients with unstable angina (USAP), and 106 patients with acute ST-elevation myocardial infarction (STEMI) treated or not treated with statins. Diagnostic accuracy of markers was determined by ROC curve analysis. Significantly lower apoA-I in all statin-treated groups and significantly higher apoB in statin-treated STEMI group compared to non-statin-treated groups were observed. CRP showed the best ROC characteristics in the assessment of STEMI patients. Lp(a) is better in the evaluation of SAP and USAP patients, considering that Lp(a) showed the highest area under the curve (AUC). Regarding atherogenic indexes, the highest AUC in SAP group was obtained for TG/apoB and in USAP and STEMI patients for TG/HDL-c. Statins lowered total cholesterol, LDL-c, and TG but fail to normalize apoA-I in patients with IHD. 1. Introduction Beside endothelial dysfunction leading to inflammatory reaction, lipid metabolism disorders represent the second key event in the initiation and rapid development of atherogenesis [1]. Many individual lipid and inflammatory markers have been considered as the factors playing an important role in atherogenesis and prognosis of related diseases. The atherogenic dyslipidemic profile, especially mild to marked elevation of apo-B containing lipoproteins, such as very low-density lipoproteins (VLDL), VLDL-remnants, intermediate-density lipoproteins (IDL), and low-density lipoproteins (LDL) (specifically small, dense LDL), and low levels of high-density lipoproteins (HDL) [2¨C4], appears to promote enhanced arterial cholesterol deposition and accelerate the progression of atherosclerotic disease. Despite the use of new and effective pharmacological drugs to lower plasma lipid concentration, cardiovascular diseases continue to be the main cause of death in western countries [5, 6]. Fenofibrate lowers the plasma level of cholesterol and triglyceride, corrects the abnormality in LDL metabolism, but has no effect on HDL-cholesterol (HDL-c) [7]. On the other hand, statins have a therapeutic effect on lipid metabolism and inflammation. They lower total and LDL-cholesterol (LDL-c), elevate HDL-c, and lower inflammatory markers such as C-reactive protein (CRP) [8¨C11]. Since antilipidemic drugs induce
%U http://www.hindawi.com/journals/crp/2011/175363/