Our understanding of the processes that determine outcomes in patients with ischaemic cardiomyopathy is based on conventional physiological concepts such as ischaemia and viability. Qualitative methods for characterising these processes tend to be binary and often fail to capture the complexity of the underlying biology. Importantly, these are perhaps inadequate to evaluate treatment effects, including the impact of coronary revascularisation.
The aim of this thesis was to deploy novel quantitative cardiac magnetic resonance (CMR) techniques to evaluate and distinguish between the pathophysiological processes that determine outcomes in patients with ischaemic cardiomyopathy, through integration of anatomical, functional, perfusion and tissue characterisation information. The work is centred around the use of coronary artery bypass graft (CABG) surgery as the method for revascularisation, and focuses on the impact of myocardial blood flow alterations on cardiac physiology and clinical outcomes.
In this work, I first evaluate the impact of surgical revascularisation on myocardial structure and function in patients with impaired left ventricular (LV) systolic function, using paired assessments before and after CABG. I found that at 6 months following revascularisation, despite improvement in functional capacity, more than a third of total myocardial segments examined are no longer considered revascularised. As a result, the overall augmentation in global myocardial blood flow (MBF) following CABG surgery is significantly blunted.
There are however technical concerns regarding the quantitative estimation of myocardial blood flow in patients with coronary artery grafts, particularly in relation to the impact of long coronary grafts on contrast kinetics. I therefore evaluated the impact of arterial contrast delay on myocardial blood flow estimation in patients with left internal mammary artery (LIMA) grafts. I showed that absolute MBF estimation is minimally affected by delayed contrast arrival in patients with LIMA grafts, and that irrespective of graft patency, residual native disease severity is a key determinant of myocardial blood flow.
Following these findings, I then assessed the prognostic impact of myocardial blood flow in a large cohort of patients with prior CABG. The only imaging study to date examining the prognostic role of quantitative perfusion indices in this population, it demonstrated that both stress MBF and myocardial perfusion reserve (MPR) independently predict adverse cardiovascular outcomes and all cause-mortality.
Finally, using the existing quantitative perfusion technique and its associated framework, I co-developed and implemented a non-invasive, in-line method of measuring pulmonary transit time (PTT) and pulmonary blood volume (PBV) during routine CMR scanning. I then found that both imaging parameters can be used as independent quantitative prognostic biomarkers in patients with known or suspected coronary artery disease
