Review
PET/CT and vascular disease: Current concepts

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Abstract

Since its introduction in 2001, positron emission tomography associated to computed tomography (PET/CT) has been established as a standard tool in cancer evaluation. Being a multimodality imaging method, it combines in a single session the sensitivity granted by PET for detection of molecular targets within the picomolar range, with an underlying submilimetric resolution inherent to CT, that can precisely localize the PET findings.

In this last decade, there have been new insights regarding the pathophysiology of atherosclerosis, particularly about plaque rupture and vascular remodeling. This has increased the interest for research on PET/CT in vascular diseases as a potential new diagnostic tool, since some PET molecular targets could identify diseases before the manifestation of gross anatomic features.

In this review, we will describe the current applications of PET/CT in vascular diseases, emphasizing its usefulness in the settings of vasculitis, aneurysms, vascular graft infection, aortic dissection, and atherosclerosis/plaque vulnerability. Although not being properly peripheral vascular conditions, ischemic cardiovascular disease and cerebrovascular disease will be briefly addressed as well, due to their widespread prevalence and importance.

Introduction

The anatomical aspects of vascular diseases have been studied for decades, and conventional imaging methods, such as computed tomography (CT), magnetic resonance imaging (MRI), and ultrasound (US), are excellent tools for evaluating morphologic changes. Nonetheless, during the last decade, scientists have gained important insights into the molecular biology of common vascular disease, such as atherosclerosis and aneurysm formation, which have increased interest in designing new diagnostic tools to evaluate these conditions.

Nuclear medicine imaging, such as positron emission tomography (PET), differs from other imaging modalities, since it has the ability to noninvasively detect molecular and cellular processes and identify diseases before the manifestation of gross anatomic features. Moreover, multimodality imaging like PET/CT is very effective, since the CT can precisely localize the PET findings. In this review, we will describe the current applications of PET/CT in vascular diseases, particularly vasculitis, aneurysms, vascular graft infection, aortic dissection, atherosclerosis/plaque vulnerability, ischemic cardiovascular disease and cerebrovascular disease.

Vasculitis is an inflammatory disease involving leukocytic infiltration of blood vessels, which affects both the veins and arteries. The disease causes reactive destruction of mural structures and the surrounding tissues and leads to infarction. The etiopathogenesis of this process is not completely understood. Vasculitis can be classified according to its etiology or the location of the affected vessels, but more commonly it is classified according to the caliber of the vessels involved [1].

The Zeek classification system is the most widely accepted method of classification for vasculitis. Using this system, vasculitis is classified by the dominant vessel involved with anti-neutrophil cytoplasmic antibodies (ANCAs) [2]. There are more recent classification systems that combine histological changes and clinical features, including Wegener's granulomatosis, microscopic polyangiitis, giant cell arteritis (GCA), and Takayasu arteritis [3].

GCA is the most frequent form of vasculitis in elderly persons born in Northern Europe. In GCA, the ascending aorta is the main site of aortic rupture, probably due to its high elastin content [4]. Takayasu arteritis is a systemic granulomatous disease of large and medium vessels that may lead to vascular lesions, such as segmental stenosis, occlusion, dilatation, and aneurysm formation in the aorta and its main branches. It mainly affects young females born in Asia, Mexico, and South America. The pathogenesis of Takayasu arteritis is still unknown [3], [4].

Diagnosing and assessing the extent of vasculitis are challenging for physicians, especially in patients presenting non-specific symptoms (e.g., fever, fatigue, night sweats, and weight loss) and signs of systemic inflammation, which are common in patients with fevers of unknown origin [5]. Other abnormalities can be present, such as polymyalgia rheumatica (which occurs in 30–40% of GCA patients), and associated diseases, including rheumatoid arthritis, syphilis, tuberculosis, and malignancy.

In laboratory tests, patients with vasculitis show persistently raised inflammatory markers (i.e., erythrocyte sedimentation rate and C-reactive protein), leucocytosis, thrombocytosis, and normochromic normocytic anemia. However, general inflammatory markers are usually poor surrogate markers for evaluating disease activity or the response to treatment for large vessel arteritis. Temporal artery biopsy is the gold standard for diagnosing giant cell arteritis, and arteriography is typically used to diagnose Takayasu arteritis, since it shows the morphology and the extent of vascular lesions. Histopathology cannot be performed during the diagnosis of Takayasu arteritis [6].

Ultrasonography is widely available, repeatable, and acceptable to patients. It provides information on the vessel lumen and wall, pulsatility, and blood-flow characteristics. However, this method cannot be used to depict structures below bone or air, and it is operator-dependent [7].

Since 1998, gadolinium-enhanced magnetic resonance imaging has been used to image large vessel anatomy and identify stenotic lesions [8]. The enhanced uptake of contrast agents by the large vessel alterations is probably due to enhanced permeability. Edema-weighted vascular magnetic resonance imaging has also been used to evaluate disease activity, but it has a poor concordance with the diagnosis of new vascular lesions [9].

PET is a non-invasive metabolic imaging method based on the regional distribution of radiolabelled 18fluoro-deoxyglucose (FDG) that is a glucose analog. After glucose enters the cell, it undergoes phosphorylation by hexokinase to form glucose-6-phosphate, which can be further utilized in glycolysis. Unlike glucose, after FDG is converted into FDG-6-phosphate, it cannot be any further metabolized, and it becomes trapped in the cytosol [40] (Fig. 1). FDG shows homogeneously increased activity in the walls of large arteries (e.g., aorta, iliac, femoral, subclavian, and carotid), which provides diagnostic clues that a patient has vasculitis. The FDG PET resolution limits detection to larger arteries, and the homogeneous FDG uptake in arterial walls decreases with effective steroid therapy. Immunosuppressive drugs (e.g., cyclophosphamide, methotrexate, azathioprine, and mycophenolate mofetil) and biological therapies, such as anti-tumor necrosis factor (anti-TNF), may be used to reduce the cumulative steroid dose [6], [7], and may also promote a significant reduction or disappearance of symptoms, with significant improvement or normalization of biochemical alterations [10], [11].

The recent advent of combining functional and anatomic imaging with PET/CT scanners allows for anatomic correlation and exact localization of lesions [12]. The combination of PET and CT imaging allows for direct correlation of pathological changes during metabolic activity with precise anatomical localization in a single fused image [10]. Ideally, FDG-PET/CT imaging should be carried out 3 h post injection of FDG. It is important to test for low serum glucose levels (<150 ng/dl) to minimize blood pool activity. Correlative imaging (CT and MRI) should be performed to evaluate arterial wall thickening, rupture, aneurysm, and vascular occlusion sequelae [11].

In a reported case where there was suspicion of autoimmune vasculitis, FDG-PET/CT scanning showed remarkable images of extensive, abnormal FDG accumulation along the walls of the thoracic and abdominal aorta, subclavian and axillary arteries, common carotid arteries, superior mesenteric arteries, iliac arteries, and the upper parts of the femoral arteries [12]. Bertagna et al. [7] showed that FDG is highly effective in detecting large-vessel vasculitis anywhere in the body and in evaluating disease extension. FDG has a high sensitivity (77–100%) and specificity (89–100%), and it is helpful in diagnosing patients with fever of unknown origin (FUO). It is a valuable tool for making a primary diagnosis of vasculitis. Moreover, FDG-PET seems to be more reliable than MRI for monitoring disease activity during immunosuppressive therapy [10], [11].

It is important to keep in mind that differential diagnoses should be performed for atherosclerosis, vascular thrombosis (Fig. 2) and vascular grafts. Generally FDG-PET shows mild heterogeneous activity and skipped regions. When intense activity is observed, it may correspond to ulcerated atherosclerotic plaques. In cases with vascular thrombosis, there is increased activity in the lumen without vascular wall invasion, and mild diffuse activity can be observed in the vascular grafts [13]. When there is intense uptake, a focal infection may be present [13].

The current risk stratification for aneurysm ruptures, such as abdominal aortic aneurysms (AAA), is based on morphologic CT parameters, including the maximum aortic diameter, aneurysm shape, AAA expansion, and computed wall stress [14]. However, some aneurysms rupture at a small size, and many large aneurysms grow to a considerable diameter without rupture. Therefore, it would be useful to define predictors of accelerated growth or increased rupture risk. Aneurysms follow a natural course, and metabolic process, such as the release of matrix metalloproteinases produced or activated by inflammatory cells, cause degradation of elastin and collagen in the vessel wall [15] facilitating ruptures. In a recent study by Reeps et al. [16], symptomatic AAA were correlated with FDG accumulation in the vessel wall, along with increased macrophage and metalloproteinase activities and collagen degradation.

A preliminary study of 26 patients using FDG-PET reported that in the 10 patients who had a positive PET, there was a trend towards forthcoming rupture (n = 1), leakage (n = 1), rapid expansion (n = 2), or increasing back pain before rupture (n = 5). Moreover, the 16 patients with a negative PET had a more benign course [17]. Of note, only patients with large sized aneurysms (mean 6.3 cm) were evaluated, and positive PET was judged visually in this study. Another study suggested that the risk of aneurysm rupture could be more accurately predicted if the high wall stress zone defined by the computed finite element analysis co-localized with the positive PET sites [18]. More studies will be necessary in the future that include a larger number of patients to standardize the protocols and criteria for this vascular PET/CT application.

Vascular graft infection (VGI) is a rare complication in vascular surgery, which occurs in 0.5–5% of implantations. Although it has a low incidence, VGI is a severe complication. Therefore, early and reliable diagnoses are necessary to provide adequate treatment and avoid further complications, such as anastomotic bleeding or sepsis, which can results in limb loss or even death [19].

FDG-PET/CT is emerging as a promising tool to detect VGI in patients. FDG-PET alone has a high sensitivity for VGI, but it lacks specificity when compared to CT [20]. Thus, adding CT to the PET camera can increase specificity when evaluating this complication. Since 2003, a number of published case reports have shown promising results in the detection of VGI using FDG [21], [22], [23], [24], [25], [26].

In a study of 39 patients (35 men and 4 women) with suspected graft infections, FDG-PET/CT was performed to form a diagnosis and localize the infection within the graft or soft tissue [27]. The final diagnosis was based on histopathologic findings and microbiologic assays obtained at surgery or based on clinical and imaging data obtained during follow-ups. There were 27 patients with foci of increased FDG uptake where infection was suspected. Of these patients, 16 had foci located in the grafts, and VGI was confirmed in 14 of these patients (88%). PET/CT excluded graft involvement in 11 patients. In 10 of these 11 patients (91%), long-term follow-ups confirmed that the infectious site was limited to the surrounding tissue only. No abnormal FDG uptake was detected in12 patients, who showed no further evidence of infection. Therefore, PET/CT had a sensitivity of 93%, specificity of 91%, positive predictive value (PPV) of 88%, and negative predictive value (NPV) of 96% for the diagnosis of VGI in this study.

Spacek et al. performed FDG-PET/CT prospectively in 76 consecutive patients in which a total of 96 vascular grafts were suspected to be infected [28]. The gold standard for diagnosis was based on histopathologic findings from surgery or a clinical follow-up of more than 6 months. Only FDG uptake around the graft was assessed, and the pattern was classified as none, inhomogeneous, or intense (focal). The CT morphologic parameters were classified as: area of infiltrate in a plane perpendicular to the long axis and excluding the graft lumen area (expressed in cm2), presence of an irregular graft boundary, or presence of a pseudoaneurysm. Subjective focal uptake was specific to VGI in 93% of prostheses (Fig. 3). Subjective focal uptake was linked with a very high PPV of 93%. On the other hand, the low rate (1.8%) of false-negative PET findings in prostheses with no focal uptake excludes VGI with a high probability of 97%. In one-fifth of the prostheses, inhomogeneous uptake was observed, which hampered the accuracy of PET alone. Moreover, under CT, the morphological appearance of the graft boundaries were irregular within this subgroup, allowing VGI to be predicted with a sensitivity of 73%, specificity of 86%, overall accuracy of 78%, and a PPV and NPV of 89% and 67%, respectively.

In a recent study, Bruggink et al. [61] prospectively evaluated 25 patients who were clinically suspected of having vascular prosthetic infections. They used dedicated PET alone and full diagnostic CT. Fifteen patients had infections diagnosed by culture. Single FDG-PET had the best results in diagnosing the patients (sensitivity 93%, specificity 70%, PPV 82%, and NPV 88%). For CT, these values were 56%, 57%, 60%, and 58%, respectively. The fusion imaging was performed using software and showed high sensitivity and specificity rates and high PPV and NPV.

Aortic dissection (AD) is one of the most frequent causes of acute chest pain, along with myocardial infarction and pulmonary embolism, and it is a potentially life-threatening disease [29]. Correct diagnoses are essential for successful outcomes because the presenting symptoms are variable, and treatments must be individualized. In type A dissections (Stanford classification), the ascending aorta is involved, while in type B dissections, only the aorta distal to the left subclavian artery is involved [30]. For type A dissections, surgical intervention is required. For type B dissections, however, it is difficult to determine whether surgery is needed and when it should be performed, and medical therapy is still poor with a mortality rate of up to 10% [31].

Some studies have shown that increased FDG uptake is a marker of active atherosclerotic inflammation within the aorta and the carotid, iliac, femoral, and vertebral arteries [32], [33]. Reeps et al. proposed that the detection of increased inflammatory changes by FDG-PET/CT may help to differentiate acute from chronic AD. In their study, they found that FDG uptake was higher in patients with acute AD than those with stable disease. This finding may be helpful when deciding whether to continue medical therapy or whether to proceed with surgical intervention. However, a prospective study with a larger number of patients is necessary to confirm these results [34]. A recent study, Kato et al. [35] reported that increased FDG uptake in the dissected aortic wall may correlate with an unfavorable outcome in acute AD patients. Corroborating these findings, Kuehl et al. [36] observed that the uptake in the aorta is increased in acute AD patients, and these patients have a worse prognosis than those with a lower FDG uptake.

Atherosclerosis is a systemic disease that affects most major arteries of the body and is the leading cause of death in developed countries. Traditionally, vascular imaging of atherosclerosis encompasses anatomic issues, such as the degree of segmental arterial stenosis and vascular calcification. During the last decade, there have been new insights regarding the pathobiology of atherosclerosis, and in particular, plaque rupture. The advancements in multimodality imaging PET/CT and its widespread use in oncology have raised interest in using this technique for metabolic vascular imaging. The PET modality has detection sensitivities for molecular targets within the picomolar range, and CT has a submillimeter resolution that can precisely localize the PET findings.

In early atherosclerosis, the total vessel area increases to maintain the lumen size and blood flow in a process called positive remodeling. Consequently, large atherosclerotic lesions can accumulate without compromising flow or producing symptoms. In an apparent contradiction to its protective role in preventing ischemia, this process has been linked to plaque vulnerability and acute coronary syndromes. Eventually, the artery can expand no further, and the plaque begins to encroach into the lumen, causing ischemia. This latter process is known as constrictive remodeling [37].

Although revascularization often effectively relieves ischemia, it has been unsuccessful in preventing myocardial infarction or prolonging life except in select patient groups [38]. Therefore, there is an urgent need to discriminate stable from unstable plaques. It has become clear that the cellular and extracellular composition of plaques is a primary determinant of plaque stability. The main characteristics that drive rupture are a thin fibrous cap, large lipid core, a paucity of smooth muscle cells, and an abundance of inflammatory cells [39].

So far, FDG is the most utilized radiopharmaceutical that is used in this scenario. Activated macrophages have a higher rate of glucose uptake than other cells in the plaque [41], so FDG can be a potential source of signal in atherosclerotic plaques.

To perform vascular PET for atherisclerosis imaging, a longer FDG uptake is required than for oncology studies to establish a better target-to-background ratio. Two hours was shown to be effective and did not produce a significant degradation of the arterial FDG signal [42]. The first prospective study using FDG to quantify inflammation was performed by Rudd et al. [43], who analyzed the carotid uptake of symptomatic lesions in patients with recent transient ischemia attacks. They observed that the carotid uptake in these patients was greater than in the contralateral asymptomatic plaque.

Several other studies have investigated inflammation in atherosclerosis in other arterial trees and in the aorta and have observed similar findings [44], [45]. One study suggested that FDG uptake by the arterial wall is related to high levels of metalloproteases (which are an atherosclerosis biomarker) [46]. Moreover, vascular uptake has been suggested as a predictor of the risk of cardiovascular events beyond standard risk factors and biomarkers. One pertinent study was published recently by Rominger et al. [47] and assessed FDG-PET/CT follow-up scans of 932 cancer patients. Of note, patients with known coronary artery disease were excluded from this analysis. Fifteen patients who had a vascular event defined as ischemic stroke, myocardial infarction, or revascularization were compared to 319 randomly selected patients who experienced no vascular events. High vascular uptake expressed as the target-to-background ratio of FDG measured in the aorta, carotid, or iliac arteries was the strongest predictor of a subsequent vascular event.

Although atherosclerosis is a systemic disease, some studies have addressed the use of FDG vascular uptake in the coronary arteries to predict cardiac events. However, there are some challenges to measuring the FDG signal in these arteries. First, the small size of coronary lesions may be missed due the limited spatial resolution of PET (3–4 mm for clinical scanners) and the partial volume effect. Second, constant movements due to respiratory and cardiac cycles result in spatial shifts between the acquisition of PET and CT data [48]. Recent developments in PET instrumentation, as the 4-D PET, promise to address these issues and generate a better temporal resolution [49]. Third, the high physiologic myocardial uptake of glucose interferes with imaging the coronary arteries. To overcome this limitation, a high fat and low carbohydrate diet has been reported to be successful [50].

One potential application of FDG-PET is to assess the response to antiatherosclerotic therapy. Tahara et al. randomized 43 patients noted to have a high baseline FDG uptake in the aorta and/or carotid arteries to either a group receiving simvastatin or a group receiving dietary management only. The extent of FDG signal reduction was positively correlated in the simvastatin group. Moreover, the decrease in FDG metabolism was linked to the increase in high-density lipoprotein cholesterol, which was also reported in another study [51].

Although FDG-PET has been proven to be a good marker of inflammation in atherosclerosis, more studies are clearly necessary to establish its use in clinical scenarios. This is more challenging for coronary imaging because of the relatively small size of cardiac lesions, cardiac and respiratory motions, and high physiologic myocardium uptake. The long term goal should be to determine whether vascular PET can serve as a predictor of future cardiovascular events.

Laitinen et al. [52] evaluated the use of a labeled vascular adhesion molecule-1 called 18F-Galacto-RGD in mouse aorta. This tracer binds to alpha(v)beta(3) integrin, which is expressed by macrophages and endothelial cells in atherosclerotic lesions. They showed a good correlation between atherosclerotic lesions in the mouse aorta and macrophage density. Additionally, the peripheral benzodiazepine receptor (PBR) is expressed in macrophages. Fujimura et al. demonstrated by in vitro autoradiography using [3H]PK 11195 that PBR is a good target for imaging inflamed plaques with a PET emitter [53].

Cardiac PET constitutes a well-developed means for detecting and tracking the progression of coronary artery disease (CAD) and diagnosing microvascular dysfunction. It has also been used as a follow-up for different therapies, offering a comprehensive approach for the work-up of CAD. Cardiac PET has potential advantages in patients with multivessel CAD as well as in subjects with large body habitus, who are prone to attenuation artifacts [54].

Cardiac PET has several technical advantages over traditional single photon emission computed tomography (SPECT), which should be appreciated. These advantages include accurate depth-independent attenuation correction, high spatial resolution (4–5 mm), high temporal resolution (5–10 s), tracers with higher extraction fractions and shorter half-lives than SPECT radiotracers, and less equivocal results because of the superior image quality in comparison to standard SPECT.

PET imaging is the most validated, noninvasive method for absolute flow quantification. Moreover, PET imaging has been applied to measure endothelial function and is capable of defining the early stage of coronary arteriosclerosis. The evaluation of coronary microcirculation in vivo relies on measuring parameters that are indices of functional status [55]. In the absence of epicardial CAD, impaired myocardial flow reserve (MFR) may reflect changes associated with cardiovascular risk factors.

82Rb PET offers several features to facilitate applying quantification of flow as a routine tool [56]. Unlike other PET tracers, 82Rb is a generator product, and it is widely available in many countries. With list mode, the gating and dynamic imaging needed for quantification can now be acquired simultaneously. This approach has been validated against microspheres in animal models, in which it was shown to be accurate, reproducible, and comparable to 13NH3. Preliminary data have indicated that the degree of MFR impairment measured using 82Rb PET can predict the likelihood of multivessel disease [57].

PET blood flow quantification has other potential clinical applications in studying nonatherosclerotic microvascular disease [58]. Cecchi et al. [59] showed that altered microvascular function is strongly associated with poor outcomes in patients with hypertrophic cardiomyopathy. Neglia et al. reported that globally impaired vasodilator capacity was associated with an increased risk of death and further progression of congestive heart failure (CHF), and it was an independent predictor of subsequent cardiac events [60]. These findings have enhanced our understanding of the role of microvascular dysfunction in these cardiac conditions, but continued research is needed to clearly ascertain the clinical role of PET flow quantification.

Currently, integrated PET/CT provides new means for attenuation correction (AC). Moreover, it allows coronary function and anatomy to be evaluated in a single setting. More studies are needed to determine whether this approach will optimize the clinical decision-making process and improve patient outcomes.

The routine clinical application of PET myocardial perfusion imaging (MPI) in evaluating CAD is now well established. The added value of hybrid data, which combines PET with coronary calcium scores and/or CT angiography, and the clinical utility of myocardial blood flow (MBF) quantification in defining early and late atherosclerosis, microvascular disease, and evaluating treatment are matters of ongoing investigation. The utility of these emerging methodologies will be judged by whether or not the added information influences clinical decisions and can positively shape patient outcomes.

At present, PET is the most accurate, noninvasive modality to provide quantitative in vivo regional measurements of both cerebral circulation and cellular metabolism in human subjects. On the other hand, due to the combination of the radionuclide's short half-life and the need for timely stroke examinations, the technique requires an on-site cyclotron and radiochemistry facility, which makes it difficult to use PET in routine clinical practice. Although PET is still mainly used as a research tool for cerebrovascular disease, it has provided valuable knowledge and insight into both ischemic and hemorrhagic stroke [62].

Stroke is the third leading cause of death worldwide, after cancer and coronary disease. Approximately 80% of all strokes are of ischemic etiology, and 25–50% of these are caused by an unstable carotid artery plaque. The risk of recurrent stroke within 90 days is 15–20% higher in patients presenting symptoms of transient ischemic attack or minor stroke [63]. Considering the aforementioned data and the fact that the current selection criteria for intervention are predominantly determined by the grade of stenosis or symptomatology alone, there is a clinical demand for factors other than plaque size and the degree of luminal obstruction when assessing the stroke risks in patients.

Cerebrovascular disease results from an imbalance of cerebral blood flow (CBF) and the local metabolic requirements of the brain parenchyma. Thus, understanding brain circulation and cellular function are fundamental to correctly treat stroke [62]. Under normal physiologic conditions, regional blood flow is closely matched to the resting regional metabolic rate of the tissue. CBF and the metabolic rates for glucose (CMRGlc) and oxygen (CMRO2) are higher in gray than in white matter. Because of this relationship between regional flow and metabolism, the fraction of available glucose and oxygen that is extracted by the brain from the blood is uniform throughout the tissue [62], [63]. When cerebral perfusion pressure (CPP) falls in the context of severe stenosis and inadequate collaterals, CBF initially changes little to nothing. This compensatory mechanism is called auto-regulation, and it is due to alterations in the diameter of small arteries or arterioles, which accommodate changes in CPP [63].

If the ischemic insult continues, then CPP falls below the autoregulatory limit, and the maximal capacity of vasodilation is achieved, causing CBF to begin declining steeply. There is also a 2–3-fold increase in the oxygen extraction fraction (OEF), which progressively approaches 100%, and is responsible for the maintenance of oxygen metabolism. Nevertheless, when the maximal OEF is no longer sufficient to meet the energy needs of the brain, further reductions in CBF occur, which produces clinical evidence of brain dysfunction due to the disruption of normal cellular metabolism [62].

Vascular imaging techniques, such as angiography, angio-CT, angio-MR, or Doppler ultrasonography, can identify the degree of stenosis and the presence of collateral vessels, but they cannot necessarily access the adequacy of the blood supply. Perfusion techniques using CT and MRI can determine the relative cerebral blood volume (CBV) and CBF. However, they do not differentiate between clinically relevant ischemia and autoregulated ischemia, since they bear no information regarding OEF. PET is the only imaging method that can determine OEF values and also provide accurate measurements of CBV, CBF, CMRO2 and CMRglc. Thus, PET potentially can assess the balance between blood flow supply and metabolic demand. However, the clinical value of these data remains to be proved through large clinical trials.

In studying hemorrhagic stroke, investigations of CBF and the metabolic rate in intracerebral hemorrhage (ICH) are limited. Still, PET can provide information on metabolism and CBF secondary to the effect of space-occupying lesions. For instance, in ICH, a study has shown that there is a reduction in OEF rather than the increase that is observed in ischemic conditions [64].

Section snippets

Conclusions

PET/CT can be used to study metabolic and physiologic processes in vivo with precise anatomic localization, which opens new clinical possibilities for evaluating vascular diseases. Further studies are necessary to define the use of PET/CT in clinical strategies more precisely, especially for atherosclerotic diseases, including plaque vulnerability, aneurysms, and aortic dissection.

Conflict of interest

The authors have nothing to disclose.

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