Outcome of pitavastatin versus atorvastatin therapy in patients with hypercholesterolemia at high risk for atherosclerotic cardiovascular disease.


Journal

International journal of cardiology
ISSN: 1874-1754
Titre abrégé: Int J Cardiol
Pays: Netherlands
ID NLM: 8200291

Informations de publication

Date de publication:
15 04 2020
Historique:
received: 09 08 2019
revised: 24 12 2019
accepted: 08 01 2020
pubmed: 29 1 2020
medline: 15 5 2021
entrez: 29 1 2020
Statut: ppublish

Résumé

There has been no report about outcome of pitavastatin versus atorvastatin therapy in high-risk patients with hypercholesterolemia. Hypercholesterolemic patients with one or more risk factors for atherosclerotic diseases (n = 664, age = 65, male = 54%, diabetes = 76%, primary prevention = 74%) were randomized to receive pitavastatin 2 mg/day (n = 332) or atorvastatin 10 mg/day (n = 332). Follow-up period was 240 weeks. The primary end point was a composite of cardiovascular death, sudden death of unknown origin, nonfatal myocardial infarction, nonfatal stroke, transient ischemic attack, or heart failure requiring hospitalization. The secondary end point was a composite of the primary end point plus clinically indicated coronary revascularization for stable angina. The mean low-density lipoprotein cholesterol (LDL-C) level at baseline was 149 mg/dL. The mean LDL-C levels at 1 year were 95 mg/dL in the pitavastatin group and 94 mg/dL in the atorvastatin group. There were no differences in LDL-C levels between both groups, however, pitavastatin significantly reduced the risk of the primary end point, compared to atorvastatin (pitavastatin = 2.9% and atorvastatin = 8.1%, HR, 0.366; 95% CI 0.170-0.787; P = 0.01 by multivariate Cox regression) as well as the risk of the secondary end point (pitavastatin = 4.5% and atorvastatin = 12.9%, HR = 0.350; 95%CI = 0.189-0.645, P = 0.001). The results for the primary and secondary end points were consistent across several prespecified subgroups. There were no differences in incidence of adverse events between the statins. Pitavastatin therapy compared with atorvastatin more may prevent cardiovascular events in hypercholesterolemic patients with one or more risk factors for atherosclerotic diseases despite similar effects on LDL-C levels.

Sections du résumé

BACKGROUND
There has been no report about outcome of pitavastatin versus atorvastatin therapy in high-risk patients with hypercholesterolemia.
METHODS
Hypercholesterolemic patients with one or more risk factors for atherosclerotic diseases (n = 664, age = 65, male = 54%, diabetes = 76%, primary prevention = 74%) were randomized to receive pitavastatin 2 mg/day (n = 332) or atorvastatin 10 mg/day (n = 332). Follow-up period was 240 weeks. The primary end point was a composite of cardiovascular death, sudden death of unknown origin, nonfatal myocardial infarction, nonfatal stroke, transient ischemic attack, or heart failure requiring hospitalization. The secondary end point was a composite of the primary end point plus clinically indicated coronary revascularization for stable angina.
RESULTS
The mean low-density lipoprotein cholesterol (LDL-C) level at baseline was 149 mg/dL. The mean LDL-C levels at 1 year were 95 mg/dL in the pitavastatin group and 94 mg/dL in the atorvastatin group. There were no differences in LDL-C levels between both groups, however, pitavastatin significantly reduced the risk of the primary end point, compared to atorvastatin (pitavastatin = 2.9% and atorvastatin = 8.1%, HR, 0.366; 95% CI 0.170-0.787; P = 0.01 by multivariate Cox regression) as well as the risk of the secondary end point (pitavastatin = 4.5% and atorvastatin = 12.9%, HR = 0.350; 95%CI = 0.189-0.645, P = 0.001). The results for the primary and secondary end points were consistent across several prespecified subgroups. There were no differences in incidence of adverse events between the statins.
CONCLUSION
Pitavastatin therapy compared with atorvastatin more may prevent cardiovascular events in hypercholesterolemic patients with one or more risk factors for atherosclerotic diseases despite similar effects on LDL-C levels.

Identifiants

pubmed: 31987664
pii: S0167-5273(19)34045-8
doi: 10.1016/j.ijcard.2020.01.006
pii:
doi:

Substances chimiques

Hydroxymethylglutaryl-CoA Reductase Inhibitors 0
Pyrroles 0
Quinolines 0
Atorvastatin A0JWA85V8F
pitavastatin M5681Q5F9P

Types de publication

Journal Article Randomized Controlled Trial

Langues

eng

Sous-ensembles de citation

IM

Pagination

139-146

Informations de copyright

Copyright © 2020 The Authors. Published by Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest Any potential conflicts of interest, including related consultancies, shareholding and funding grants: Dr. Moroi received a research grant from, Bayer Yakuhin, Ltd, Sanofi KK, MSD KK, Novartis Pharma, Ltd., Teijin Pharma Ltd., Mitsubishi Tanabe Pharma Corporation, Takeda Pharmaceutical Co., Ltd., and Nihon Mediphysics, Ltd. Dr. Shiba received grants and personal fees from Mitsubishi Tanabe Pharma, grants and personal fees from Daiichi Sankyo Company, Limited, grants and personal fees from Ono Pharmaceutical Co., Ltd., personal fees from Eli Lilly Japan K.K., personal fees from Boehringer Ingelheim, personal fees from Merck Sharp & Dohme (MSD), personal fees from Novartis Pharma, personal fees from Novo Nordisk Pharma Ltd., outside the submitted work. The remaining authors have nothing to disclose.

Auteurs

Masao Moroi (M)

Division of Cardiovascular Medicine (Ohashi), Department of Internal Medicine, Faculty of Medicine, Toho University, Tokyo, Japan. Electronic address: moroi@med.toho-u.ac.jp.

Daiji Nagayama (D)

Nagayama Clinic, Oyama City, Tochigi, Japan.

Fumihiko Hara (F)

Division of Cardiovascular Medicine (Omori), Department of Internal Medicine, Faculty of Medicine, Toho University, Tokyo, Japan.

Atsuhito Saiki (A)

Division of Diabetes, Endocrinology and Metabolism (Sakura), Department of Internal Medicine, Faculty of Medicine, Toho University, Chiba, Japan.

Kazuhiro Shimizu (K)

Division of Cardiovascular Medicine (Sakura), Department of Internal Medicine, Faculty of Medicine, Toho University, Chiba, Japan.

Mao Takahashi (M)

Division of Cardiovascular Medicine (Sakura), Department of Internal Medicine, Faculty of Medicine, Toho University, Chiba, Japan.

Naoko Sato (N)

Pharmaceutical Unit, Toho University Sakura Medical Center, Chiba, Japan.

Teruo Shiba (T)

Division of Diabetes and Metabolism (Ohashi), Department of Internal Medicine, Faculty of Medicine, Toho University, Tokyo, Japan.

Hideki Sugimoto (H)

Division of Neurology (Ohashi), Department of Internal Medicine, Faculty of Medicine, Toho University, Tokyo, Japan.

Toshiki Fujioka (T)

Division of Neurology (Ohashi), Department of Internal Medicine, Faculty of Medicine, Toho University, Tokyo, Japan.

Tatsuo Chiba (T)

Department of Pharmacy, Toho University Omori Medical Center, Tokyo, Japan.

Kosuke Nishizawa (K)

Department of Pharmacy, Toho University Omori Medical Center, Tokyo, Japan.

Shuki Usui (S)

Division of Diabetes, Endocrinology and Metabolism (Omori), Department of Internal Medicine, Faculty of Medicine, Toho University, Tokyo, Japan.

Yasuo Iwasaki (Y)

Division of Neurology (Omori), Department of Internal Medicine, Faculty of Medicine, Toho University, Tokyo, Japan.

Ichiro Tatsuno (I)

Division of Diabetes, Endocrinology and Metabolism (Sakura), Department of Internal Medicine, Faculty of Medicine, Toho University, Chiba, Japan.

Kaoru Sugi (K)

Division of Cardiovascular Medicine (Ohashi), Department of Internal Medicine, Faculty of Medicine, Toho University, Tokyo, Japan.

Junichi Yamasaki (J)

Division of Cardiovascular Medicine (Omori), Department of Internal Medicine, Faculty of Medicine, Toho University, Tokyo, Japan.

Shigeo Yamamura (S)

Faculty of Pharmaceutical Sciences, Josai International University, Chiba, Japan.

Kohji Shirai (K)

Division of Diabetes, Endocrinology and Metabolism (Sakura), Department of Internal Medicine, Faculty of Medicine, Toho University, Chiba, Japan.

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