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Effect of Alirocumab on Lipoprotein(a) and Cardiovascular Risk After Acute Coronary Syndrome. / ODYSSEY OUTCOMES Committees and Investigators.

In: Journal of the American College of Cardiology, Vol. 75, No. 2, 21.01.2020, p. 133-144.

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Harvard

ODYSSEY OUTCOMES Committees and Investigators 2020, 'Effect of Alirocumab on Lipoprotein(a) and Cardiovascular Risk After Acute Coronary Syndrome', Journal of the American College of Cardiology, vol. 75, no. 2, pp. 133-144. https://doi.org/10.1016/j.jacc.2019.10.057

APA

ODYSSEY OUTCOMES Committees and Investigators (2020). Effect of Alirocumab on Lipoprotein(a) and Cardiovascular Risk After Acute Coronary Syndrome. Journal of the American College of Cardiology, 75(2), 133-144. https://doi.org/10.1016/j.jacc.2019.10.057

Vancouver

ODYSSEY OUTCOMES Committees and Investigators. Effect of Alirocumab on Lipoprotein(a) and Cardiovascular Risk After Acute Coronary Syndrome. Journal of the American College of Cardiology. 2020 Jan 21;75(2):133-144. https://doi.org/10.1016/j.jacc.2019.10.057

Author

ODYSSEY OUTCOMES Committees and Investigators. / Effect of Alirocumab on Lipoprotein(a) and Cardiovascular Risk After Acute Coronary Syndrome. In: Journal of the American College of Cardiology. 2020 ; Vol. 75, No. 2. pp. 133-144.

BibTeX

@article{d108bfc369c94e7c99199365ed3afdac,
title = "Effect of Alirocumab on Lipoprotein(a) and Cardiovascular Risk After Acute Coronary Syndrome",
abstract = "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.",
keywords = "acute coronary syndromes, alirocumab, low-density lipoprotein cholesterol, major adverse cardiovascular events, proprotein convertase subtilisin/kexin type 9 inhibition, REDUCING LIPIDS, EFFICACY, DISEASE, SAFETY, CHOLESTEROL, NIACIN",
author = "{ODYSSEY OUTCOMES Comm Inv} and Bittner, {Vera A.} and Michael Szarek and Aylward, {Philip E.} and Bhatt, {Deepak L.} and Rafael Diaz and Edelberg, {Jay M.} and Zlatko Fras and Goodman, {Shaun G.} and Sigrun Halvorsen and Corinne Hanotin and Harrington, {Robert A.} and Jukema, {J. Wouter} and Virginie Loizeau and Moriarty, {Patrick M.} and Angele Moryusef and Robert Pordy and Roe, {Matthew T.} and Peter Sinnaeve and Sotirios Tsimikas and Robert Vogel and White, {Harvey D.} and Doron Zahger and Zeiher, {Andreas M.} and Gabriel Steg and Schwartz, {Gregory G.} and Aylward, {Philip E.} and Heinz Drexel and Peter Sinnaeve and Mirza Dilic and Lopes, {Renato D.} and Gotcheva, {Nina N.} and Goodman, {Shaun G.} and Juan-Carlos Prieto and Huo Yong and Patricio Lopez-Jaramillo and Ivan Pecin and Zeljko Reiner and Petr Ostadal and Poulsen, {Steen Hvitfeldt} and Margus Viigimaa and Nieminen, {Markku S.} and Nicolas Danchin and Vakhtang Chumburidze and Nikolaus Marx and Evangelos Liberopoulos and {Montenegro Valdovinos}, {Pablo Carlos} and Hung-Fat Tse and Victor Gurevich and Tatiana Sotnikova and Konstantin Nikolaev",
year = "2020",
month = jan,
day = "21",
doi = "10.1016/j.jacc.2019.10.057",
language = "Английский",
volume = "75",
pages = "133--144",
journal = "Journal of the American College of Cardiology",
issn = "0735-1097",
publisher = "Elsevier",
number = "2",

}

RIS

TY - JOUR

T1 - Effect of Alirocumab on Lipoprotein(a) and Cardiovascular Risk After Acute Coronary Syndrome

AU - ODYSSEY OUTCOMES Comm Inv

AU - Bittner, Vera A.

AU - Szarek, Michael

AU - Aylward, Philip E.

AU - Bhatt, Deepak L.

AU - Diaz, Rafael

AU - Edelberg, Jay M.

AU - Fras, Zlatko

AU - Goodman, Shaun G.

AU - Halvorsen, Sigrun

AU - Hanotin, Corinne

AU - Harrington, Robert A.

AU - Jukema, J. Wouter

AU - Loizeau, Virginie

AU - Moriarty, Patrick M.

AU - Moryusef, Angele

AU - Pordy, Robert

AU - Roe, Matthew T.

AU - Sinnaeve, Peter

AU - Tsimikas, Sotirios

AU - Vogel, Robert

AU - White, Harvey D.

AU - Zahger, Doron

AU - Zeiher, Andreas M.

AU - Steg, Gabriel

AU - Schwartz, Gregory G.

AU - Aylward, Philip E.

AU - Drexel, Heinz

AU - Sinnaeve, Peter

AU - Dilic, Mirza

AU - Lopes, Renato D.

AU - Gotcheva, Nina N.

AU - Goodman, Shaun G.

AU - Prieto, Juan-Carlos

AU - Yong, Huo

AU - Lopez-Jaramillo, Patricio

AU - Pecin, Ivan

AU - Reiner, Zeljko

AU - Ostadal, Petr

AU - Poulsen, Steen Hvitfeldt

AU - Viigimaa, Margus

AU - Nieminen, Markku S.

AU - Danchin, Nicolas

AU - Chumburidze, Vakhtang

AU - Marx, Nikolaus

AU - Liberopoulos, Evangelos

AU - Montenegro Valdovinos, Pablo Carlos

AU - Tse, Hung-Fat

AU - Gurevich, Victor

AU - Sotnikova, Tatiana

AU - Nikolaev, Konstantin

PY - 2020/1/21

Y1 - 2020/1/21

N2 - 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.

AB - 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.

KW - acute coronary syndromes

KW - alirocumab

KW - low-density lipoprotein cholesterol

KW - major adverse cardiovascular events

KW - proprotein convertase subtilisin/kexin type 9 inhibition

KW - REDUCING LIPIDS

KW - EFFICACY

KW - DISEASE

KW - SAFETY

KW - CHOLESTEROL

KW - NIACIN

U2 - 10.1016/j.jacc.2019.10.057

DO - 10.1016/j.jacc.2019.10.057

M3 - статья

VL - 75

SP - 133

EP - 144

JO - Journal of the American College of Cardiology

JF - Journal of the American College of Cardiology

SN - 0735-1097

IS - 2

ER -

ID: 88169504