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Published on: April 17, 2021
Diminished response to statins predicts the occurrence of heart failure after acute myocardial infarction
Kosuke Tsuda1,2, Yu Kataoka1, Soshiro Ogata3
1Department of Cardiovascular Medicine, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan.
Insights
Poor response to statin therapy significantly increases heart failure risk in acute myocardial infarction patients. Identifying statin hyporesponse is crucial for managing heart failure (HF) risk post-myocardial infarction (AMI).
Area of Science:
- Cardiology
- Pharmacogenomics
- Preventive Medicine
Background:
- Statin therapy is vital for managing low-density lipoprotein cholesterol (LDL-C) after acute myocardial infarction (AMI).
- While statins reduce atherosclerotic events, their impact on heart failure (HF) occurrence and individual response variability requires further investigation.
- Understanding statin response variability is key to optimizing HF prevention post-AMI.
Purpose of the Study:
- To investigate the association between statin response variability and the incidence of heart failure (HF) in patients following acute myocardial infarction (AMI).
Main Methods:
- Analysis of 505 statin-naïve AMI patients treated with atorvastatin, rosuvastatin, or pitavastatin post-primary percutaneous coronary intervention (PCI).
- Statin hyporesponse defined as <15% LDL-C reduction at 1 month.
- Comparison of HF outcomes between statin hyporesponders and non-hyporesponders over a median 4.4-year follow-up.
Main Results:
- Statin hyporesponse occurred in 15.2% of subjects.
- Statin hyporesponders showed a significantly higher risk of HF (HR=3.01, P=0.01).
- This association remained significant across multivariate Cox models, propensity score-matched cohorts, and inverse probability of treatment weights analyses.
Conclusions:
- Hyporesponse to statins is a significant risk factor for developing heart failure (HF) after acute myocardial infarction (AMI).
- Identifying patients with statin hyporesponse is critical for risk stratification and targeted HF prevention strategies.
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:
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:
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:
Hyporesponse to statins increases HF risk after AMI. Our findings highlight statin hyporesponse as a high-risk feature associated with HF events.
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