Diminished response to statins predicts the occurrence of heart failure after acute myocardial infarction.

Acute myocardial infarction (AMI) heart failure low-density lipoprotein cholesterol (LDL-C) statin

Journal

Cardiovascular diagnosis and therapy
ISSN: 2223-3652
Titre abrégé: Cardiovasc Diagn Ther
Pays: China
ID NLM: 101601613

Informations de publication

Date de publication:
Aug 2020
Historique:
entrez: 24 9 2020
pubmed: 25 9 2020
medline: 25 9 2020
Statut: ppublish

Résumé

Lowering low-density lipoprotein cholesterol (LDL-C) levels using a statin is a cornerstone of preventive therapeutic management following acute myocardial infarction (AMI). In addition to its anti-atherosclerotic effects, recent studies reported a lower occurrence of heart failure (HF) under statin therapy. However, there is a wide variability in statin response. The association between the response to statin and the occurrence of HF in AMI subjects remains unclear. The purpose of present study is to examine whether the variability in statin response affects HF risk after AMI. We analyzed 505 statin-naïve AMI subjects undergoing primary percutaneous coronary intervention (PCI) who commenced atorvastatin, rosuvastatin, or pitavastatin. Statin hyporesponse was defined as a reduction in LDL-C levels <15% from baseline to 1 month after statin therapy. HF outcomes were compared between patients with and without statin hyporesponse. Statin hyporesponse was identified in 15.2% (77/505) of study subjects. During a median 4.4-year observational period, statin hyporesponse was associated with a greater likelihood of HF [hazard ratio (HR) =3.01, 95% confidence interval (CI): 1.27-6.79, P=0.01]. This increased HF risk in statin hyporesponders was consistently observed in a multivariate Cox proportional hazards model (HR =2.74, 95% CI: 1.01-6.75, P=0.04), a propensity score-matched cohort (HR =12.30, 95% CI: 1.50-100.3, P=0.01) and in an inverse probability of treatment weights analysis with average treatment effects (coefficient =7.02, 95% CI: 2.29-21.58, P=0.0006). Hyporesponse to statins increases HF risk after AMI. Our findings highlight statin hyporesponse as a high-risk feature associated with HF events.

Sections du résumé

BACKGROUND BACKGROUND
Lowering low-density lipoprotein cholesterol (LDL-C) levels using a statin is a cornerstone of preventive therapeutic management following acute myocardial infarction (AMI). In addition to its anti-atherosclerotic effects, recent studies reported a lower occurrence of heart failure (HF) under statin therapy. However, there is a wide variability in statin response. The association between the response to statin and the occurrence of HF in AMI subjects remains unclear. The purpose of present study is to examine whether the variability in statin response affects HF risk after AMI.
METHODS METHODS
We analyzed 505 statin-naïve AMI subjects undergoing primary percutaneous coronary intervention (PCI) who commenced atorvastatin, rosuvastatin, or pitavastatin. Statin hyporesponse was defined as a reduction in LDL-C levels <15% from baseline to 1 month after statin therapy. HF outcomes were compared between patients with and without statin hyporesponse.
RESULTS RESULTS
Statin hyporesponse was identified in 15.2% (77/505) of study subjects. During a median 4.4-year observational period, statin hyporesponse was associated with a greater likelihood of HF [hazard ratio (HR) =3.01, 95% confidence interval (CI): 1.27-6.79, P=0.01]. This increased HF risk in statin hyporesponders was consistently observed in a multivariate Cox proportional hazards model (HR =2.74, 95% CI: 1.01-6.75, P=0.04), a propensity score-matched cohort (HR =12.30, 95% CI: 1.50-100.3, P=0.01) and in an inverse probability of treatment weights analysis with average treatment effects (coefficient =7.02, 95% CI: 2.29-21.58, P=0.0006).
CONCLUSIONS CONCLUSIONS
Hyporesponse to statins increases HF risk after AMI. Our findings highlight statin hyporesponse as a high-risk feature associated with HF events.

Identifiants

pubmed: 32968627
doi: 10.21037/cdt-20-415
pii: cdt-10-04-705
pmc: PMC7487383
doi:

Types de publication

Journal Article

Langues

eng

Pagination

705-716

Informations de copyright

2020 Cardiovascular Diagnosis and Therapy. All rights reserved.

Déclaration de conflit d'intérêts

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at http://dx.doi.org/10.21037/cdt-20-415). YK serves as an unpaid editorial board member of Cardiovascular Diagnosis and Therapy from Jul 2019 to Jun 2021. The other author has no conflicts of interest to declare.

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Auteurs

Kosuke Tsuda (K)

Department of Cardiovascular Medicine, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan.
Department of Cardiology, Osaka Medical College, Takatsuki, Osaka, Japan.

Yu Kataoka (Y)

Department of Cardiovascular Medicine, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan.

Soshiro Ogata (S)

Department of Preventive Medicine and Epidemiology, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan.

Kunihiro Nishimura (K)

Department of Preventive Medicine and Epidemiology, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan.

Ryo Nishikawa (R)

Department of Cardiovascular, Renal and Metabolic Medicine, Sapporo Medical University School of Medicine, Hokkaido, Japan.

Takahito Doi (T)

Department of Cardiovascular Medicine, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan.

Takahiro Nakashima (T)

Department of Cardiovascular Medicine, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan.

Hayato Hosoda (H)

Department of Cardiovascular Medicine, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan.

Satoshi Honda (S)

Department of Cardiovascular Medicine, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan.

Shoji Kawakami (S)

Department of Cardiology, Aso Iizuka Hospital, Iizuka, Fukuoka, Japan.

Masashi Fujino (M)

Department of Cardiovascular Medicine, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan.

Kazuhiro Nakao (K)

Department of Cardiovascular Medicine, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan.

Shuichi Yoneda (S)

Department of Cardiovascular Medicine, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan.

Kensaku Nishihira (K)

Department of Cardiology, Miyazaki Medical Association Hospital Cardiovascular Center, Miyazaki, Japan.

Fumiyuki Otsuka (F)

Department of Cardiovascular Medicine, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan.

Yoshio Tahara (Y)

Department of Cardiovascular Medicine, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan.

Yasuhide Asaumi (Y)

Department of Cardiovascular Medicine, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan.

Masaaki Hoshiga (M)

Department of Cardiology, Osaka Medical College, Takatsuki, Osaka, Japan.

Teruo Noguchi (T)

Department of Cardiovascular Medicine, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan.

Satoshi Yasuda (S)

Department of Cardiovascular Medicine, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan.

Classifications MeSH