Tissue Characterisation in Acquired Heart Disease with Cardiovascular Magnetic Resonance Imaging

Objectives: To apply and refine conventional and developing cardiac magnetic resonance (CMR) imaging tissue characterisation techniques, with the aim of applying them to better understand cardiac remodelling in health, disease and as an outcome surrogate in clinical trials.

Background: Cardiac structure, function and perfusion are routinely assessed with a range of imaging modalities in both research and clinical practice. Cardiac magnetic resonance (CMR) imaging is emerging as the gold standard tool for many of these assessments. The use of gadolinium containing contrast agents in CMR protocols allows the detection of myocardial scar and focal fibrosis and provides important prognostic information. The developing field of T1 mapping allows measurement of the extracellular volume, a surrogate for fibrosis that offers further insights into diffuse myocardial change not previously possible.

Methods: CMR tissue characterisation techniques were applied in sequential studies of: ischaemic cardiomyopathy, health, athletic cardiac adaptation and in a randomised controlled study examining the effects of spironolactone in heart failure with preserved ejection fraction.

Results & Conclusions: Late gadolinium enhancement (LGE) imaging is of limited application in predicting functional recovery of dysfunctional segments in ischaemic cardiomyopathy (Chapter 3). Modified Look-Locker Inversion recovery (MOLLI) T1 and extracellular mapping techniques can be applied reproducibly in health and following either bolus or split dose gadolinium administration (Chapters 4 & 5). T1 mapping provides important insights into athletic cardiac remodelling that may allow its application in distinguishing between athletic and myopathic change (Chapter 6). Individuals with heart failure with preserved ejection fraction (HF-PEF) have diffuse myocardial fibrosis as measured with T1 mapping. Early results of a randomised controlled study suggest that the beneficial effects of spironolactone in HF-PEF may in part be due to regression of diffuse myocardial fibrosis (Chapter 7).