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Non-invasive/Invasive imaging
Molecular imaging of atherosclerosis: clinical state-of-the-art
  1. Farouc A Jaffer1,
  2. Johan W Verjans1,2
  1. 1Massachusetts General Hospital, Harvard Medical School, Cardiovascular Research Center, Boston, Massachusetts, USA
  2. 2Department of Cardiology, Division of Heart and Lungs, University Medical Center Utrecht, Utrecht, the Netherlands
  1. Correspondence to Dr Farouc A Jaffer, Massachusetts General Hospital, Harvard Medical School, Cardiovascular Research Center, 185 Cambridge Street, Simches Building, Room 3206, Boston, MA 02114, USA; fjaffer{at}

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Physicians depend greatly on imaging techniques that help them make clinical decisions. However, when a diagnosis is made on the basis of anatomical imaging alone, the disease process has often advanced beyond the point where preventative therapy can be applied. In many cardiovascular diseases, it is vital to detect pathological and normal processes at an early, subclinical stage, to enable early and improved diagnosis, prediction and treatment (figure 1A). This is particularly relevant to atherosclerosis, which can be clinically silent for decades and then manifest suddenly as an acute myocardial infarction (MI) or stroke.

Figure 1

Clinical molecular imaging concepts. (A) Schematic representation of the value of molecular imaging in the detection of early disease or even pre-disease changes in patients, compared to anatomical imaging capabilities. Patient symptoms usually occur in a later phase where physiological and/or anatomical changes have occurred. (B) Comparative overview table of electromagnetic energy, spatiotemporal resolution of clinical systems, and advantages/disadvantages of molecular imaging modalities. PET, positron emission tomography; SPECT, single photon emission CT.

The holy grail in cardiovascular prevention is to identify individuals at risk for MI or stroke. At present, structural imaging tools such as CT or intravascular ultrasound (IVUS) cannot reliably identify ‘vulnerable’ patients with a high risk plaque that will lead to thrombotic occlusion of a coronary or cerebral artery.w1 w2 Our current understanding of such plaques is largely defined by postmortem studies, but is limited by processing and only provides a single snapshot in the lifetime of a culprit lesion. These studies demonstrate that culprit lesions in acute MI demonstrate acute plaque rupture in ∼60% of cases, plaque erosion in ∼25%, and other mechanisms in the remainder of cases (calcified nodule, other). Plaque rupture is biologically driven by inflammatory cells (macrophages, lymphocytes), destabilising proteases (matrix metalloproteinases, cathepsins), reactive oxygen species, fragile …

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  • Contributors FAJ designed the review, wrote the paper, and critically reviewed the final manuscript. JWV co-wrote the paper, and critically reviewed the final manuscript.

  • Funding NIH R01 HL108229, AHA Grant-in-Aid 13GRNT1760040, MGH SPARK Award, Rubicon Grant 825.12.013/Netherlands Organisation for Scientific Research (JWV).

  • Competing interests In compliance with EBAC/EACCME guidelines, all authors participating in Education in Heart have disclosed potential conflicts of interest that might cause a bias in the article. FAJ has received research support from Abbott Vascular, Merck, and Kowa Ltd. JWV has no competing interests

  • Provenance and peer review Commissioned; externally peer reviewed.

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