Effects Of Statins On Plasma Lipids And Inflammation Factors In Patients With Acute Myocardial Infarction

Objective: In recent years, the incidence of coronary atheroscleroticheart disease is increasing rapidly with mortality, and patients are gettingyounger and younger age of onset. Hyperlipidemia is a major risk factor forcoronary heart disease. MIRACLE trial showed that intervention forhyperlipidemia in patients with acute coronary syndrome is effective. Foracute myocardial infarction patients after admission, starting lipid-loweringtherapy, particularly the use of statins, has become the basis of drug measuresand one of the most important contents. Statins have a role independent ofother lipid-lowering effects, which is called pleiotropic effects, includinganti-inflammatory, antioxidant, improvement of endothelial function, plaquestabilization, reduction of neuroendocrine activation. Acute coronarysyndrome is a kind of inflammatory response, which has been considered as asign throughout the various stages of atherosclerosis, ranging from thedysfunction of endothelial cells to atherosclerotic plaque rupture. Studies haveshown that coronary plaque rupture and secondary thrombosis directlycontribute to acute coronary syndrome. The hs-CRP and IL-6are importantindicators of the inflammatory response in coronary atherosclerotic lesions.Currently there are trials, researches about effects of different statins, testingthe lipid-lowering and anti-inflammatory function after long-term applicationin patients with acute coronary syndrome. The experiments always include abroad range of subjects, a single time point for monitoring index. The studyamount is still small when it comes to the use of statins in the very patientswith acute myocardial infarction during acute phase. At the same time, thedynamic changes of the inflammatory factors on themselves in patients withacute myocardial infarction are often not concerned, which can also influencethe experiment results, that is, natural anti-inflammation condition cannot be reflected exactly. This test launched special study to compare the functions ofstatins, or different statin doses in lowering lipids and suppressinginflammation in patients with acute myocardial infarction during the acutephase or convalescence. This trial is to compare effects of atorvastatin,fluvastatin and rosuvastatin on serum low density lipoprotein-cholesterol(LDL-C), high density lipoprotein-cholesterol(HDL-C), total cholesterol(TC)and inflammatory factor high-sensitivity C-reactive protein (hs-CRP),interleukin-6(IL-6) in patients with acute myocardial infarction. During thebody’s metabolism disorders characterized by inflammation, lipid metabolismwill also change. Patients with acute coronary syndrome have a series ofchanges in lipid metabolism during acute phase response, plasma levels oftriglycerides and very low density lipoproteins increase, HDL-C, LDL-C andTC levels reduce. Lipoprotein homeostasis is a complex process, and not allelements are atherosclerotic evenly. This three kinds of statins achieve themain therapeutic effect, including LDL-C reduction and HDL-C increase, byinhibiting endogenous lipoprotein synthesis and raising expression ofmembrane bound LDL-C receptors. With the stimulation of IL-1, IL-6andother cytokines from activated macrophages, CRP can be produced by thesmooth muscle cells located in coronary atherosclerotic lesions and directlyparticipate in atherosclerosis and cardiovascular complications in the rightlesion. In the acute phase response, hs-CRP and IL-6levels also appear tochange dynamically. This experiment compares anti-inflammatory effects ofstatins by measuring the change in the amount of inflammatory markers.Methods: From March to December in2013, chose100cases whoattended in the CCU Branch of the First Hospital of Qin Huangdao within24hof onset of acute myocardial infarction and received emergency percutaneouscoronary intervention successfully to get coronary revascularization, everyonemet diagnostic criteria of the American College of Cardiology (ACC) andAmerican Heart Association (AHA), including the clinical history of ischemicchest pain, ECG dynamic evolution, elevated markers of myocardial injury.Emergency coronary intervention was performed in compliance with guidelines, all patients underwent emergency coronary stenting. All thepatients had not received statin therapy during the former month. Dividedthem into four groups randomly, each group was given atorvastatin20mg,atorvastatin40mg, fluvastatin80mg, or rosuvastatin10mg orally once a nightfor four weeks. Tested the serum LDL-C, HDL-C, TC, hs-CRP and IL-6levelsbefore, one and four weeks after medication in each group.Results: After medication for one week, LDL-C levels are all loweramong the four groups comparing with the base line before treatment (P<0.05),and there is no remarkable difference between atorvastatin20mg group andfluvastatin group, fluvastatin group and the rosuvastatin group (P>0.05), butrosuvastatin has stronger influence than atorvastatin20mg(P<0.05),atorvastatin40mg is the strongest(P<0.05). HDL-C leves of atorvastatin40mggroup increase(P<0.05), Fluvastatin group has no significant change inHDL-C leves(P>0.05), the remaining two groups reduce (P<0.05), There is noremarkable difference in△-value between atorvastatin20mg group androsuvastatin group(P>0.05). TC levels of four groups decrease (P<0.05), thereis no significant difference in the amount of change between each twogroups(P>0.05). hs-CRP levels of atorvastatin40mg decrease(P<0.05), theother three groups increase(P<0.05), there is no significant difference in theamount of change between each two groups(P>0.05). For IL-6, neitheratorvastatin20mg group nor fluvastatin group has significant differencebetween before and after medication therapy(P>0.05), IL-6levels ofatorvastatin40mg group and rosuvastatin group reduce comparing with thelevel before treatment (P<0.05), there is no remarkable difference between thelatter two change amounts (P>0.05). After four weeks’ medication, the serumLDL-C, TC, hs-CRP and IL-6levels all decrease(P<0.05), HDL-C levesincrease(P>0.05), For every index, there is no significant difference betweeneach two groups(P>0.05).Conclusions: The four groups, atorvastatin20mg, atorvastatin40mg,fluvastatin80mg, and rosuvastatin10mg all have lipid-lowering effects,atorvastatin40mg has strongest effects in reducing LDL-C, followed by rosuvastatin10mg, and the atorvastatin20mg, fluvastatin80mg group are inthe end, with the latter two undifferentiated. Atorvastatin40mg and fluvastatin80mg can make HDL-C higher than atorvastatin20mg and rosuvastatin10mg.There is no significant difference between each two groups in reducing thelevels of TC. Atorvastatin40mg, rosuvastatin10mg group can suppressinflammation in patients with acute myocardial infarction, and atorvastatin40mg group is stronger.