There has been a significant growth in hybrid single-photon emission computed tomography and computed tomography (SPECT–CT) and positron emission tomography computed tomography (PET–CT) systems over the past decade, driven in large part by oncologic imaging. A fortuitous byproduct of this has been the development, application, and validation of myocardial perfusion imaging (MPI) using these hybrid systems. Cardiac hybrid SPECT–CT and PET–CT systems offer distinct advantages compared with traditional SPECT or PET MPI. The CT provides for excellent attenuation correction and improves the sensitivity and specificity of MPI, CT-derived coronary artery calcium (CAC) score adds substantial incremental diagnostic and prognostic information to MPI, and hybrid scanners offer the ability to combine a physiologic assessment of perfusion, function, or metabolism with an anatomic assessment of atherosclerosis and structural heart disease. By doing so, hybrid SPECT–CT and PET–CT imaging offers unprecedented opportunities for molecular cardiology research. The primary focus of this chapter is to discuss the clinical applications of hybrid radionuclide MPI with calcium scoring and coronary CTA.
The hardware of SPECT–CT and PET–CT scanners comprises a conventional SPECT scanner or a PET scanner coupled with a CT scanner of various configurations. While all SPECT–CT and PET–CT scanners offer CT-based attenuation correction, calcium scoring (≥4 slice MDCT) and coronary CTA (≥64 slice MDCT) may be performed only on certain hybrid SPECT–CT and PET–CT scanners. Sample hybrid PET–CT and SPECT–CT protocols are shown in Figure 25-1A and B, respectively. The CAC score and/or coronary CTA study can be performed sequentially right before or after the SPECT or PET scan or at a separate setting.
Attenuation correction using transmission scanning employing external radioactive sources or cardiac CT improves the count uniformity of the image and helps distinguish attenuation artifacts from real defects. It also offers the possibility of stress-only imaging, with potential savings of time, cost, and radiation dose as discussed in more detail in Chapter 9. Also, accurate attenuation correction enables precise measurements of absolute radiotracer concentration in the myocardium making feasible noninvasive quantitative estimation of myocardial blood flow in mL/g/min.
External radionuclide source transmission scans pose some challenges including: (1) degradation of the radionuclide source over time which adversely impacts image quality, (2) longer acquisition time when compared with the CT transmission scans, and (3) a small additional radiation dose (in addition to the emission scan). CT attenuation correction, on the other hand, is rapid (takes a few seconds) and of excellent quality. SPECT–CT and PET–CT utilize a low-dose x-ray transmission computed tomogram for attenuation correction (CTAC). But, due to inherent differences in image resolution between CT and SPECT or PET MPI, the CTAC and SPECT or PET myocardial perfusion images may be misregistered (not appropriately aligned) resulting in artifacts. Accurate registration is critical for improving the diagnostic yield of CT attenuation-corrected MPI (Fig. 25-2A and B).
Figure 25-2
(A and B) The top panel demonstrates stress and rest rubidium-82 myocardial perfusion images. The bottom panel shows the overlay of the CT transmission and rubidium-82 emission images. In “A,” the emission images demonstrate a reversible anterolateral myocardial perfusion defect, and the fusion images demonstrate that the stress transmission and emission images are misregistered. Using software, the transmission and emission images were realigned and the images reconstructed with a new appropriately registered attenuation map, resulting in normal myocardial perfusion images (B).
SPECT–CT MPI has been validated in patients with and without underlying CAD.1,2 Multiple studies of SPECT MPI with radionuclide attenuation correction compared with non–attenuation-corrected images demonstrated that test specificity and normalcy are improved while maintaining sensitivity to detect obstructive CAD.3–6 Importantly, attenuation correction of MPI increases the normalcy rate, a term used to define the percentage of normal studies in a low-risk cohort. Figure 25-3 demonstrates the effect of attenuation correction using a hybrid SPECT–CT system. Recent publications have demonstrated the improved prognostic capability of attenuation-corrected SPECT MPI.7,8 However, radionuclide attenuation correction with SPECT MPI is not easy to use and widespread clinical adaptation of this technique has been slow.
In contrast, PET MPI with attenuation correction has been widely used clinically (Fig. 25-4) and for research applications, but PET MPI without attenuation correction is significantly degraded by attenuation and is not interpreted clinically or for research purposes.9 Multiple studies demonstrated the excellent diagnostic10 and prognostic value11 of PET MPI. Furthermore, noninvasive quantitative assessment of myocardial blood flow with PET has emerged as a powerful tool to diagnose microvascular dysfunction, follow progression or regression or CAD, and identify localized ischemia, transplant vasculopathy, and balanced ischemia.9 Absolute myocardial blood flow and coronary flow reserve assessed by PET accurately predicts future adverse cardiovascular outcomes; in particular, a normal coronary flow reserve offers excellent negative predictive value to exclude high risk CAD.12–15
Figure 25-4
Dipyridamole stress and rest rubidium-82 PET–CT myocardial perfusion images demonstrate a large-sized and severe perfusion defect in the entire anteroseptal wall, the mid and apical anterior walls, and LV apex that was reversible, consistent with reversibility in the left anterior descending artery (Panel A). In addition, there was a medium-sized and severe perfusion defect in the entire inferior wall and the basal inferoseptal wall that was reversible consistent with reversibility in posterior descending artery. There was transient ischemic dilation of the left ventricle (TID ratio = 1.3) and a rest left ventricular ejection fraction of 26% that decreased to 21% during peak stress (high-risk features). Polar plots of perfusion are shown in panel B. Coronary angiography demonstrated severe disease in the right coronary artery, left anterior descending artery, and left circumflex artery (Panel C).
Advances in multidetector row CT scanners have tremendously improved the noninvasive diagnosis of CAD using CAC score, coronary CTA, combined imaging of myocardial perfusion and anatomy,16 as well as CT-derived estimates of fractional flow reserve (CT-FFR).17 For attenuation correction, low-resolution CT (nondiagnostic CT), 2-slice CT or ≥4-slice multidetector-row CT-based hybrid scanners can be used. For CAC scoring, at least 4-slice CT is required (≥6-slice recommended). For coronary CTA, at least a 16-slice scanner is required (≥64-slice multidetector-row CT recommended), with imaging capability for slice width of 0.4 to 0.6 mm and temporal resolution of 500 ms or less (≤350 ms is preferred).18
Coronary artery calcification is a specific marker of coronary atherosclerosis and a powerful indicator of increased cardiovascular risk (see Chapter 28).19,20 CAC score in addition to MPI can be of great value both to the clinician and the patient and stimulate further discussions regarding patient’s risk factor management.21 Likewise, extensive literature (as discussed in Chapter 28) supports the role of coronary CTA alone or in conjunction with MPI in the diagnosis and management of individuals with known or suspected CAD. Extensive coronary artery calcification, high or irregular heart rates, and high body mass index may limit the diagnostic accuracy of coronary CTA; ischemia evaluation may provide incremental diagnostic value in those instances. Furthermore, revascularization decisions guided by functional testing with SPECT MPI22 or invasive fractional flow reserve23 may improve clinical outcomes.
With hybrid SPECT/CT and PET/CT systems a prospectively gated calcium score scan can be acquired along with the MPI or the CTAC obtained during PET–CT or SPECT–CT MPI can be visually assessed for coronary artery calcification with good accuracy.24,25 Several studies wherein subjects underwent both a CAC score study and MPI (at the same setting or at different settings) have demonstrated that subjects with normal MPI may have extensive underlying calcified atherosclerosis, and this finding may influence physicians to prescribe aspirin and lipid-lowering agents.26 The frequency of ischemia in subjects with Agatston calcium score of >400 is high (>20%)27–31; a myocardial perfusion study is considered appropriate among individuals with CAC score >400 or among individuals with high CHD risk and CAC score 100 to 400 independent of symptoms.32 As with CAC score, investigators33 have evaluated the diagnostic and prognostic value of a zero CAC score in conjunction with stress SPECT MPI in patients presenting to the emergency room with chest pain. In that study, 0.8% of patients had an abnormal MPI (5/625 patients, four of whom had no CAD on subsequent invasive angiography), and 0.3 event rate (mildly elevated troponin, no cardiac death) over a mean follow-up of 7 months. These authors33 concluded that most of the patients with chest pain in the ED have a calcium score of 0, which predicts both a normal stress SPECT result and an excellent short-term outcome. A recent meta-analysis by Bavishi et al.34 confirmed that zero to low CAC scores were infrequently associated with ischemia, but there was a wide variance in the frequency of ischemia among patients with intermediate to high CAC scores (Tables 25-1 and 25-2).
| First Author | Year of Publication | Sample Size | Patient Characteristics | Age (years) | Male (%) | HTN (%) | DM (%) | HL (%) | CAC Categories | Ischemia Prevalence (%) |
|---|---|---|---|---|---|---|---|---|---|---|
| Anand | 2004 | 220 | Asymptomatic, suspected CAD | 56 ± 11 | 72 | 35 | 30 | 30 | 100–399, ≥400 | 30 |
| Anand | 2006 | 180 | Asymptomatic, Type II DM | 53 ± 8 | 61 | 22 | 100 | 62 | ≤10, 11–100, 101–400, 401–1000, >1,000 | 31.7 |
| Blumethal | 2006 | 260 | Siblings of premature CAD | 51 ± 8 | 38 | 60 | 14 | 38 | 0, 1–10, 11–100, 101–399, ≥400 | 18.8 |
| Chang | 2015 | 946 | Suspected CAD | 58 ± 9 | 75 | 50 | 10 | 57 | 0–10, 11–100, 101–400, ≥400 | 10.9 |
| Estevez | 2008 | 80 | Symptomatic, suspected CAD | 62 ± 15 | 39 | 80 | 30 | 38 | 0, >0 | 15.5 |
| Fathala | 2011 | 157 | Suspected CAD | 64 ± 10 | 60 | 18 | 17 | 16 | 0, >10 | 31.8 |
| Ghardi | 2013 | 462 | Known or suspected CAD | 63 ± 11 | 68 | 53 | 17 | 40 | 0, >0 | 22.9 |
| He | 2000 | 411 | Suspected CAD | 53 ± 8 | 69 | 39 | 6 | 54 | 0, 1–10, 11–100, 101–399, ≥400 | 19.7 |
| Ho | 2007 | 703 | Suspected CAD | 59 ± 9 | 79 | 48 | 7 | 69 | 0–10, 11–100, 101–400, 401–1000, >1000 | 7.4 |
| Moser | 2003 | 102 | Asymptomatic, suspected CAD | NR | NR | NR | NR | NR | 0–100, 101–400, ≥400 | 18.6 |
| Nishida | 2005 | 83 | Symptomatic, suspected CAD | 68 | 66 | 63 | 27 | 48 | 0, >0 | 42.2 |
| Piers | 2008 | 531 | Suspected CAD | 55 ± 11 | 57 | 57 | 12 | 41 | <10, 10–99, 100–399, ≥400 | 13.9 |
| Ramakrishna | 2007 | 835 | Suspected CAD | 55 ± 10 | 77 | 42 | 14 | 67 | 0, 1–10, 11–100, 101–400, >400 | 8.3 |
| Rozanski | 2007 | 1153 | Suspected CAD | 58 ± 10 | 74 | 38 | 8 | 65 | 0, 1–9, 10–99, 100–399, 400–999, ≥1,000 | 5.6 |
| Rosman | 2006 | 126 | Asymptomatic, Suspected CAD | 59 ± 11 | 67 | 39 | 10 | 72 | 0, 1–99, 100–399, 400–999, ≥1000 | 18.3 |
| Schenker | 2008 | 621 | Suspected CAD patients | 61 ± 11 | 40 | 74 | 28 | 54 | 0, 1–399, ≥400 | 28.8 |
| Schepis | 2007 | 77 | Suspected CAD Patients | 66 ± 9 | 62 | 73 | 18 | NR | ≤10, 11–100, 101–400, 401–1,000, ≥1000 | |
| Scholte | 2008 | 100 | Asymptomatic, Type II DM | 53 ± 10 | 65 | 51 | 100 | 53 | 0, 1–10, 11–100, 101–400, 401–1000, ≥1000 | 23 |
| Seyahi | 2011 | 35 | Renal Transplant | 37 ± 11 | 67 | 81 | 6 | NR | 101–400, ≥400 | 17.1 |
| Yao | 2004 | 73 | Suspected CAD | 53 ± 11 | NR | NR | NR | NR | 0, 1–10, 11–100, 101–399, ≥400 | 42.5 |
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