Remodeling after acute myocardial infarction: mapping ventricular dilatation using three dimensional CMR image registration
1 Robert Steiner MRI Unit, MRC Clinical Sciences Centre, Imperial College London, Hammersmith Hospital Campus, Du Cane Road, London, W12 0NN, UK
2 Department of Computing, Imperial College London, South Kensington Campus, Exhibition Road, London, SW7 2AZ, UK
3 Department of Imaging, Imperial College Healthcare NHS Trust, Hammersmith Hospital, Du Cane Road, London, W12 0HS, UK
4 Department of Cardiology, Imperial College Healthcare NHS Trust, London, Hammersmith Hospital, Du Cane Road, London, W12 0HS, UK
Journal of Cardiovascular Magnetic Resonance 2012, 14:41 doi:10.1186/1532-429X-14-41Published: 21 June 2012
Progressive heart failure due to remodeling is a major cause of morbidity and mortality following myocardial infarction. Conventional clinical imaging measures global volume changes, and currently there is no means of assessing regional myocardial dilatation in relation to ischemic burden. Here we use 3D co-registration of Cardiovascular Magnetic Resonance (CMR) images to assess the long-term effects of ischemia-reperfusion injury on left ventricular structure after acute ST-elevation myocardial infarction (STEMI).
Forty six patients (age range 33–77 years) underwent CMR imaging within 7 days following primary percutaneous coronary intervention (PPCI) for acute STEMI with follow-up at one year. Functional cine imaging and Late Gadolinium Enhancement (LGE) were segmented and co-registered. Local left ventricular wall dilatation was assessed by using intensity-based similarities to track the structural changes in the heart between baseline and follow-up. Results are expressed as means, standard errors and 95% confidence interval (CI) of the difference.
Local left ventricular remodeling within infarcted myocardium was greater than in non-infarcted myocardium (1.6% ± 1.0 vs 0.3% ± 0.9, 95% CI: -2.4% – -0.2%, P = 0.02). One-way ANOVA revealed that transmural infarct thickness had a significant effect on the degree of local remodeling at one year (P < 0.0001) with greatest wall dilatation observed when infarct transmurality exceeded 50%. Infarct remodeling was more severe when microvascular obstruction (MVO) was present (3.8% ± 1.3 vs −1.6% ± 1.4, 95% CI: -9.1% – -1.5%, P = 0.007) and when end-diastolic volume had increased by >20% (4.8% ± 1.4 vs −0.15% ± 1.2, 95% CI: -8.9% – -0.9%, P = 0.017).
The severity of ischemic injury has a significant effect on local ventricular wall remodeling with only modest dilatation observed within non-ischemic myocardium. Limitation of chronic remodeling may therefore depend on therapies directed at modulating ischemia-reperfusion injury. CMR co-registration has potential for assessing dynamic changes in ventricular structure in relation to therapeutic interventions.