Adenosine-Induced Stress Myocardial Perfusion Imaging Using Dual-Source Cardiac Computed Tomography
Ron Blankstein, MD*, ,*,
Leon D. Shturman, MD*,
Ian S. Rogers, MD, MBA*,
Jose A. Rocha-Filho, MD*,
David R. Okada, MD*,
Ammar Sarwar, MD*,
Anand V. Soni, MD*,
Hiram Bezerra, MD*, ,
Brian B. Ghoshhajra, MD, MBA*,
Milena Petranovic, MD*,
Ricardo Loureiro, MD*,
Gudrun Feuchtner, MD*, ,
Henry Gewirtz, MD*,
Udo Hoffmann, MD, MPH*,
Wilfred S. Mamuya, MD, PhD*,||,
Thomas J. Brady, MD* and
Ricardo C. Cury, MD*,¶
* Cardiac MR PET CT Program, Department of Radiology and Division of Cardiology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts
Noninvasive Cardiovascular Imaging Program, Department of Medicine and Radiology, Brigham and Women's Hospital, Boston, Massachusetts
Harrington McLaughlin Heart and Vascular Institute, Case Western Reserve University, Cleveland, Ohio
Department of Radiology, Innsbruck Medical University, Innsbruck, Austria
|| Lown Cardiovascular Group, Brookline, Massachusetts
¶ Cardiovascular MR and CT Program, Baptist Cardiac and Vascular Institute, Miami, Florida

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Figure 1 Flow Diagram of Patients Eligible for Recruitment and Reasons for Exclusion
Of 767 patients meeting inclusion criteria, 369 were excluded; 42 patients completed the computed tomography (CT) stress perfusion scan, out of which 34 also underwent invasive angiography. ACS = acute coronary syndrome; CABG = coronary artery bypass grafting surgery; ECG = electrocardiogram.
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Figure 2 Comprehensive Computed Tomography Protocol
See the Methods section for detailed explanation. After scout images and test bolus were performed, adenosine infusion was started at 140 µg/kg/min. Three minutes later, a contrast-enhanced stress perfusion scan was acquired using retrospective gating and tube current modulation. Once the heart rate returned to baseline, the rest perfusion scan was acquired. This was a contrast-enhanced scan using prospective triggering. Approximately 7 min later, a low tube voltage, prospectively triggered delayed enhancement scan was acquired.
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Figure 3 Radiation Exposure of Stress Cardiac CT Versus SPECT MPI
Estimated effective radiation dose in milisiverts (mSv) is shown for cardiac computed tomography (CT) (blue bars) and single-photon emission computed tomography (SPECT) myocardial perfusion imaging (MPI) (red bars). The total effective radiation dose was equivalent for the 2 modalities.
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Figure 4 Example of Single-Vessel Disease Identified by All Modalities
A 59-year-old obese man with no prior cardiac history who presented with chest pain and dyspnea on exertion. A CT perfusion showed a large perfusion defect in the anteroseptal, anterior, and anterolateral walls (A). (B) The CT angiography showed large noncalcified plaque in the proximal LAD; (C) SPECT MPI images with fully reversible defect throughout the mid and apical anterior wall. (D) Invasive angiography in the left anterior oblique caudal view showing severe stenosis in LAD before the takeoff of the first diagonal branch. LAD = left anterior descending; other abbreviations as in Figure 3.
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Figure 5 Example of CT Perfusion Identifying Multivessel Disease
A 60-year-old man with diabetes, dyslipidemia, hypertension, and a prior LAD stent who presented with chest pain. The CT perfusion (arrows) showed a perfusion defect throughout the anteroseptum, anterior, anterolateral, and inferolateral segments. On invasive angiography, the patient had severe disease in the proximal LAD and moderate stenosis in the left circumflex vessel. The SPECT study was read as normal with attenuation-related artifact in the inferior wall. It is likely that the apparently normal SPECT was caused by balanced myocardial ischemia. Abbreviations as in Figures 3 and 4.
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Figure 6 Example of Peri-Infarct Ischemia
A 63-year-old man with diabetes mellitus, hypertension, dyslipidemia, and prior myocardial infarction presented with near syncope. The CT perfusion (A) during adenosine infusion revealed a focal perfusion defect in the mid inferolateral segment. The rest CT showed a very small subendocardial perfusion defect in the same territory. Delayed-enhancement CT (B) showed subendocardial delayed enhancement along the inferolateral wall consistent with prior infarction in this region, smaller than the stress perfusion defect. On invasive angiography (C; right anterior oblique caudal projection), the patient had a subtotal occlusion of the mid left circumflex coronary artery. Nuclear SPECT imaging (D) also showed a small infarct in the inferolateral wall with peri-infarct ischemia. Abbreviations as in Figure 3.
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Figure 7 Example of False-Positive CT Perfusion
An 84-year-old man with hypertension, dyslipidemia, and tobacco use who presented with pre-syncope. Evaluation of CT myocardial perfusion during adenosine infusion showed a circumferential subendocardial perfusion defect that on blinded reading was thought to represent multivessel disease. The SPECT MPI and invasive angiography did not reveal any significant disease. Given that the patient has multiple risk factors for microvascular disease, it is possible that the perfusion abnormalities identified in this case are consistent with microvascular disease in the absence of significant epicardial coronary artery disease. Abbreviations as in Figure 3.
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