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Clinical Feasibility of Molecular Imaging of Plaque Inflammation in Atherosclerosis

¹ University of California, Irvine, California; ² Kurume University School of Medicine, Kurume, Japan; and ³ Cardiovascular Pathology Institute, Gaithersburg, Maryland

View larger version (87K): [in this window] [in a new window]   FIGURE 1.  Increasing inflammation, with evolving severity of atherosclerotic process. Columns of histopathologic sections demonstrate normal vessel, pathologic intimal thickening, early and late fibroatheroma, thin-cap fibroatheroma, and plaque rupture. First 2 rows represent sections in low and high magnification. Corresponding sections in last 2 rows are immunohistochemical staining with CD68 antibody (color reaction, brown), representing magnitude of inflammation. Note increasing severity of inflammation. It is hypothesized that there would be a threshold value for noninvasive detection of inflammation by either 18F-FDG or AA5 imaging and that positive scan results will represent instability. PIT = pathologic intimal thickening; FA = fibroatheroma; TCFA = thin-cap fibroatheroma.

View larger version (107K): [in this window] [in a new window]   FIGURE 2.  Clinical imaging of plaque inflammation. (A) Imaging of macrophage prevalence with radiolabeled LDL. Carotid angiogram shows extensive stenosis (arrow) and mural irregularities (arrowheads) involving distal common and proximal internal carotid arteries (left panel). Left carotid angiogram showed only minor degree of internal carotid stenosis. External image 9 h after injection of 99mTc-LDL (481 MBq [13 mCi]) shows focal, asymmetric accumulation in right common carotid artery at bifurcation and proximal internal carotid artery (arrows), which corresponds to angiographic lesion (middle panel). Photograph of bisected right carotid endarterectomy specimen showing tight stenosis (arrow) and extensive intraplaque hemorrhage (right panel); histologic section demonstrates lesion with numerous foam cells and macrophages adjacent to hemorrhage (hematoxylin and eosin, x200). In clinically most feasible molecular imaging, 18F-FDG is selectively taken up by infiltrating macrophages in plaques. (Image modified from (8).) (B) Carotid artery ultrasound imaging demonstrates carotid vascular disease in patient with recent acute vascular event (left panel). Plaques reveal homogeneous ultrasonic appearance, with irregular surfaces. Abnormal focal 18F-FDG uptake visualized in 18F-FDG PET images is concordant with ultrasonic information (right panel). (Image modified from (15).) (C) In contrast to 18F-FDG, annexin A5 selectively binds to dying macrophages, which are abundant in unstable plaques. Coronal SPECT view in patient with left-sided transient ischemic attack 3 d before surgery (left panel). Although this patient had clinically significant stenosis of both carotid arteries, annexin uptake was evident only in culprit lesion (arrow). Histopathologic analysis of endarterectomy specimen (polyclonal rabbit anti–annexin antibody, x400) shows substantial infiltration of macrophages into neointima, with extensive binding of AA5 (brown) (right panel). (Image modified from (11).)

View larger version (79K): [in this window] [in a new window]   FIGURE 3.  18F-FDG imaging of coronary inflammation. (A) Incidental 18F-FDG uptake is seen in left main coronary artery region in 71-y-old patient undergoing PET for evaluation of recurrence of colon malignancy and metastatic disease (modified from (16)) (left panel). This patient had multiple coronary risk factor; hence, CT angiography was performed that showed noncalcified plaque in left main coronary and proximal left anterior descending artery (arrow) (middle panel). Corresponding image after fusion with 18F-FDG PET/CT localized inflammatory PET signal with maximal standardized uptake value of 2.1 (arrow) (right panel). (B) On the other hand, prospective study has recently demonstrated potential feasibility of detecting inflammation in culprit plaque in patients presenting with acute coronary syndrome. In 1 such patient who had undergone primary coronary intervention, 18F-FDG imaging was performed. Radiotracer uptake is clearly visible (left) at site of coronary stent placement (right), suggesting that culprit lesion was inflamed. 18F-FDG uptake in myocardium was suppressed by high-fat, low-carbohydrate diet and β-blocker administration. Stent sites in patients with chronic stable angina did not show 18F-FDG uptake. MI = myocardial infarction. Figure 3B was provided by Ahmed Tawakol, Massachusetts General Hospital, Boston, Massachusetts.