Abstract:
Background. Transient ischaemic dilation (TID) and left ventricular (LV) stunning on nuclear myocardial perfusion imaging (MPI) are important findings that convey a high risk of subsequent cardiac events. However, the mechanisms leading to TID or stunning on MPI, are not well elucidated. Further, detailed analysis of the clinical factors that may influence the present of TID, apart from severe coronary artery disease, have not been studied. The aim of this thesis was (1) explore the clinical significance of LV stunning on MPI, (2) to determine the likely pathophysiology of both TID and stunning on MPI using concurrent multimodality imaging, and (3) to undertake a careful multivariate analysis of likely clinical risks. Methods. The four published research papers that comprise the body of this research were prospective (3/4) and retrospective (1/4) and used database analysis of multiple clinical and imaging variables. They relied on assessment of both MPI functional data, on concurrent echocardiographic assessment of LV mass index and volumes, and on quantitative coronary analysis of angiographic correlative data (see METHODS section in each chapter). Results and Conclusions; (1) The presence of regional wall motion abnormalities on MPI are highly specific for high grade coronary angiographic stenoses. The sensitivity of a wall motion abnormality is higher than the presence of a perfusion defect (in stenoses >80%), which has important clinical relevance in reducing the false negative results in MPI, particularly in patients with significant left main disease. (2) All patients with TID had diabetes, LVH or both, suggesting the pathophysiology of these disease processes may play an integral role in the manifestation of TID on MPI. (3) The significant drop in both LVEF and increase in LV volumes measured in patients with TID on Adenosine MPI were not measurable on concurrent echocardiography. This suggests that TID on Adenosine MPI is not related to true myocardial stunning, but is a reflection of the severity of the underlying coronary flow reserve abnormality. This also explains the increased incidence of TID in patients with diseases affecting coronary microvascular function such as LVH and diabetes.
