| Summary: | Immune-mediated inflammatory diseases (IMID) are a group distinguished by specific pathways of immune-dysregulation that lead to inflammation, organ damage and dysfunction, of which Rheumatoid Arthritis (RA) and Giant Cell Arteritis (GCA) are two examples. An increased risk of cardiovascular disease (CVD) is observed in patients with IMID. Inflammation plays an important role in atherosclerosis. The inflammatory process has confounding effects on lipid and glucose metabolism, blood pressure and haemostatic factors. RA is a chronic inflammatory arthritis and one of the most common systemic autoimmune diseases affecting approximately 1% of the UK population. In RA, the risk of myocardial infarction (MI) is independent of, and incremental to, traditional CVD risk factors. CVD, as a direct result of the IMID process and independent of atherosclerosis can be an additional insult and seen in GCA. GCA is associated with an increased mortality mainly due to CVD, including aortic syndromes. Aortic involvement in GCA may manifest clinically as a syndrome of systemic inflammation without specific symptoms, or even be asymptomatic until aortic dissection or rupture supervenes with life-threatening consequences. The early identification of disease can benefit patients clinically by initiation of earlier disease modifying therapy, potentially reducing morbidity and mortality. Determining disease phenotype is important to develop effective screening strategies. This thesis aims to identify subclinical cardiovascular (CV) change using cardiovascular magnetic resonance (CMR) in the IMIDs of RA and GCA. It is also tested whether therapeutic interventions can modulate surrogate markers of CV outcomes in RA. Using CMR, this thesis demonstrates the presence of CV abnormalities in early RA (ERA) and established GCA. Changes in vascular function, myocardial tissue composition and ventricular geometry/performance are present in ERA, inferring an increased risk of CVD at the earliest stages of the RA disease continuum. There are thoracic aortic structural changes in established, treated, GCA. Dilatation of the thoracic aorta is common in GCA, with polymyalgic symptoms a possible risk factor. Patients with GCA also had increased aortic arterial stiffness than controls. CMR is able to detect subclinical CV change in asymptomatic ERA and established GCA patients without known CVD. Surrogate markers of CV events can be modulated in ERA with early aggressive RA therapy and CMR can identify silent aortic dilatation, associated with adverse outcomes, in GCA. CMR can aid the early and appropriate diagnosis of disease and complications, and potentially identify those at the highest risk of adverse outcomes.
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