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Updated: May 21, 2026
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Primary Outcome Assessment in a Pig Model of Acute Myocardial Infarction
Published on: October 14, 2016
Remodeling after acute myocardial infarction: mapping ventricular dilatation using three dimensional CMR image
Declan P O'Regan1, Wenzhe Shi, Ben Ariff
1Robert Steiner MRI Unit, MRC Clinical Sciences Centre, Imperial College London, Hammersmith Hospital Campus, Du Cane Road, London W12 0NN, UK. declan.oregan@imperial.ac.uk
Summary
Cardiovascular Magnetic Resonance (CMR) imaging reveals that the severity of heart attack (STEMI) significantly impacts long-term left ventricular remodeling. Limiting ischemia-reperfusion injury may reduce chronic heart remodeling.
Area of Science:
- Cardiology
- Medical Imaging
- Biomedical Engineering
Background:
- Progressive heart failure results from myocardial remodeling post-myocardial infarction, a leading cause of death.
- Current imaging methods assess global heart changes, lacking regional assessment of myocardial dilatation relative to ischemic burden.
- 3D co-registration of Cardiovascular Magnetic Resonance (CMR) images is utilized to evaluate long-term effects of ischemia-reperfusion injury on left ventricular structure after acute ST-elevation myocardial infarction (STEMI).
Purpose of the Study:
- To assess long-term left ventricular structural changes after acute ST-elevation myocardial infarction (STEMI) using 3D co-registered CMR.
- To investigate the relationship between regional myocardial dilatation and ischemic burden.
- To evaluate the impact of ischemia-reperfusion injury on left ventricular remodeling.
Main Methods:
- Forty-six STEMI patients underwent CMR imaging within 7 days and at one year post-primary percutaneous coronary intervention (PPCI).
- Functional cine imaging and Late Gadolinium Enhancement (LGE) were segmented and co-registered.
- Intensity-based similarities tracked local left ventricular wall dilatation between baseline and follow-up.
Main Results:
- Local left ventricular remodeling was significantly greater in infarcted (1.6%±1.0) versus non-infarcted myocardium (0.3%±0.9).
- Transmural infarct thickness significantly affected remodeling, with greatest dilatation observed when infarct transmurality exceeded 50%.
- Remodeling was more severe with microvascular obstruction (MVO) and increased end-diastolic volume (>20%).
Conclusions:
- Ischemic injury severity significantly influences local ventricular wall remodeling, with minimal dilatation in non-ischemic areas.
- Limiting chronic remodeling may necessitate therapies targeting ischemia-reperfusion injury.
- CMR co-registration shows potential for assessing dynamic ventricular structural changes and therapeutic intervention effects.
