机构：[a]Division of Cardiovascular Disease, University of Alabama at Birmingham, Birmingham, Alabama[b]State University ofNew York, Downstate School of Public Health, Brooklyn, New York[c]South Australian Health and Medical Research Institute,Flinders University and Medical Centre, Adelaide, South Australia, Australia[d]Brigham and Women’s Hospital Heart & VascularCenter and Harvard Medical School, Boston, Massachusetts[e]Estudios Cardiológicos Latinoamérica, Instituto Cardiovascular deRosario, Rosario, Argentina[f]Sanofi, Bridgewater, New Jersey[g]Division of Medicine, Department of Vascular Medicine,Preventive Cardiology Unit, University Medical Centre Ljubljana, Ljubljana, Slovenia[h]Medical Faculty, University of Ljubljana,Ljubljana, Slovenia[i]Canadian VIGOUR Centre, University of Alberta, Edmonton, Alberta, Canada[j]St. Michael’s Hospital,University of Toronto, Toronto, Ontario, Canada[k]Department of Cardiology, Oslo University Hospital, Oslo, Norway[l]Universityof Oslo, Oslo, Norway[m]Sanofi, Paris, France[n]Stanford Center for Clinical Research, Department of Medicine, StanfordUniversity, Stanford, California[o]Department of Cardiology, Leiden University Medical Center, Leiden, the Netherlands[p]Divisionof Clinical Pharmacology, University of Kansas Medical Center, Kansas City, Kansas[q]Regeneron Pharmaceuticals Inc., Tarrytown,New York[r]Duke Clinical Research Institute, Duke University Medical Center, Durham, North Carolina[s]Division of Cardiology,Department of Medicine, Duke University School of Medicine, Durham, North Carolina[t]Department of Cardiovascular Medicine,University Hospitals Leuven, Leuven, Belgium[u]University of Leuven, Leuven, Belgium[v]Division of Cardiovascular Medicine,University of California San Diego, La Jolla, California[w]Division of Cardiology, University of Colorado School of Medicine, Aurora,Colorado[x]Green Lane Cardiovascular Services Auckland City Hospital, Auckland, New Zealand[y]Soroka University MedicalCenter, Faculty of Health Sciences, Ben Gurion University of the Negev, Beer Sheva, Israel[z]Department of Medicine III, GoetheUniversity, Frankfurt am Main, Germany[aa]Assistance Publique-Hôpitaux de Paris, Hôpital Bichat, Université de Paris, FACT(French Alliance for Cardiovascular Trials), INSERM U1148, Paris, France[bb]National Heart and Lung Institute, ImperialCollege, Royal Brompton Hospital, London, United Kingdom.
BACKGROUND Lipoprotein(a) concentration is associated with cardiovascular events. Alirocumab, a proprotein convertase subtilisin/kexin type 9 inhibitor, lowers lipoprotein(a) and low-density lipoprotein cholesterol (LDL-C). OBJECTIVES A pre-specified analysis of the placebo-controlled ODYSSEY Outcomes trial in patients with recent acute coronary syndrome (ACS) determined whether alirocumab-induced changes in lipoprotein(a) and LDL-C independently predicted major adverse cardiovascular events (MACE). METHODS One to 12 months after ACS, 18,924 patients on high-intensity statin therapy were randomized to alirocumab or placebo and followed for 2.8 years (median). Lipoprotein(a) was measured at randomization and 4 and 12 months thereafter. The primary MACE outcome was coronary heart disease death, nonfatal myocardial infarction, ischemic stroke, or hospitalization for unstable angina. RESULTS Baseline lipoprotein(a) levels (median: 21.2 mg/dl; interquartile range [IQR]: 6.7 to 59.6 mg/dl) and LDL-C [corrected for cholesterol content in lipoprotein(a)] predicted MACE. Alirocumab reduced lipoprotein(a) by 5.0 mg/dl (IQR: 0 to 13.5 mg/dl), corrected LDL-C by 51.1 mg/dl (IQR: 33.7 to 67.2 mg/dl), and reduced the risk of MACE (hazard ratio [HR]: 0.85; 95% confidence interval [CI]: 0.78 to 0.93). Alirocumab-induced reductions of lipoprotein(a) and corrected LDL-C independently predicted lower risk of MACE, after adjustment for baseline concentrations of both lipoproteins and demographic and clinical characteristics. A 1-mg/dl reduction in lipoprotein(a) with alirocumab was associated with a HR of 0.994 (95% CI: 0.990 to 0.999; p = 0.0081). CONCLUSIONS Baseline lipoprotein(a) and corrected LDL-C levels and their reductions by alirocumab predicted the risk of MACE after recent ACS. Lipoprotein(a) lowering by alirocumab is an independent contributor to MACE reduction, which suggests that lipoprotein(a) should be an independent treatment target after ACS. (ODYSSEY Outcomes: Evaluation of Cardiovascular Outcomes After an Acute Coronary Syndrome During Treatment With Alirocumab; NCT01663402) (C) 2020 The Authors. Published by Elsevier on behalf of the American College of Cardiology Foundation.
基金：
Fondation Assistance Publique - Hopitaux de Paris, Paris, France
第一作者机构：[a]Division of Cardiovascular Disease, University of Alabama at Birmingham, Birmingham, Alabama
推荐引用方式(GB/T 7714)：
Vera A. Bittner,Michael Szarek,Philip E. Aylward,et al.Effect of Alirocumab on Lipoprotein(a) and Cardiovascular Risk After Acute Coronary Syndrome[J].JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY.2020,75(2):133-144.doi:10.1016/j.jacc.2019.10.057.
APA：
Vera A. Bittner,Michael Szarek,Philip E. Aylward,Deepak L. Bhatt,Rafael Diaz...&Gregory G. Schwartz.(2020).Effect of Alirocumab on Lipoprotein(a) and Cardiovascular Risk After Acute Coronary Syndrome.JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY,75,(2)
MLA：
Vera A. Bittner,et al."Effect of Alirocumab on Lipoprotein(a) and Cardiovascular Risk After Acute Coronary Syndrome".JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY 75..2(2020):133-144
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