Cardiovascular magnetic resonance of the carotid arterial wall

Abstract

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.