Background
Atherosclerosis is a leading cause of death [Lloyd-Jones 2009; Murray 1997] involving
inflammatory processes throughout [Libby 2002]. Cardiovascular disease (CVD) incidence is
increased in generalised inflammatory conditions [Esdaile 2001; Watson 2003; Rosenfeld
2011; Triant 2012]. However, the presence and burden of atherosclerosis in groups with
such conditions but low traditional cardiovascular risk is unclear. The means to reduce
cardiovascular risk in individuals without conventional modifiable risk factors remains
unknown. Carotid arterial wall imaging allows assessment of atheroma burden and the
effects of treatments to reduce it. Cardiovascular magnetic resonance (CMR) is non-invasive,
radiation-free, and allows volumetric measures to be obtained.

Methods and Results
Using previously validated carotid CMR imaging techniques we undertook a series of studies
in two conditions associated with inflammation and increased CVD: systemic lupus
erythematosus (SLE) and HIV. We recruited SLE patients with LDL-cholesterol <3.4mmol/L
into a 2-year placebo-controlled trial of rosuvastatin and evaluated vascular effects: no
benefit from statin therapy on carotid arterial parameters was seen (Chapter 9). We
combined baseline findings with results from a pilot study to further investigate the extent of
CVD in SLE, demonstrating an excess of subclinical atherosclerosis (Chapter 8). In HIV, we
investigated two cohorts using CMR: a group with adult-acquired HIV-infection that revealed
evidence of early subclinical atherosclerosis (Chapter 10) and a group of perinatally infected
young adults that revealed no apparent abnormalities suggesting early atherosclerosis
(Chapter 11).

Conclusions
CMR allows quantification of atherosclerosis in different patient groups. Low traditional CVD
risk SLE and adult HIV-infected patients exhibit subclinical atherosclerosis. It emerges that
clearer assessment of CMR’s limitations, the abnormalities seen in patient subgroups and of
the different arterial wall pathophysiological changes in different inflammatory conditions is
needed before employing carotid parameters as surrogates for assessing the effect of
established or novel treatments on CVD risk.