New methods to image unstable atherosclerotic plaques

Abstract

Atherosclerotic plaque rupture is the primary mechanism responsible for myocardial infarction and stroke, the top two killers worldwide. Despite being potentially fatal, the ubiquitous prevalence of atherosclerosis amongst the middle aged and elderly renders individual events relatively rare. This makes the accurate prediction of MI and stroke challenging. Advances in imaging techniques now allow detailed assessments of plaque morphology and disease activity. Both CT and MR can identify certain unstable plaque characteristics thought to be associated with an increased risk of rupture and events. PET imaging allows the activity of distinct pathological processes associated with atherosclerosis to be measured, differentiating patients with inactive and active disease states. Hybrid integration of PET with CT or MR now allows for an accurate assessment of not only plaque burden and morphology but plaque biology too. In this review, we discuss how these advanced imaging techniques hold promise in redefining our understanding of stable and unstable coronary artery disease beyond symptomatic status, and how they may refine patient risk-prediction and the rationing of expensive novel therapies.

Keywords: Computed tomography; Positron emission tomography; Unstable plaque.

Fig. 1.

Schematic representation of morphological and biological targets for unstable plaque imaging.

Fig. 2.

FDG performance in early phase clinical trials. (A) CT on the left with corresponding PET image on the right demonstrating FDG uptake in culprit carotid plaque (B) How FDG PET CT imaging can be applied to the aorta and myocardium.

Fig. 3.

Detection of coronary atherosclerotic inflammation by 68Ga DOTATATE. The panels in the top row show the culprit lesion in the circumflex artery with corresponding angiogram (A), CT (B), and PET CT with 68GA DOTATATE (C) and FDG (D). The bottom row of panels illustrates a bystander lesion in the proximal right coronary artery which is appears of moderate stenosis on angiography (A), appears non-calcified and positively remodeled on CT angiography (F) and has a clear correlation of DOTATATE (G) and FDG (H) uptake [78].

Fig. 4.

FMISO quantifies hypoxia in carotid plaques. (A) Plaque in left internal carotid on contrast enhanced cr. Co-registered PET images with FDG (B) and FMISO (C) demonstrate a strong correlation of tracer uptake.

Fig. 5.

CT characteristics of ¹⁸F-NaF uptake. Coronary angiography in LAO caudal view showing severe proximal LAD lesion (A, arrowed). Note co-localised PET uptake in (B, arrowed). CT allows assessment of plaque density in (C) (<30 Hounsfield units). Hybrid PET CT in (D) shows co-localisation of 18-fluoride uptake.

Fig. 6.

A potential novel definition of stable and unstable coronary artery disease. Note: this proposal would require extensive research and investigation before it could be recommended in routine clinical practice. Pending this current guideline, recommendations for revascularsation and the prescription of optimal medical therapy should be followed.