The future of imaging in cardiovascular disease intervention trials: 2017 and beyond - PubMed (original) (raw)

Review

The future of imaging in cardiovascular disease intervention trials: 2017 and beyond

Mhairi K Doris et al. Curr Opin Lipidol. 2016 Dec.

Abstract

Purpose of review: As our understanding of cardiovascular disease has advanced over the past decades, multiple novel treatment strategies have been developed with the hope of reducing the global morbidity and mortality associated with this condition. Large-scale trials to test such novel therapies using clinical end points are expensive, leading to interest in phase II clinical trials with imaging-derived outcome measures.

Recent findings: Noninvasive imaging techniques that assess changes in both atherosclerotic disease burden and plaque composition in response to therapy are well established. With the advent of molecular techniques and hybrid imaging, we now have the ability to assess disease activity alongside these standard anatomic assessments. This multifaceted approach has the potential to provide a more comprehensive assessment of the actions and efficacy of novel therapies in the carotids, aorta and coronary arteries.

Summary: This review will examine how advanced noninvasive imaging strategies have been used to investigate drug efficacy in intervention trials to date, and crucially how these approaches are set to evolve and play a central role in developing the next generation of atherosclerotic medication.

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Conflict of interest statement

Conflicts of Interest

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Figures

Figure 1

Figure 1. The impact of therapy on plaque composition

Patient treated with statins. T1 weighted MRI sequences demonstrate a high-intensity plaque (HIP) with a PMR of 1.68 in the proximal segment of the left anterior descending artery (LAD) at baseline (A, yellow dotted circle). This HIP corresponds to the low-density coronary plaque with positive remodeling in the proximal portion of the LAD on CTA (B). Cross-sectional CTA images of this HIP lesion show positive remodeling with low attenuation plaque (LAP) (a, b, c). After 12 months of intensive statin treatment, PMR decreased to 1.08 (C, yellow dotted circle). CTA at follow-up shows a decrease in LAP volume (D, d, e, f). Patient not treated with statins. Noncontrast T1-weighted imaging at baseline does not show any HIPs. The PMR was 0.92 in a lesion in the proximal segment of the right coronary artery (E, yellow dotted circle,), which corresponds to a minor coronary plaque on CTA (F, a, b, c). However, after 12 months, a representative HIP was observed at the same lesion in the right coronary artery (G, yellow dotted circle), accompanied by an increase in the PMR to 1.35. CTA shows significant progression of coronary plaque morphology (H, d, e, f). PMR: Plaque to Myocardium Ratio Figure reproduced from Noguchi et al. J Am Coll of Cardiol. 2015;66(3):245–56.

Figure 2

Figure 2. The effect of therapy on disease activity

T2*-weighted imaging of a left common carotid artery before and after ultrasmall superparamagnetic iron oxide (USPIO) infusion at 0 (A and B), and 12 weeks (C and D). (B) USPIO uptake can clearly be seen in the plaque at baseline (yellow arrowhead). (C) Pre-USPIO imaging remains very similar at 12 weeks (red arrowhead). (D) Signal enhancement post-USPIO can be seen with no evidence of signal voids (blue arrowheads) (indicating minimal USPIO uptake and a lack of activated macrophages). Effects of simvastatin on 18FDG uptake in atherosclerotic plaque inflammation (E–H). FDG-PET images and fused PET/CT image demonstrate FDG signal in the aortic arch and carotid arteries (E and F). Repeat imaging following simvastatin reveals attentuation of FDG signal (G and H) Figures A–D reproduced from Tang et al J Am Coll Cardiol, 2009; 53(22):2039–2050. Figures E–H reproduced from Tahara N et al. J Am Coll Cardiol 2006;48(9):1825–31.

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