detected both broad-spectrum MMP activity and apoptosis in inflamed rabbit plaques via combined 99mTc-RP805 (MMP) and 111In-annexin A5 imaging (macrophages/apoptosis) (25)

detected both broad-spectrum MMP activity and apoptosis in inflamed rabbit plaques via combined 99mTc-RP805 (MMP) and 111In-annexin A5 imaging (macrophages/apoptosis) (25). studies, of particular benefit in the management of cardiovascular disease (CVD). Molecular imaging investigations of CVD continue to increase each year. Over the past year, significant gains in clinical applications and new technology have been achieved in vascular and myocardial imaging. In this update, we have the privilege to highlight recent outstanding clinical and translational molecular imaging (MOLI) studies of CVD. II. Vascular Imaging A. Atherosclerosis Atherosclerosis remains a dominant focus for CVD molecular imaging studies. This field is driven by the quest to identify biologically high-risk vulnerable plaques (e.g. heightened plaque inflammation, neovascularization, or apoptosis). Molecular imaging therefore complements traditional anatomical imaging approaches that identify plaque structure and composition. Clinical molecular Lamin A antibody imaging studies of atherosclerosis have grown substantially in recent years. The two leading clinical platforms remain 18F-fluorodeoxyglucose (FDG) imaging of plaque metabolic activity/inflammation by positron emission tomography (PET), and ultrasmall superparamagnetic iron oxide (USPIO) nanoparticle-enhanced MRI of plaque macrophages. These modalities primarily interrogate the carotid arteries and larger vascular beds, although recent preliminary reports suggest the potential for noninvasive coronary plaque imaging. Clinical 18FDG PET molecular imaging studies of atherosclerosis 18FDG is a glucose analog trapped intracellularly by metabolically active cells, and Nitro blue tetrazolium chloride therefore enables PET-based detection of metabolism. 18FDG has been used extensively in cancer and myocardial viability studies. Pioneering work from the last decade demonstrated that 18FDG could enable PET imaging of inflamed subsets of carotid atheromata of human subjects. Subsequent correlational Nitro blue tetrazolium chloride analyses established a link between 18FDG signals and plaque macrophages, or inflammation. Consistent with the widespread ability to perform clinical 18FDG PET imaging, large vessel atherosclerosis metabolism/inflammation studies have grown substantially in the last several years. Several recent 18FDG plaque investigations have shed new light on the clinical utility, pathophysiology, and spatial distribution of plaque metabolism/inflammation. In an observational 18FDG PET/CT study of 932 cancer patients, increased 18FDG uptake (mean large vessel plaque target-to-background ratio (TBR) 1.7) was the strongest predictor of a future vascular event, which occurred in 1.6% of patients at a median follow-up time of 29 months (1). Importantly, the 18FDG signal was 4-fold-more predictive of a future vascular event compared to the degree of plaque calcification noted on co-registered CT. A retrospective study of 200 patients demonstrated a correlation between cardiovascular risk factors and the number of 18FDG-positive plaques, and an inverse association between statin therapy and 18FDG-positive plaques (2). In new pathophysiologic studies, 18FDG plaque signals rarely overlapped with plaque calcification, further suggesting that CT-detected calcification may indicate a burnt-out plaque phenotype. 18FDG plaque uptake was greater in patients with a history of CAD and also associated with the inflammatory serum biomarkers matrix metalloproteinase (MMP)-3 and MMP-9 (3). In multimodal 18FDG PET/CT and MRI studies of carotid plaques, one MRI study found that lipid-rich plaques had higher 18FDG signal intensities than collagen-rich Nitro blue tetrazolium chloride or calcified plaques (4), while another study noted weak correlations between 18FDG plaque indicators and plaque compositional variables produced from CT and MRI (5). Finally a report of ten carotid endarterectomy sufferers further connected 18FDG uptake to plaque irritation (6). The inflammatory mRNA markers macrophage Compact disc68, cathepsin K, matrix metalloproteinase (MMP)-9, and interleukin-18 correlated with the 18FDG TBR favorably, with Compact disc68 getting the most powerful association (r=0.71, p=0.02). Within an interesting preliminary progress, 18FDG Family pet/CT allowed the noninvasive recognition of coronary plaque fat burning capacity/irritation (Amount 1) (7). Nitro blue tetrazolium chloride History suppression from the typically extreme myocardial 18FDG indication was performed with patients consume a minimal carbohydrate, high-fat food the entire evening before, and imbibe a veggie essential oil beverage before the research then. In topics with great myocardial suppression, focal 18FDG indication (albeit at limited quality) was discovered in CT-demarcated coronary arterial sections, and tended to become more widespread in sufferers with angiographically-confirmed CAD. Potential research are had a need to determine whether 18FDG measures of coronary plaque inflammation shall predict coronary events. Open in another window Amount 1 Family pet/CT imaging of coronary arterial irritation/metabolic activity via 18F-fluorodeoxyglucose (FDG)..