Advances in Molecular Imaging: Plaque Imaging

Here’s the abstract of a review we published recently in Current Cardiovascular Imaging Reports:-

Recent advances in nuclear plaque imaging aim to achieve noninvasive identification of vulnerable atherosclerotic plaques using positron emission tomography (PET) with 18F-fluorodexoyglucose (FDG) and novel tracers targeting molecular markers of inflammation and other active metabolic processes.

Nuclear imaging of atherosclerosis has been demonstrated in multiple vascular beds, including the carotid, aorta, peripheral and coronary arteries—but significant challenges remain, especially for coronary imaging. The advantage of PET over other molecular imaging modalities is its superior sensitivity, however, low spatial resolution means that images must be co-registered with computed tomography (CT) or magnetic resonance imaging (MRI) for precise anatomical localization of the PET signal.

Such hybrid techniques provide the best hope for early detection of prospective culprit lesions—which may, in the coronary vasculature, appear falsely low-risk using conventional coronary angiography or stress imaging.

Current hot topics in nuclear plaque imaging include the use of FDG-PET for therapeutic monitoring in drug development, identification of imaging biomarkers to evaluate cardiovascular risk, and the development of novel tracers against an array of biologically important markers of atherosclerosis.

The purpose of this article is to review these recent advances in nuclear plaque imaging.

The full article is available here, behind a paywall. I can send reprints as PDFs on request.

Advice for aspiring cardiologists from Harvard Professor Peter Libby

This short interview with Peter Libby from Harvard contains some good advice for those considering an academic cardiology career. Some highlights:

  • Try and continue to do some clinical cardiology alongside research
  • Research is a vocation. It is something you can't help yourself from doing.
  • Most experiments don't work
  • Be prepared for disappointment
  • Discovering something new is phenomenally exciting

Here is a link to the video

Risk factor control or drug therapy in lowering cardiovascular deaths

I'm not sure exactly how this intriguing graph was constructed, but it demonstrates that nearly half of the reduction in CHD deaths over the past 50 years is due to new therapies, whilst most of the remainder stems from better risk factor control.

From the ESC Guidelines

Another approach to understanding the changes in CVD mortality and incidence rates is by applying models such as the IMPACT mortality model. Based on information on changes in coronary risk factors and in treatment as obtained from the results of RCTs regarding the effectiveness of different treatment modalities, it estimates the expected influence on CHD mortality by age and gender. This model has been applied in different countries; the results from these studies are rather consistent and similar to what has been observed in other studies of the same subject, as summarised in Figure 1. Beneficial reductions in major risk factors—in particular smoking, BP, and cholesterol—accounted for more than half of the decrease in CHD deaths, although they were counteracted by an increase in the prevalence of obesity and type 2 diabetes; 40% of the decline in CHD death rates is attributed to better treatments of acute myocardial infarction, heart failure, and other cardiac conditions. Results from clinical trials and natural experiments also show that a decline in CHD mortality can happen rapidly after individual or population-wide changes in diet or smoking.

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Percentage of the decrease in deaths from coronary heart disease attributed to treatments and risk factor changes in different populations (adapted from Di Chiara et al. Does surveillance impact on cardiovascular prevention? Eur Heart J 2009;30:1027–1029.)

British Heart Foundation's Reflections of Research Competition

A video that we submitted to the British Heart Foundation's "Reflections of Research" competition has won in the best video category.

We made this video to highlight the variety of imaging methods that we have at our disposal to image atherosclerosis and its consequences.

Some more coverage on the Cambridge BRC website and the Addenbrooke's Hospital homepage.

Click here to view the other winning entries.

Imaging of progression of carotid atherosclerosis - case unproven

A study I recently read in the Lancet reports results of an individual patient data meta-analysis, which show that cIMT progression is not associated with incident myocardial infarction, stroke, or vascular death in the general population (hazard ratio 0·98, 95% CI 0·95–1·01, adjusted for age, sex, mean common carotid artery intima-media thickness, and vascular risk factors).

A single measure of carotid IMT may be useful for predicting risk in asymptomatic intermediate risk adults, although far less so than calcium scoring by CT according to the most recent guidelines.

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Interaction of calcification and inflammation in atherosclerosis

Cocker J Nucl Cardiol 2012 Imaging atherosclerosis with hybrid  18F fluorodeoxyglucose positron emission tomographycomputed tomography imaging What Leonardo da Vinci could not see pdf  page 10 of 15

The diagram above seems a logical appraisal of the situation, published recently by Cocker and colleagues.

A proposed schematic staging inflammatory and calcification activity within atherosclerotic lesions with FDG and NaF as imaging biomarkers. During early stages of atherosclerosis, inflammation is the predominant mechanism active within plaque. During these stages, [18F]FDG may be taken up by the lesion. As inflammation peaks, the risk of plaque rupture may increase. Inflammation also contributes toward initiating calcium metabolism within lesions that results in the formation of early calcium deposits. This would be reflected by uptake of both FDG and hydroxyapatite-specific [18F]sodium fluoride (NaF). Once the density of calcium deposits exceeds a certain threshold, it becomes visible with CT. During active calcification, plaque may still be vulnerable. Eventually, the calcification and mineralization processes exceed the inflammatory activity present within plaque, which might be demarcated by only NaF uptake (in the absence of FDG), as well as calcium deposits on CT. Ongoing calcification eventually leads to forming an end- stage stable atheroma that is densely calcified with only evidence for calcium on CT. Model of plaque progression (top bar) is adapted from Koenig and Khuseyinova.