Cardiovascular magnetic resonance in ST-segment elevation myocardial infarction (CMR in STEMI)

• Main Author: McAlindon, Elisa
• Published: University of Bristol 2015
• Subjects: 616.1
• Online Access: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.681480

Myocardial infarction is a leading cause of morbidity and mortality in the developed world. Cardiovascular magnetic resonance (CMR) is an imaging technique that provides non-invasive tissue characterisation of the myocardium. CMR can, therefore, quantify myocardial infarct characteristics in vivo. This aim of this work is to investigate the CMR parameters used to assess and quantify injury following myocardial infarction. The research questions in this thesis are: • How reliable are the CMR parameters found in myocardial infarction? • Can newer sequences impact on the reliability of the assessment of myocardial oedema? • Are existing sequences available for infarct size measurement interchangable? • How does a functional measure of microvascular dysfunction relate to microvascular obstruction identified on CMR? • What can new T1 and T2 mapping sequences contribute to the assessment of myocardial infarction by CMR? CMR is increasingly being used to quantify surrogate endpoints used in myocardial infarction studies. In Chapter 4, pilot work identified that the reproducibility of these end points can vary depending on the expertise of the observer. Chapter 5 determined the most reliable method available for quantifying myocardial · oedema and myocardial infarction was manual contouring. This technique was then used in Chapter 7 to establish the repeatability of CMR parameters used as surrogate endpoints in clinical trials. Chapter 7 identified that the least reproducible CMR parameter measured in acute myocardial infarction was myocardial oedema. Chapter 8 sought to address this issue by evaluating 4 sequences to identify and quantitate myocardial oedema. Of these, a new T2 mapping sequence was the most reproducible for quantitating myocardial oedema. New mapping sequences, both Tl and T2 mapping were further evaluated in Chapter 11 to investigate a cut off value for T2 value in oedematous myocardium following acute myocardial infarction. Chapter 11 also established that infarct characteristics affect the T2 value in affected myocardium. The association between native Tl and T2 mapping and between the extracellular volume and myocardial oedema was also determined. Chapter 7 also highlighted that quantification of myocardial infarction could be improved. Single shot steady state free precession (SS -SSFP) late gadolinium enhancement imaging was assessed against the standard inversion recovery gradient echo sequences in Chapter 9. Although the identification of myocardial infarction was acceptable with the SS-SSFP, quantification was suboptimal with this sequence and therefore should not be used for quantification of infarct size. Despite restoration of flow to the epicardial infarct related artery following acute myocardial infarction, flow is not necessarily optimal in the microvasculature. Chapter 10 provides an in vivo functional insight into microvascular obstruction (MVO) identified on CMR following ST segment elevation myocardial infarction (STEM!) using an invasive measure (the index of microcirculatory resistanceIMR) at the time of primary angioplasty. There is a good association between the IMR and MVO on CMR