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Nuclear Cardiac Stress Testing in the Era of Molecular Medicine^*

View larger version (29K): [in this window] [in a new window]   FIGURE 1.  Timeline of signal and detector advances in the history of nuclear cardiac stress testing and accuracy of current techniques. (A) Time points of initial recognition that ECG and radiotracers provide diagnostic information for myocardial perfusion and metabolism. (B) Time span of use of detection modalities in cardiac stress testing. (C) Diagnostic information provided by stress testing as change from pretest to posttest likelihood of angiographically confirmed CAD. Bayesian curves are derived from current levels of sensitivity (Sens) and specificity (Spec) for each protocol: ECG-Exercise (16), SPECT (17), and PET (18).

View larger version (129K): [in this window] [in a new window]   FIGURE 2.  CT angiography in a patient who underwent percutaneous coronary intervention of the left anterior descending (LAD) coronary artery in the past and now complains of recurrent angina. Multiple lesions, partially calcified, can be seen in the proximal LAD (D and E) as well as the stent in mid-LAD. A complete 3-dimensional reconstruction of the heart (A) shows a significant lesion in the LAD (arrow) and the high-density stent (arrowhead). Only a small section of the LAD can be visualized on a single axial slice (B), whereas multiplanar reformations can be created along the vessel and show extended sections (C). Curved multiplanar reformations (D) and maximum-intensity projections (E) can be used to show the entire vessel in a single image. Panels F, G, and H show cross-sections of the LAD at the proximal reference, the stenosis, and the distal reference level, respectively. MO = marginal branch; DO = diagonal branch; V = cardiac vein. (Adapted from (29).)

View larger version (24K): [in this window] [in a new window]   FIGURE 3.  82Rb time–activity curves at rest (A) and after adenosine stress (B). Solid circles represent the activity concentration in left atrium and open circles represent the activity concentration in myocardial tissue. Although the first few minutes after infusion of 82Rb are not usually included in clinical acquisition protocols, it is precisely this period that is of interest if myocardial perfusion is to be quantified. Dynamic imaging of the heart during this time allows analysis of the 82Rb concentration in both arterial blood and myocardial tissue as a function of time. Disparity between myocardial perfusion SPECT and 82Rb PET studies is shown (C). Clinically indicated adenosine dual-isotope gated SPECT images (left panel) without attenuation correction show regional 99mTc-sestamibi perfusion defect in anterior and inferior regions (arrow). On the rest 201Tl images, the anterior defect became reversible while the inferior defect persisted. Corresponding 82Rb PET myocardial perfusion tomograms performed in the same patient are shown on the right panel. PET images were acquired after an infusion of adenosine and 1,110 MBq of 82Rb (top) and at rest after another 1,110-MBq infusion of 82Rb (bottom). 82Rb PET images show normal distribution of radiotracer in all myocardial regions, without evidence for reversible or fixed defects to suggest myocardial ischemia or infarction. Although high-energy positrons of 82Rb degrade spatial resolution and the short half-life increases statistical noise, high-quality images free from attenuation artifacts can be produced with 82Rb PET with only 1,110-MBq injected dose. (Adapted from (28).)

View larger version (32K): [in this window] [in a new window]   FIGURE 4.  Single-photon-emission tomograms demonstrating delayed recovery of regional fatty acid metabolism after transient exercise-induced ischemia, termed ischemic memory. Representative stress (left) and rest reinjection (middle) short-axis thallium tomograms demonstrate a reversible inferior defect consistent with ischemic but viable myocardium. 123I-BMIPP tomogram (right) injected and acquired at rest 22 h after exercise-induced ischemia shows persistent metabolic abnormality in inferior region despite complete recovery of regional perfusion at rest, as evidenced by thallium reinjection image. (Adapted from (44).)

View larger version (104K): [in this window] [in a new window]   FIGURE 5.  Simultaneous myocardial perfusion and metabolism imaging after dual intravenous injection of 99mTc-sestamibi and 18F-FDG at peak exercise. Dual-isotope simultaneous acquisition was performed 40–60 min after exercise study was completed. Rest 99mTc-sestamibi imaging was performed separately. In this patient with angina and no prior myocardial infarction, there is evidence of extensive reversible perfusion defect in anterior, septal, and apical regions (arrows). Coronary angiogram showed 90% stenosis of left anterior descending and 60% of left circumflex coronary arteries. The corresponding 18F-FDG image shows intense uptake in regions with reversible sestamibi defects (arrows), reflecting the metabolic correlate of exercise-induced myocardial ischemia. Ex = exercise; R = rest. (Adapted from (45).)

View larger version (114K): [in this window] [in a new window]   FIGURE 6.  Polar map of myocardial tracer uptake during adenosine vasodilation is shown in a patient with CAD. (A) Relative distribution of the radiotracer (as would be the case with SPECT studies) suggests single-vessel disease in the territory of left anterior descending (LAD) artery. (B) Quantitative assessment of regional myocardial blood flow reserve with 13N-ammonia PET. In a vascular territory without significant coronary artery stenosis, a normal myocardial blood flow reserve is approximately 3 mL/min/g. As such, quantitative myocardial blood flow assessment identifies abnormal flow reserve in all 3 vascular territories in this patient; 1.37 mL/min/g in LAD territory, 1.65 mL/min/g in left circumflex (LCX) territory, and 1.91 mL/min/g in right coronary artery (RCA) territory. The clinical implication for the presumed diagnosis of 1-vessel disease on evaluation of relative myocardial radiotracer uptake versus 3-vessel CAD on quantitative assessment of myocardial blood flow reserve is important and not inconsequential. Moreover, follow-up polar maps (C and D) acquired 1-y after medical therapy with pravastatin show significant improvement in myocardial flow reserve in all 3 vascular territories when compared with baseline values (A and B). The extent of the stress-induced defect decreased from 51% of LAD vascular territory to only 3%. Moreover, there is increase and normalization in myocardial blood flow reserve in LCX and RCA vascular territories, which could be detected only on quantitative measurements of myocardial blood flow (D) but not on evaluation of the relative radiotracer uptake (C). (Adapted from (65).)

View larger version (84K): [in this window] [in a new window]   FIGURE 7.  Transverse CT, PET, and integrated PET/CT images of the heart from a patient with ischemic cardiomyopathy are shown. (A) CT image shows abnormal thinning of the apical and apicolateral regions of the LV and preserved wall thickness in the septal and lateral regions. (B) Corresponding 18F-FDG PET image shows preserved metabolic activity in septal and lateral regions and relatively decreased metabolic activity in apical and apicolateral regions. (C) Integrated PET/CT image (C) provides accurate coregistration of the limited-spatial-resolution metabolic signal of PET with the high-resolution anatomic signal of CT. (Adapted from (30).)