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Purpose: Myocardial infarction (MI) triggers complex cellular responses essential for tissue repair and remodeling, including myofibroblast activation. Fibroblast activation protein alpha (FAP) identifies activated myofibroblasts post-MI, however its spatial distribution relative to the scar and area at risk (AAR) is unclear. Non-invasive FAP-imaging with PET radiotracer 68 Ga-FAPI-46 shows uptake beyond the infarct scar. We therefore aimed to characterize FAP expression in the AAR using a myocardial ischemia–reperfusion (MI/R) model in mice.We induced MI/R in male C57BL/6N mice. The AAR was identified by in vivo lectin staining, and expression of FAP, CD68, and hypoxic tissues were measured using immunohistochemistry. Spatial FAP was further interrogated by 68 Ga-FAPI-46 in mice by autoradiography and humans by PET. Additionally, human cardiac tissues from acute MI patients were examined for fibroblasts and inflammatory cells by expression of FAP, CD13, and α-smooth muscle actin.FAP expression peaked three days post-MI/R predominantly within the AAR (p < 0.05 vs. d0). Consistent between murine models and human tissues, FAP+ myofibroblasts accumulated within the infarct scar and borderzone, occasionally extending into non-ischemic myocardium. CD68+ macrophages peaked similarly at three days post-MI/R (p < 0.05 vs. d0). FAP expression weakly correlated with CD68 but not with extent of ischemic or hypoxic territory post-MI/R. FAP imaging in mice and humans revealed aligned non-uniform 68 Ga-FAPI-46 uptake extending from the infarct scar into surviving myocardium after MI.Our findings demonstrate a distinct FAP expression pattern post-MI/R. The alignment of ex vivo68 Ga-FAPI-46 signal with myofibroblasts in the AAR supports its identification of a unique substrate in myocardial injury complementing other non-invasive imaging measurements of perfusion, viability and fibrosis.Procedures: Myocardial infarction (MI) triggers complex cellular responses essential for tissue repair and remodeling, including myofibroblast activation. Fibroblast activation protein alpha (FAP) identifies activated myofibroblasts post-MI, however its spatial distribution relative to the scar and area at risk (AAR) is unclear. Non-invasive FAP-imaging with PET radiotracer 68 Ga-FAPI-46 shows uptake beyond the infarct scar. We therefore aimed to characterize FAP expression in the AAR using a myocardial ischemia–reperfusion (MI/R) model in mice.We induced MI/R in male C57BL/6N mice. The AAR was identified by in vivo lectin staining, and expression of FAP, CD68, and hypoxic tissues were measured using immunohistochemistry. Spatial FAP was further interrogated by 68 Ga-FAPI-46 in mice by autoradiography and humans by PET. Additionally, human cardiac tissues from acute MI patients were examined for fibroblasts and inflammatory cells by expression of FAP, CD13, and α-smooth muscle actin.FAP expression peaked three days post-MI/R predominantly within the AAR (p < 0.05 vs. d0). Consistent between murine models and human tissues, FAP+ myofibroblasts accumulated within the infarct scar and borderzone, occasionally extending into non-ischemic myocardium. CD68+ macrophages peaked similarly at three days post-MI/R (p < 0.05 vs. d0). FAP expression weakly correlated with CD68 but not with extent of ischemic or hypoxic territory post-MI/R. FAP imaging in mice and humans revealed aligned non-uniform 68 Ga-FAPI-46 uptake extending from the infarct scar into surviving myocardium after MI.Our findings demonstrate a distinct FAP expression pattern post-MI/R. The alignment of ex vivo68 Ga-FAPI-46 signal with myofibroblasts in the AAR supports its identification of a unique substrate in myocardial injury complementing other non-invasive imaging measurements of perfusion, viability and fibrosis.Results: Myocardial infarction (MI) triggers complex cellular responses essential for tissue repair and remodeling, including myofibroblast activation. Fibroblast activation protein alpha (FAP) identifies activated myofibroblasts post-MI, however its spatial distribution relative to the scar and area at risk (AAR) is unclear. Non-invasive FAP-imaging with PET radiotracer 68 Ga-FAPI-46 shows uptake beyond the infarct scar. We therefore aimed to characterize FAP expression in the AAR using a myocardial ischemia–reperfusion (MI/R) model in mice.We induced MI/R in male C57BL/6N mice. The AAR was identified by in vivo lectin staining, and expression of FAP, CD68, and hypoxic tissues were measured using immunohistochemistry. Spatial FAP was further interrogated by 68 Ga-FAPI-46 in mice by autoradiography and humans by PET. Additionally, human cardiac tissues from acute MI patients were examined for fibroblasts and inflammatory cells by expression of FAP, CD13, and α-smooth muscle actin.FAP expression peaked three days post-MI/R predominantly within the AAR (p < 0.05 vs. d0). Consistent between murine models and human tissues, FAP+ myofibroblasts accumulated within the infarct scar and borderzone, occasionally extending into non-ischemic myocardium. CD68+ macrophages peaked similarly at three days post-MI/R (p < 0.05 vs. d0). FAP expression weakly correlated with CD68 but not with extent of ischemic or hypoxic territory post-MI/R. FAP imaging in mice and humans revealed aligned non-uniform 68 Ga-FAPI-46 uptake extending from the infarct scar into surviving myocardium after MI.Our findings demonstrate a distinct FAP expression pattern post-MI/R. The alignment of ex vivo68 Ga-FAPI-46 signal with myofibroblasts in the AAR supports its identification of a unique substrate in myocardial injury complementing other non-invasive imaging measurements of perfusion, viability and fibrosis.Conclusions: Myocardial infarction (MI) triggers complex cellular responses essential for tissue repair and remodeling, including myofibroblast activation. Fibroblast activation protein alpha (FAP) identifies activated myofibroblasts post-MI, however its spatial distribution relative to the scar and area at risk (AAR) is unclear. Non-invasive FAP-imaging with PET radiotracer 68 Ga-FAPI-46 shows uptake beyond the infarct scar. We therefore aimed to characterize FAP expression in the AAR using a myocardial ischemia–reperfusion (MI/R) model in mice.We induced MI/R in male C57BL/6N mice. The AAR was identified by in vivo lectin staining, and expression of FAP, CD68, and hypoxic tissues were measured using immunohistochemistry. Spatial FAP was further interrogated by 68 Ga-FAPI-46 in mice by autoradiography and humans by PET. Additionally, human cardiac tissues from acute MI patients were examined for fibroblasts and inflammatory cells by expression of FAP, CD13, and α-smooth muscle actin.FAP expression peaked three days post-MI/R predominantly within the AAR (p < 0.05 vs. d0). Consistent between murine models and human tissues, FAP+ myofibroblasts accumulated within the infarct scar and borderzone, occasionally extending into non-ischemic myocardium. CD68+ macrophages peaked similarly at three days post-MI/R (p < 0.05 vs. d0). FAP expression weakly correlated with CD68 but not with extent of ischemic or hypoxic territory post-MI/R. FAP imaging in mice and humans revealed aligned non-uniform 68 Ga-FAPI-46 uptake extending from the infarct scar into surviving myocardium after MI.Our findings demonstrate a distinct FAP expression pattern post-MI/R. The alignment of ex vivo68 Ga-FAPI-46 signal with myofibroblasts in the AAR supports its identification of a unique substrate in myocardial injury complementing other non-invasive imaging measurements of perfusion, viability and fibrosis. [ABSTRACT FROM AUTHOR]

Purpose of Review Cardiac magnetic resonance (CMR) has emerged in recent years as a reliable tool to assess, in a single examination after a reperfused myocardial infarction, the initially area at risk (AAR), the final infarct size (IS), and from their difference the salvaged myocardium (SM). The aim of the present review is to summarize recent advances in the CMR imaging of SM. Recent Findings While there is consensus on the use of late gadolinium enhancement (LGE) to calculate IS, how to assess the AAR is a debated topic. The use of T2-weighted short-TI inversion recovery (T2W-STIR) is to date supported by a large amount of data, but it is affected by several limitations. Newer techniques have been developed to overcome T2W-STIR limitations, some of them have been already used in randomized clinical trials (RCTs) while others are showing promising results. The use of CMR to generate surrogate endpoints in RCTs is gaining attention; in this context, analysis of data from recent RCTs suggests that the assessment of SM as outcome measure could be useful to reduce sample sizes and costs of trials. Summary CMR is a reliable technique for the assessment of SM. LGE is the gold standard for IS measurement, while which is the best technique for the evaluation ofAAR is still debated. When using CMR-derived endpoints in RCTs, the assessment of SM is advisable. [ABSTRACT FROM AUTHOR]

Objectives: The purpose of this study was to estimate the myocardial area at risk (MAAR) using coronary computed tomography angiography (CTA) and Voronoi algorithm-based myocardial segmentation in comparison with single-photon emission computed tomography (SPECT). Methods: Thirty-four patients with coronary artery disease underwent 128-slice coronary CTA, stress/rest thallium-201 SPECT, and coronary angiography (CAG). CTA-based MAAR was defined as the sum of all CAG stenosis (>50 %) related territories (the ratio of the left ventricular volume). Using automated quantification software (17-segment model, 5-point scale), SPECT-based MAAR was defined as the number of segments with a score above zero as compared to the total 17 segments by summed stress score (SSS), difference (SDS) score map, and comprehensive SPECT interpretation with either SSS or SDS best correlating CAG findings (SSS/SDS). Results were compared using Pearson's correlation coefficient. Results: Forty-nine stenoses were observed in 102 major coronary territories. Mean value of CTA-based MAAR was 28.3 ± 14.0 %. SSS-based, SDS-based, and SSS/SDS-based MAAR was 30.1 ± 6.1 %, 20.1 ± 15.8 %, and 26.8 ± 15.7 %, respectively. CTA-based MAAR was significantly related to SPECT-based MAAR ( r = 0.531 for SSS; r = 0.494 for SDS; r = 0.814 for SSS/SDS; P < 0.05 in each). Conclusions: CTA-based Voronoi algorithm myocardial segmentation reliably quantifies SPECT-based MAAR. Key points: • Voronoi algorithm allows for three-dimensional myocardial segmentation of coronary CT angiography • Stenosis-related CT myocardial territories correlate to SPECT based area at risk • CT angiography myocardial segmentation may assist in clinical decision-making [ABSTRACT FROM AUTHOR]

Area at risk (AAR) is an important parameter for the assessment of the salvage area after revascularization in acute myocardial infarction (AMI). By combining AAR assessment by T2-weighted imaging and scar quantification by late gadolinium enhancement imaging cardiovascular magnetic resonance (CMR) offers a promising alternative to the 'classical' modality of Tc99m-sestamibi single photon emission tomography (SPECT). Current T2 weighted sequences for edema imaging in CMR are limited by low contrast to noise ratios and motion artifacts. During the last years novel CMR imaging techniques for quantification of acute myocardial injury, particularly the T1-mapping and T2-mapping, have attracted rising attention. But no direct comparison between the different sequences in the setting of AMI or a validation against SPECT has been reported so far. We analyzed 14 patients undergoing primary coronary revascularization in AMI in whom both a pre-intervention Tc99m-sestamibi-SPECT and CMR imaging at a median of 3.4 (interquartile range 3.3-3.6) days after the acute event were performed. Size of AAR was measured by three different non-contrast CMR techniques on corresponding short axis slices: T2-weighted, fat-suppressed turbospin echo sequence (TSE), T2-mapping from T2-prepared balanced steady state free precession sequences (T2-MAP) and T1-mapping from modified look locker inversion recovery (MOLLI) sequences. For each CMR sequence, the AAR was quantified by appropriate methods (absolute values for mapping sequences, comparison with remote myocardium for other sequences) and correlated with Tc99m-sestamibi-SPECT. All measurements were performed on a 1.5 Tesla scanner. The size of the AAR assessed by CMR was 28.7 ± 20.9 % of left ventricular myocardial volume (%LV) for TSE, 45.8 ± 16.6 %LV for T2-MAP, and 40.1 ± 14.4 %LV for MOLLI. AAR assessed by SPECT measured 41.6 ± 20.7 %LV. Correlation analysis revealed best correlation with SPECT for T2-MAP at a T2-threshold of 60 ms (ms) (slope = 0.99, Pearson's r = 0.94), and for MOLLI at T1-threshold of 1,075 ms (slope 0.86, r = 0.91, Pearson's r = 0.45). For the assessment of AAR in AMI, the novel T2-mapping technique correlates best with SPECT size, T1-mapping with MOLLI and standard T2-weighted imaging showed similar good correlations. [ABSTRACT FROM AUTHOR]

Myocardial in vivo tissue characterization is of great importance because it can provide meaningful information to understand pathophysiological processes underlying different cardiac diseases. Ex vivo histologic analyses of tissue samples have been classically considered the gold standard in the study of tissue properties and its composition. However, over the past decade, there has been a growing interest in the in vivo myocardial characterization with different imaging techniques, which can potentially be translated into the clinics in order to make an early diagnosis and evaluate serial changes, opening the possibility of dynamic evaluation. Animal models have become an essential tool to achieve this goal. This article aims at concisely reviewing recent and significant developments in the field of imaging techniques-mostly cardiac magnetic resonance-in relevant animal models of tissue characterization of area at risk, edema, and fibrosis. [ABSTRACT FROM AUTHOR]

To evaluate the myocardial area at risk (AAR) measured by the endocardial surface area (ESA) method on late gadolinium enhancement (LGE) cardiovascular magnetic resonance (CMR) when applied after scar remodeling (3 months after index infarction) compared to T2-weighted CMR imaging. One hundred and sixty nine patients with ST-elevation myocardial infarction, treated with primary percutaneous coronary intervention, underwent one CMR within 1 week after index treatment to determine the AAR with T2-weighted imaging and a second scan 3 months after to measure AAR with the ESA method. There was a moderate correlation between the two methods (r = 0.86; P < 0.001). The AAR was significantly higher measured with T2-weighted imaging than with the ESA methods (32 ± 11% of left ventricle (LV) vs. 26 ± 10%LV; P < 0.001). The mean difference was 6 ± 6%LV. Furthermore, the mean difference between the two methods was statistical higher in the patients with myocardial salvage index ≥0.90 than in the remaining patients (9 ± 8%LV vs. 6 ± 5%LV; P = 0.02). The ESA method performed after scar remodeling (3 months following STEMI) yields significantly lower AAR′s and myocardial salvage indices compared to the T2-weighted method. Therefore, T2-weighted CMR plus LGE is the method of choice to assess AAR and myocardial salvage index using CMR. However, the ESA method is an easy and valid method for determining AAR, which can be used in settings where T2-weighted imaging has not been obtained in the acute phase. [ABSTRACT FROM AUTHOR]

The purpose of this study was to compare the accuracy of post-reperfusion cardiac magnetic resonance (CMR) and pre-reperfusion multidetector computed tomography (MDCT) imaging to measure the size of the area at risk (AAR), using pathology as a reference technique in a porcine acute myocardial infarction model. Fifteen pigs underwent balloon-induced coronary artery occlusion for 40 min followed by reperfusion. The AAR was assessed with arterial enhanced MDCT performed during occlusion, while two different T2 weighted (T2W) CMR imaging sequences and the contrast-enhanced (ce-) CMR endocardial surface length (ESL) were performed after 90 min of reperfusion. Animals were euthanized and the AAR was assessed by pathology. Additional measurements of the myocardial water content in the AAR, remote and the AAR border zones were performed. AAR by pathology best correlated with measurements made by MDCT (R 2 = 0.88; p < 0.001) with little bias on Bland–Altman plots (bias 2.5%, SD 6.1% LV area). AAR measurements obtained by T2W STIR, T2W ACUTE sequences or the ESL on ce-CMR showed a fair correlation with pathology (R 2 = 0.72, R 2 = 0.65 and R 2 = 0.69, respectively; all p ≤ 0.001), but significantly overestimated the size of the AAR with important bias (17.4 ± 10.8% LV area; 11.7 ± 11.0% LV area; 13.0 ± 10.3% LV area, respectively). The myocardial water content in the AAR border zones was significantly higher than the remote (82.8 vs. 78.8%; p < 0.001). Our data suggest that post-reperfusion imaging methods overestimated the AAR likely due to the presence of edema outside of the boundaries of the AAR. Pre-reperfusion arterial enhanced MDCT showed the greatest accuracy for the assessment of the AAR. [ABSTRACT FROM AUTHOR]

Acute myocardial infarction (MI) results in reversible and irreversible injury to the myocardium, including stunning, edema, myocyte necrosis, and microvascular obstruction. Because of its unique tissue characterization capabilities, cardiovascular magnetic resonance provides a reliable means of visualizing and quantifying the extent of these injuries. Such characterization is readily achieved through a comprehensive examination including function, first-pass perfusion, T2 (edema), and late enhancement imaging sequences. This helps to predict the prognosis, assess the success of reperfusion, detect acute phase complications, localize the area of the acute event, and confirm the diagnosis in clinical scenarios with clinical presentations similar to that of acute MI. Finally, one emerging application is the role cardiovascular magnetic resonance (CMR) may play in detecting some infarcts very early on in their evolution. This article covers the established and emerging clinical applications of CMR in the settings of reperfused and nonreperfused infarcts and in acute myocardial ischemia, the step immediately preceding actual irreversible injury. [ABSTRACT FROM AUTHOR]

Clinical investigations have suggested that the defects in SPECT images of a free fatty acid analog, I-123 beta-methyliodophenyl pentadecanoic acid (BMIPP) may indicate the ischemic risk area. To elucidate whether I-123 BMIPP can indicate the area at risk of ischemia, ex-vivo autoradiography was performed in rats whose left coronary artery was occluded for 60 min and then reperfused. I-123 BMIPP was injected at the acute stage (n = 10), or the subacute stage (7 days after reperfusion; n = 9). Infarction and the area at risk were identified by triphenyl tetrazolium chloride staining and injection of methylene blue during religation just before sacrifice, respectively. The BMIPP uptake in the risk area was significantly lower than that in the remote area at the acute (risk, 53.7+/-23.3% of the uptake at right ventricle, mean +/- SD; remote, 109.3+/-11.8%; p < 0.01) and subacute (risk, 52.5+/-11.5%; remote, 97.9+/-14.3%; p < 0.01) stages. In addition, the area with reduced uptake of I-123 BMIPP showed a significant correlation with the area at risk both at the acute (r = 0.98, p < 0.01) and subacute (r = 0.92, p < 0.01) stages. In conclusion, the area at risk can be evaluated by I-123 BMIPP both at the acute and subacute stages. [ABSTRACT FROM AUTHOR]

Previous studies have indicated that iodine-123 labelled β-methyliodophenyl pentadecanoic acid (BMIPP), an iodinated fatty acid analogue, can identify persistent alteration of fatty acid metabolism after restoration of blood flow. To assess whether fatty acid imaging can delineate areas at risk following successful revascularization in patients with acute myocardial infarction (AMI), BMIPP findings at 1 week post AMI were compared with perfusion imaging before and after revascularization therapy. Sixty-five patients with AMI underwent technetium-99m tetrofosmin single-photon emission tomography (SPET) before m (TF0) and 1 week (TF1) after successful revascularization therapy. BMIPP SPET was also performed under a fasting state at 1 week (BM1) post AMI. The extent scores were calculated from the defect scores in 20 segments. The BM1 score (7.7±3.9) was similar to the TF0 score (8.8±4.2) ( r=0.86, P<0.0001), but significantly higher than the TF1 score (5.8±3.9) ( P<0.0001). A significant correlation was observed between the BM1 score and TF0 score ( r=0.86, P<0.0001). Among a total of 1300 segments, the BM1 score was identical to the TF0 score in 1156 (88.9%). These data indicate that the ability of BMIPP imaging at 1 week post AMI to identify areas at risk is similar to that of tetrofosmin perfusion imaging in the acute phase. This may be due to the impairment of fatty acid uptake and metabolism reflecting prior severe ischaemic insult which persists at least 1 week after recovery of perfusion in the acute phase of AMI. [ABSTRACT FROM AUTHOR]

Myocardial function around the border of ischemia was investigated in eight open-chest dogs using video mapping of epicardial deformation. With this method, 40-60 white markers attached to the left ventricular epicardium were traced in time automatically. Before and 5-10 min after coronary artery occlusion, blood flow and epicardial deformation were determined in 30-40 regions with a spatial resolution of about 5 mm. Epicardial deformation was expressed as subepicardial fiber shortening and surface area decrease during the ejection phase. The latter indicates local contribution to stroke volume. The absolute values of these variables were normalized relative to the central ischemic (= 0%) and remote non-ischemic area (= 100%). The 50% contour line of a variable was defined as its border. The average distance between the borders of perfusion and function was not significantly different from zero, due to considerable variation in this distance both within one heart (± 5.7 mm) and between mean distances for different hearts (± 4.4 mm). The width of the transition zone (distance between the 20% and 80% contour lines) of surface area decrease and subepicardial fiber shortening was significantly larger (20.5 and 15.0 mm, respectively) than those of transmural and subepicardial blood flow (8.5 and 9.5 mm, respectively). The present results demonstrate that in a 20-mm zone around the border of ischemia, major discrepancies are present between perfusion and deformation. [ABSTRACT FROM AUTHOR]

In a canine model of coronary artery occlusion and reperfusion, we assessed the amount of myocardium at risk for necrosis using both post-mortem perfusion staining with triphenyltetrazoliumchloride (TTC) and autoradiography following in vivo injection ofCe microspheres. Twenty-four transverse slices of 5 dog hearts were analyzed. In the same heart slice planimetry was performed both on the calibrated colour picture taken after TTC staining (A) and on the autoradiogram (B). The values for the area at risk, as determined by both methods, were very closely correlated and almost identical: A=0.977 B+31.4 mm, r=0.99, p<0.001. This is in contrast to an earlier report where a different autoradiographic technique was used. In short-term experimental models of coronary artery occlusion, autoradiography delineates an area at risk, matching very closely the area at risk obtained after TTC staining. [ABSTRACT FROM AUTHOR]

The determination of the myocardium at risk before intervention and the change in that region after intervention constitute a promising measurement tool for the assessment of acute therapy. A newTc labeled myocardial blood flow tracer,Tc tetrofosmin, is expected to enable the evaluation of myocardium at risk because of the absence of redistribution. This preliminary study was performed in 9 patients with acute coronary syndrome (4 unstable angina and 5 acute myocardial infarction) to investigate whether recovery of perfusion by tetrofosmin imaging parallels mechanical improvement. Tetrofosmin imaging was performed acutely and 3-30 days later. Visual analysis of defect severity was assessed in both studies. Segments with improvement in perfusion were accompanied by significant wall motion recovery compared with normal and unimproved segments (Δ WMI: normal segments 0.40±0.67, improved segments 1.79±0.68, unimproved segments −0.15±0.16, p< 0.01 for improved segments compared with other groups), suggesting the efficacy of this tracer for the assessment of the acute therapy. These data suggest thatTc tetrofosmin imaging is a useful method for the assessment of the myocardial area at risk and the efficacy of acute therapy in acute myocardial infarction and unstable angina. [ABSTRACT FROM AUTHOR]

The aim of this study was to directly compare three currently used quantitative methods of analysis of technetium-99m sestamibi images in patients with selective balloon-induced transmural ischaemia. The area at risk (AR) was assessed in 19 patients undergoing singlevessel percutaneous transluminal coronary angioplasty by injecting theTc-sestamibi at the time of coronary artery occlusion during balloon inflation. After imaging, the patients were classified according to localization of the perfusion defect as having anteroseptal (group I, 11 patients) or posterolateral defects (group II, eight patients). The planimetric technique based on polar maps, proposed by Verani et al. ( J Am Coll Cardiol, 1988) (method A), the method described by Tamaki et al. ( Circulation, 1982) (method B) and the technique validated by O'Connor et al. ( Eur J Nucl Med, 1990) (method C) were tested. Three threshold values of 45%, 50% and 60% of the maximum left ventricular count were used to define the limits of the perfusion defect. The mean values of the AR calculated by the three techniques with the original cut-off level (method A=16.5%±12.9; method B=10.4%±7.6%; method C=29.6%±15.7%) were statistically different (one-way analysis of variance: P<0.001; paired t test: method A vs B, P=0.003; method B vs C and method A vs C, P<0.0001). There was no significant difference between the mean values of the AR estimated by the three methods using the same cut-off levels. The use of 60% of the maximum left ventricular count provided the best correlation between the techniques (method A vs B, r=0.95; method B vs C, r=0.92; method A vs C, r=0.95). Nevertheless, a difference >10% between the values of AR assessed by the three methods was found in four subjects. There was no significant difference between the three methods in the evaluation of AR in the subjects of group I and group II. Reproducibility was good for all methods. It is concluded that the three methods of analysis of the AR byTc-sestamibi SPET imaging showed comparable performance and good reproducibility using the same cut-off level. The location of perfusion defect does not affect the comparability of the three techniques. We suggest the use of a cut-off level of 60% for all three methods in the assessment of the AR byTc-sestamibi SPET imaging. [ABSTRACT FROM AUTHOR]