title: Effect of statin treatment in patients with acute myocardial infarction and left ventricular systolic dysfunction according to the level of high-sensitivity C-reactive protein.
abstract: The effects of statins on the prognosis of patients with left ventricular (LV) systolic dysfunction remain controversial. The aim of this study was to assess the effect of statin treatment on clinical outcomes in acute myocardial infarction (AMI) patients with LV systolic dysfunction. A total of 5,119 AMI patients with LV ejection fraction less than 50% on the initial echocardiogram were analyzed in the Korean Acute Myocardial Infarction Registry. The study population was divided into 4 groups according to the level of high sensitivity C-reactive protein (hs-CRP) and statin treatment: low hs-CRP (hs-CRP ≤ 2.0 mg/L) and high hs-CRP (hs-CRP > 2 mg/L) with or without statin therapy. We evaluated the incidence of major adverse cardiac events (MACEs) including cardiac death, reinfarction, target lesion revascularization, and coronary artery bypass grafting during a 12-month period in each group. Statin therapy did not significantly prevent the MACEs in the low hs-CRP groups (with statin: 10.1% versus without statin: 12.0%, P = 0.249). In the high hs-CRP groups, however, the incidence of MACEs was significantly decreased with statin treatment (with statin: 11.3%, without statin: 20.8%, P < 0.001). These findings were consistently observed in all subgroups of the high-hs CRP group, including the subgroup with an LV ejection fraction less than 40%. In a multivariable logistic regression analysis of the high hs-CRP group, lack of statin therapy was a significant predictor of MACE incidence (odds ratio: 1.573, 95% confidence interval: 1.079-2.293, P = 0.018). The statin treatment was associated with better outcome in AMI and LV dysfunction patients with hs-CRP ≥ 2 mg/dL.
authors.affiliation: Chonnam National University Hospital.
authors.forename: Hae Chang
authors.initials: HC
authors.lastname: Jeong
authors.forename: Youngkeun
authors.initials: Y
authors.lastname: Ahn
authors.forename: Keun-Ho
authors.initials: KH
authors.lastname: Park
authors.forename: Doo Sun
authors.initials: DS
authors.lastname: Sim
authors.forename: Young Joon
authors.initials: YJ
authors.lastname: Hong
authors.forename: Ju Han
authors.initials: JH
authors.lastname: Kim
authors.forename: Myung Ho
authors.initials: MH
authors.lastname: Jeong
authors.forename: Young Jo
authors.initials: YJ
authors.lastname: Kim
authors.forename: Shung Chull
authors.initials: SC
authors.lastname: Chae
authors.forename: Myeong Chan
authors.initials: MC
authors.lastname: Cho
authors.forename: Jei Keon
authors.initials: JK
authors.lastname: Chae
authors.forename: Chong Jin
authors.initials: CJ
authors.lastname: Kim
authors.forename: Seung-Woon
authors.initials: SW
authors.lastname: Rha
authors.forename: Yang Soo
authors.initials: YS
authors.lastname: Jang
authors.forename: Seok Kyu
authors.initials: SK
authors.lastname: Oh
authors.forename: In Whan
authors.initials: IW
authors.lastname: Seong
authors.forename: Kwang Soo
authors.initials: KS
authors.lastname: Cha
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism*; D004452:Echocardiography; D004562:Electrocardiography; D005260:Female; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000503:physiopathology; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction / Q000502:physiology*; D009203:Myocardial Infarction / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology; D011379:Prognosis; D012189:Retrospective Studies; D013318:Stroke Volume; D013599:Systole; D018487:Ventricular Dysfunction, Left / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology; D016277:Ventricular Function, Left / Q000502:physiology*
chemical_list: D015415:Biomarkers; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D002097:C-Reactive Protein