- Oral presentation
- Open Access
Role of T1 and T2-mapping in assessing the myocardial interstitium in hypertrophic cardiomyopathy: a cardiovascular magnetic resonance study
© Ismail et al; licensee BioMed Central Ltd. 2013
- Published: 30 January 2013
- Cardiovascular Magnetic Resonance
- Late Gadolinium Enhancement
- Hypertrophic Cardiomyopathy
- Late Gadolinium Enhancement Image
- Cardiovascular Magnetic Resonance Study
Fibrosis is thought to play an important role in the pathogenesis of the adverse sequelae of hypertrophic cardiomyopathy (HCM). Late gadolinium enhancement (LGE) cardiovascular magnetic resonance detects replacement fibrosis but cannot presently detect interstitial fibrosis. The latter is thought to be a very early feature of HCM and can be triggered by inflammation, which can also expand the size of the myocardial interstitium. We sought to determine whether extracellular volume (ECV) mapping by T1-relaxometry in concert with T2-mapping can identify interstitial changes in HCM and whether these were related to myocardial edema.
Twenty HCM patients (mean±SD age: 59.9±9.1 years, 15 male) and 13 healthy volunteers (46.1±11.5 years, 7 male) were studied. Left ventricular T1 and T2 maps were acquired at the base, mid-ventricle and apex in patients and at the mid-ventricle in controls using a modified Look-Locker inversion recovery sequence and a T2-prepared steady-state free precession mapping sequence. Post-contrast T1 maps were acquired a minimum of 15 min after 0.1 mmol/kg gadolinium together with conventional LGE images. After motion correction, pre- and post-contrast T1 parameter maps were co-registered to generate ECV parameter maps. Parameter maps and LGE images were viewed side-by-side and regions of interest (ROI) were drawn in areas with and without LGE. Data were analysed using a linear mixed effects model to account for clustering of ROI within patients.
ECV mapping in HCM detects replacement fibrosis, but was unable to detect interstitial fibrosis. There was no evidence of edema in areas of LGE suggesting that this was not a major contributor to ECV expansion in our HCM cohort.
Characteristic - Mean±SD
Hypertrophic Cardiomyopathy (n=20)
Male - n(%)
Age - years
LV wall thickness - mm
LV-EDV index - ml/m2
LV-ESV index - ml/m2
LV ejection fraction - %
LV Mass Index - g/m2
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