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Fig. 19.3 Co-registered 18F-NaF-PET/CT images show- ing uptake in the coronary arteries. (a) No uptake seen in patient without coronary calcium. (b) Patient with extensive LAD calcication without NaF uptake. (c) Patient with extensive LAD calcication with focal NaF uptake. (d) Patient with LAD calcication with NaF uptake adjacent to the calcied segment suggesting expanding micro-

calcication. (e) Patient with recent ACS in the RCA territory with corresponding NaF uptake in the proximal RCA. (f) Angiogram of patient from (e) showing ulcerated plaque and thrombus in the proximal RCA corresponding to the area of NaF uptake. (Reproduced with permission from Dweck etal. [59])

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Fig. 19.4 Comparison of 18F-NaF and 18F-FDG uptake in patients with CAD. (a) Coronary angiogram of patient with proximal LAD STEMI. (b) NaF-PET showing intense proximal LAD uptake. (c) FDG-PET without signicant focal uptake at the culprit proximal LAD lesion. Yellow arrow denotes myocardial uptake in the LAD distribution. Blue arrow denotes esophageal uptake. (d) Coronary angiogram of patient with proximal LAD ACS (non-STEMI) (red arrow) and bystander non-culprit CAD in the LCx (white arrow), both of which were stented. (e) NaF uptake shown in the culprit stented LAD without signicant uptake in the bystander stented LCx. (f

) FDG- PET without tracer

uptake in either the culprit LAD or the bystander LCx in the same patient. (g) Coronary angiogram showing nonobstructive disease in the proximal to mid RCA in a patient with stable angina. (h) NaF-PET showing tracer uptake in the mid RCA lesions (red) but not in the proximal RCA (yellow). (i) Intravascular ultrasound of the NaF-negative lesion showing predominantly brofatty inltration (green) and conuent macrocalcications (white) without signicant necrosis (red). (j) Intravascular ultrasound of the NaFpositive lesion shows microcalcications (white) and signicant necrotic core (red), consistent with high-risk features. (Reproduced with permission from Joshi etal. [1])

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colocalizes with peri-coronary adipose tissue as recognized by low-attention plaques on coronary CT and often identied in proximity to culprit lesions of ACS [63]. Although both elevated CAC score and presence of high-risk, partially calcied or low-attenuation plaques on coronary CT are proportional to the uptake of NaF, the presence of obstructive disease (>70% stenosis or >50% stenosis of the left main or proximal left anterior descending (LAD) arteries) was not predictive of increased maximum TBR of NaF, highlighting its complementary qualitative information in personalized risk assessment [55].

NaF Imaging inProspective Risk Assessment

Additional work has sought to identify the utility of NaF imaging in prospective trials to predict lesions at impending risk of rupture and subsequent myocardial infarction. Initial reports of association of age, male sex, and low HDL serum concentrations with increased NaF uptake provided evidence of a direct correlation of signal intensity with risk for adverse cardiovascular outcomes [59].

A study evaluated 293 patients who underwent NaF imaging, coronary CT co-registration, and invasive coronary angiography for either symptomatic stable angina or recent myocardial infarction [64]. By quantifying global NaF uptake in the coronary vascular tree, 69% of subjects were found to have a non-zero NaF signal. Over 42months, 7% of the subjects experienced a fatal or non-fatal myocardial infarction, all of whom had increased NaF uptake, with zero subjects without positive NaF signal experiencing an adverse cardiovascular outcome. Although the overall event number was low during the period of the study, it is notable that neither CAC score nor the presence of obstructive lesions on coronary CT was predictive of subsequent myocardial infarction. Indeed, in this study only NaF uptake emerged as a statistically signicant predictor of adverse cardiovascular events with several standard clinical scoring systems failing to demonstrate a reliable prognostic linkage. Furthermore,

elevated NaF TBR carried a statistically signicant hazard ratio of 4.6 for the risk of subsequent infarction [64].

A second, smaller study looked at the coregistration of NaF-PET imaging with coronary CT for the prospective evaluation of adverse coronary events over 2 years of follow-up [65]. Coronary events occurred in 11 of the 32 patients that completed follow-up, with analysis demonstrating a signicantly increased uptake of NaF imaging during the initial evaluation. Furthermore, correlation with increased CAC score as well as the presence of partially calcied or high-risk plaque features on coronary CT (dened as low density <30 Hounseld Units, or with a remodeling index of >1.1) were found in all patients that had increased NaF uptake. While most patients in this study had baseline obstructive lesions identied on coronary CT, dened as a 2mm segment with ≥50% stenosis, in two of the noted coronary events coronary CT did not reveal obstructive stenosis of the culprit lesion while NaF uptake was increased at the culprit site prior to intervention, implicating the potential complementary role of molecular NaF imaging in high-risk patients [65].

An NaF-based strategy may also help differentiate patients identied as high-risk by modalities such as CAC scoring into patients with stable, mature coronary calcications as opposed to those with active inammation and concomitant microcalcication that may benet from more aggressive interventions [59]. However, robust prospective clinical studies will need to be performed to establish the proposed ability of NaF to identify metabolically active, high-risk coronary atherosclerotic lesions.

Limitations andFuture Directions

Although early results and imaging correlations with NaF have been promising, other studies have shown less signicant associations with increased tracer uptake. Indeed, a study of 88 patients with diabetes mellitus imaged prospectively with NaF PET failed to identify a signicant number of potentially high-risk plaques as

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would be expected in such an at-risk population. Additional studies are underway with improved long-term clinical monitoring after imaging to identify subjects with cardiac events to better elucidate this potential [66]. Increased radiation exposure may also be restrictive in some clinical centers with baseline NaF-PET/CT scans associated with 8–9 mSv of radiation [67]. The PET spatial resolution limitation of 3–4mm may also impede the utility of NaF for individualized assessment of smaller, focal atherosclerotic lesions [68]. Ultimately, longer term prospective clinical studies will need to be undertaken to better understand the prognostic utility of NaF-PET imaging in atherosclerotic disease and the promising role that NaF-PET may play as a complementary tool in the screening and serial evaluation of high-risk patient populations.

68Ga-Pentixafor Imaging ofCXCR4 Inammation

There has been continued progress in identifying targeted tracers that provide more specic and potentially predictive data in regard to CAD activity and risk for adverse clinical outcomes. One of the most promising developments from this work has been the identication of the CXCmotif chemokine receptor 4 (CXCR4) which, when bound to the associated ligand CXC-motif chemokine ligand 12 (CXCL12), is associated with leukocyte-mediated inammatory processes that are seen in models of ischemic injury [69]. Histologic evaluation of inammatory coronary plaques has revealed CXCR4-positive leukocyte populations, primarily monocyte/macrophages, although populations of smooth muscle cells, endothelial cells, T-cells, B-cells, and thrombocytes have also shown signicant CXCR4 expression in atherosclerotic zones [69, 70].

The CXCR4 Signaling Pathway

CXCR4 is a transmembrane G-protein-coupled chemokine receptor that has been implicated in a variety of inammatory and autoimmune diseases, as well as in cancer progression where it has been studied as a potential therapeutic target to interrupt metastasis [70]. Additionally, the CXCR4 signaling axis has been implicated in the evolution of coronary plaque through its role in development and growth of smooth muscle and endothelial progenitor cells. The precise pathways through which endothelial and smooth muscle cells are integrated into the CXCR4 signaling pathway are incompletely characterized, but it appears to play a homeostatic role in helping to recruit inammatory populations to areas of vascular microinjury, ultimately leading to endothelial proliferation and repair of the vascular bed [69]. CXCR4 is implicated in the activation and recruitment of intralesional macrophages in atherosclerotic plaques and in the early post myocardial infarction period [69, 70] (Fig.19.5). Indeed, this process is cumulative throughout the development of atherosclerotic plaques and, as such, offers promise as a targeted molecule for evaluation of patients with high-risk for cardiovascular disease [69]. As the density of macrophages increases, the risk of thrombotic events increases due to the release of cytokines and macrophage-associated proteases such as matrix metalloproteases, compromising the thin brous cap and leading to further local inammation. By targeting one of the key cell types that is integral to the progression of advanced atherosclerotic plaques, CXCR4 offers increased specicity with a narrower bandwidth signal than currently more established tracers such as FDG and NaF [69]. Even more intriguingly, early animal studies have evaluated the therapeutic potential of CXCR4 blockade with small molecules such as the allo-

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Fig. 19.5 68Ga-Pentixafor uptake in a patient with ACS after reperfusion. (a) Coronary angiogram with acute LAD occlusion (red arrow). (b) Coronary angiogram showing reperfusion of the LAD after stenting. (c) Fused

steric antagonist AMD3100 (Plerixafor) that can even lead to improved function and recovery after acute myocardial infarction when delivered within a narrow therapeutic window of time post infarct [71].

Nuclear Imaging ofCXCR4 inCoronary Atherosclerosis

To take advantage of this promising molecular target, the radiotracer 68Ga-pentixafor was developed as a highly specic ligand of CXCR4. Early studies demonstrated the potential clinical utility of this targeted radiotracer by comparing the con-

Pentixafor-PET/CT scan showing focal tracer uptake at the mid-site of the LAD stent (red arrow). (Reproduced with permission from Derlin etal. [74])

cordance of Pentixafor uptake in patients recently diagnosed with ACS with myocardial inammation on cardiac magnetic resonance imaging (cMRI), suggesting a role for CXCR4 signaling to promote inammatory remodeling. Although tracer uptake was not ubiquitous across all subjects in this population, all Pentixafor positive segments corresponded to regions of infarct on cMRI, and uptake appeared to be proportional to the extent of infarct as measured by troponin elevation level, serving as an early proof of concept on the clinical utility of Pentixafor imaging [72].

Further efforts were undertaken to study the association of Pentixafor uptake with high-risk patient demographics. In a retrospective study of

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38 patients who underwent Pentixafor-PET imaging for oncologic purposes, the large arteries and branches in the thorax were evaluated and showed that arterial uptake from inammatory plaque macrophages may serve to highlight areas with coronary vascular disease [73]. In another study, patients that surpassed a dened average threshold of Pentixafor tracer uptake in prespecied arterial segments, as dened by the average TBR of tracer uptake, demonstrated markedly higher rates of comorbidities such as diabetes, hypertension, hyperlipidemia, and history of prior known cardiovascular disease, demonstrating the ability to identify at-risk lesions in patients at higher risk of cardiovascular disease [69]. The prevalence of these risk factors was often at least four times greater in the high TBR group, and indeed, there was an overall 12% increase in tracer uptake in patients with any high-risk demographic features for atherosclerotic disease [69]. This type of “dose-dependent” relationship between Pentixafor signal intensity and high-risk features may also help establish relative cut-offs in tracer uptake that can be used to identify plaques at highest risk of potential rupture.

More specically than association with clinical syndromes, considerable study has gone into the evaluation of the colocalization of Pentixafor uptake with arterial neo-intimal calcications [15]. A retrospective analysis of patients that underwent Pentixafor-PET/CT imaging showed that nearly 34% of sites with Pentixafor uptake were also found to have calcications on CT, but conversely, only 7% of the total calcied arterial lesions showed Pentixafor uptake [69]. This underlines the hypothesis that CXCR4 may be more associated with early plaque development through its role in the recruitment of macrophages and subsequent release of metal-

loproteases and cytokines, which lead to plaque destabilization.

Comparison of18F-FDG and68Ga-Pentixafor Imaging

When compared to more established tracers such as FDG, there are notable similarities and differences in the Pentixafor tracer uptake prole for CAD evaluation. In a retrospective study of 92 patients who underwent FDG and Pentixafor imaging, both tracers showed similar inversely proportional uptake to degree of arterial calcications with over 30% higher average TBR in noncalcied, metabolically active lesions as compared to severely calcied lesions (1.4 vs. 1.9 for Pentixafor and 1.1 vs. 1.5 for FDG) [70]. Conversely, 35% of patients demonstrated Pentixafor uptake without any FDG uptake, indicating the utility of this tracer to recognize factors beyond focal macrophage metabolic activity [70]. However, due to the inability to biopsy the coronary vasculature in clinical evaluations, Pentixafor studies to date lack histopathologic corroboration of the cell populations responsible for uptake of the tracer. Efforts to address this have included evaluation of cadaveric heart samples or explants from carotid endarterectomies [74]. These studies have been able to conrm the high density of CXCR4-positive cells in areas of atherosclerosis without signicant CXCR4 expression in healthy vascular segments (5% CXCR4-positive cells vs. negligible number in healthy segments). Interestingly, these ex vivo analyses have also identied direct correlations between Pentixafor uptake intensity and symptomatic carotid artery disease (15% CXCR4positive cells in symptomatic lesions vs. 2% CXCR4-positive cells in asymptomatic lesions),

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further implicating the ability of CXCR4 targeting imaging to identify clinically relevant inammatory regions in diseased arteries [74].

Clinical Applications of CXCR4- Targeted Imaging

In animal models of myocardial infarction designed for early testing of CXCR4 antagonists, Pentixafor uptake intensity was directly related to time after infarct, with highest signal intensity 3days after infarct, consistent with the timing of inammatory recruitment to the infarct zone [71]. Most recently, several groups have worked to demonstrate the clinical utility of CXCR4- targeted nuclear imaging in prospective studies of patients with known CAD or recent ACS. Evaluation of human subjects post infarction with Pentixafor imaging co-registered with cMRI demonstrated increased uptake in culprit arterial segments, with uptake intensity related to severity of ischemic burden as characterized by edema and late gadolinium enhancement [71]. However, the generalizability of this correlation as a predictor of ACS rather than a sequela continues to be studied. In one study of 37 patients imaged within 1 week of an acute ST-elevation myocardial infarction (STEMI) after undergoing stent-based reperfusion, Pentixafor uptake was quantied in both culprit lesions that were stented as well as non-culprit, non-stented regions [74] (Fig.19.6). Although both demonstrated signicant uptake, maximum SUV in the dened regions of interest was over 30% higher in stented culprit lesions compared to stented non-culprit lesions, and over 60% higher than non-stented non-culprit calcied lesions, suggesting that some CXCR4 activity

could also be attributed to direct intravascular injury from revascularization [74].

A theranostic approach, evaluating the potential use of CXCR4 pathways for treatment of acute infarction, is underway [75]. Pentixafor uptake after induced infarction in mice becomes measurable in the myocardial infarct zone within hours after infarct and peaks within 1–3 days, with a subsequent decline to baseline levels by 1 week [75]. Interestingly, subjects with catastrophic post-infarct complications such as ventricular rupture showed a 30% higher tracer uptake in the infarcted myocardium at 3 days post infarct as compared to surviving subjects, suggesting a pathologic consequence to sustained CXCR4 activation [75]. Indeed, the use of the competitive inhibitor of CXCR4 receptor binding, AMD3100, at day 3 after infarct demonstrated a threefold reduction (8% vs. 23%) in the incidence of ventricular rupture and improved long-term ventricular function as compared to untreated subjects [75]. Additionally, there was a 15% improvement in left ventricular ejection fraction without affecting infarct size [75]. However, as a testament to the dynamic and multifaceted role of the CXCR4 signaling cascade, subjects not treated until 7days after infarction actually experience an increased risk of left ventricular rupture (31% vs. 8%) without the benet of improved ventricular function seen in subjects treated at the day 3 inammation peak [75]. These observations indicate CXCR4 can be used to identify subjects with sustained or severe inammation that may benet from more advanced therapies due to increased risk of delayed complications. In fact, retrospective evaluation of 50 patients after acute myocardial infarction demonstrated that the intensity of Pentixafor uptake 3–5 days after infarct was

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Fig. 19.6 68Ga-Pentixafor uptake in various coronary lesions (top row=CT scan, bottom row=Pentixafor- PET, middle row=fused image). (a) Calcied LAD plaque without Pentixafor uptake. (b) Partially calcied lesion with Pentixafor uptake in the proximal LAD (yellow arrow). (c) Pentixafor uptake in the stented portion of a non-culprit

inversely proportional to resultant ventricular function several months later (correlation coefcient of -0.41 comparing ejection fraction versus maximum CXCR4 SUV) [75].

Although the specicity of the CXCR4 signaling pathway has shown promise in targeted identication of at-risk atherosclerotic lesions, the incompletely understood and diverse functions that CXCR4 plays in other local cell types merit further studies. CXCR4 expression in mature endothelial and smooth muscle cells has been associated with maintenance of arterial wall integrity and endothelial barrier function in animal models, highlighting the importance of evaluating clinical context and complementary data when interpreting Pentixafor-based imaging in the evaluation of CAD [69].

LCx lesion. (d) Scatter plot of Pentixafor uptake intensity in control calcied plaques versus Pentixafor-positive plaques showing highest uptake in culprit stented lesions with modest uptake in non-culprit stented lesions and lowest uptake in stable calcied plaques. (Reproduced with permission from Derlin etal. [74])

Emerging Tracers

Continued understanding of the disease pathobiology, identication of novel molecular tracers, as well as improvement in imaging techniques will continue to advance the utility of PET imaging of atherosclerosis using targeted molecular tracers. Additionally, this may allow the development of predictive algorithms determining risk of adverse events in a lesion-specic manner, and surveillance methods for plaque stabilization. Several additional PET radiotracers are being studied that target atherosclerosis through metabolic pathways such as biosynthesis of nucleotides [76] and phospholipids [77, 78], and markers of endothelium activation and immune cell recruitment [79].

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In response to atherosclerotic immune activation, cells entering the proliferative stage require nucleotides as building blocks [80]. One study in mice, rabbits, and humans demonstrated signicantly higher uptake of 18F-labeled thymidine (18F-FLT) in subjects with atherosclerosis compared to controls [76]. Similarly, taking advantage of cholesterol, fatty acid, and phospholipid biosynthesis in proliferating macrophages, 11C- and 18F-labeled choline, a phospholipid precursor, has shown increased atherosclerotic plaque uptake in mice [77] and humans [78]. In addition to probes targeting metabolic pathways, investigators are also exploring cell surface molecules that are upregulated during atherosclerosis for molecular PET imaging. Evaluation of 68Ga-DOTATATE, a derivative of the somatostatin analog octreotide that targets somatostatin receptor subtype-2, which is upregulated in macrophages, has shown excellent specicity and superior coronary lesion discriminating features compared to

F-FDG in mice [81] and humans [82]. Additional studies with 64Cu-DOTATATE have also shown promising results in human studies [83]. Moreover, another tracer targeting upregu- lated translocator protein expression in macrophages, 11C-PK11195, has also shown higher uptake in symptomatic carotid plaques of humans [84]. Finally, in an effort to further improve target specicity, smaller antibody fragment- based radiotracers or nano-tracers are being developed and investigated in atherosclerosis [85–87]. While prospective trials are required to rmly establish the clinical utility of these agents, molecular PET imaging holds the promise of providing a targeted approach to assist practitioners in the diagnosis and treatment of inammatorily active coronary atherosclerotic lesions.

Acknowledgments VA Merit BX004558, UCLA Cardiovascular Discovery Fund/Lauren B.Leichtman and Arthur E.Levine Investigator Award.

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