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AIMS: To determine the myocardial salvage index, the extent of infarction needs to be related to the myocardium at risk (MaR). Thus, the ability to assess both infarct size and MaR is of central clinical and scientific importance. The aim of the present study was to explore the relationship between T2-weighted cardiac magnetic resonance (CMR) and contrast-enhanced steady-state free precession (CE-SSFP) CMR for the determination of MaR in patients with acute myocardial infarction. METHODS AND RESULTS: Twenty-one prospectively included patients with first-time ST-elevation myocardial infarction underwent CMR 1 week after primary percutaneous coronary intervention. For the assessment of MaR, T2-weighted images were acquired before and CE-SSFP images were acquired after the injection of a gadolinium-based contrast agent. For the assessment of infarct size, late gadolinium enhancement images were acquired. The MaR by T2-weighted imaging and CE-SSFP was 29 ± 11 and 32 ± 12% of the left ventricle, respectively. Thus, the MaR with T2-weighted imaging was slightly smaller than that by CE-SSFP (-3.0 ± 4.0%; P < 0.01). There was a significant correlation between the two MaR measures (r(2)= 0.89, P < 0.01), independent of the time after contrast agent administration at which the CE-SSFP was commenced (2-8 min). CONCLUSION: There is a good agreement between the MaR assessed by T2-weighted imaging and that assessed by CE-SSFP in patients with reperfused acute myocardial infarction 1 week after the acute event. Thus, both methods can be used to determine MaR and myocardial salvage at this point in time. (Less)

OBJECTIVES: Our goal was to validate myocardium at risk on T2-weighted short tau inversion recovery (T2-STIR) cardiac magnetic resonance (CMR) over time, compared with that seen with perfusion single-photon emission computed tomography (SPECT) in patients with ST-segment elevation myocardial infarction, and to assess the amount of salvaged myocardium after 1 week. BACKGROUND: To assess reperfusion therapy, it is necessary to determine how much myocardium is salvaged by measuring the final infarct size in relation to the initial myocardium at risk of the left ventricle (LV). METHODS: Sixteen patients with first-time ST-segment elevation myocardial infarction received (99m)Tc tetrofosmin before primary percutaneous coronary intervention. SPECT was performed within 4 h and T2-STIR CMR within 1 day, 1 week, 6 weeks, and 6 months. At 1 week, patients were injected with a gadolinium-based contrast agent for quantification of infarct size. RESULTS: Myocardium at risk at occlusion on SPECT was 33 +/- 10% of the LV. Myocardium at risk on T2-STIR did not differ from SPECT, at day 1 (29 +/- 7%, p = 0.49) or week 1 (31 +/- 6%, p = 0.16) but declined at week 6 (10 +/- 12%, p = 0.0096 vs. 1 week) and month 6 (4 +/- 11%, p = 0.0013 vs. 1 week). There was a correlation between myocardium at risk demonstrated by T2-STIR at week 1 and myocardium at risk by SPECT (r(2) = 0.70, p < 0.001), and the difference between the methods on Bland-Altman analysis was not significant (-2.3 +/- 5.7%, p = 0.16). Both modalities identified myocardium at risk in the same perfusion territory and in concordance with angiography. Final infarct size was 8 +/- 7%, and salvage was 75 +/- 19% of myocardium at risk. CONCLUSIONS: This study demonstrates that T2-STIR performed up to 1 week after reperfusion can accurately determine myocardium at risk as it was before opening of the occluded artery. CMR can also quantify salvaged myocardium as myocardium at risk minus final infarct size.

BACKGROUND: The amount of myocardium at risk (MaR) during acute coronary occlusion and the duration of occlusion are important determinants of final infarct size. The main goal of early reperfusion therapy is to salvage ischemic myocardium, thereby preserving left ventricular function. The aims of the present study were to test the feasibility of developing polar plot representations of MaR, for perfusion single photon emission computed tomography (SPECT), regional wall thickening by magnetic resonance imaging (MRI), and distribution of ST-segment changes. A second aim was to test the hypothesis that these different modalities display similar localization of the MaR in patients with reperfused first-time myocardial infarction. METHODS: Eleven patients with first-time myocardial infarction with ST-elevation received (99m)Tc tetrofosmin before primary percutaneous coronary intervention, SPECT imaging within 3 hours, and cardiac MRI of the left ventricle within 24 hours. The results for SPECT, MRI, and electrocardiogram (ECG) were developed into polar plots, and two expert observers designated the culprit coronary artery as assessed by angiography. RESULTS: The perfusion SPECT, MRI wall thickening, and ST changes are presented in side-by-side polar plots. In total, the culprit artery, based on the location of the MaR, was correctly designated in 91%, 82%, and 91% of cases by SPECT, MRI, and ECG, respectively. CONCLUSIONS: Polar representation for localization of the MaR by SPECT perfusion, MRI wall thickening, and ECG ST-segment deviation is feasible. All 3 modalities have the potential to be used for indirect visual designation of the culprit artery in patients with first-time acute coronary occlusion. (Less)

This study describes and validates a new method for automatic segmentation of left ventricular mass (LVM) in myocardial perfusion SPECT (MPS) images. This is important for estimating the size of a perfusion defect as percentage of the left ventricle. METHODS: A total of 101 patients with known or suspected coronary artery disease underwent both rest and stress MPS and MRI. A new automated algorithm was trained in 20 patients (40 MPS studies) and tested in 81 patients (162 MPS studies). The algorithm, which segmented the left ventricle in the MPS images, is based on Dijkstra's algorithm and finds an optimal mid-mural line through the left ventricular wall. From this line, the endocardium and epicardium are identified on the basis of an individually estimated wall thickness and signal intensity. The algorithm was validated by comparing LVM in both stress and rest MPS, with LVM of the manually segmented left ventricle from MRI as the reference standard. For comparison, LVM was quantified using the software quantitative perfusion SPECT (QPS). RESULTS: The mean difference +/- SD in LVM between MPS and MRI was lower for the new method (6% +/- 15% LVM) than for QPS (18% +/- 19% LVM) for both mean difference (P < 0.001) and SD (P = 0.015). Linear regression analysis of LVM, comparing MPS and MRI, yielded R(2) = 0.83 using the new method and R(2) = 0.80 using QPS. Interstudy variability, measured as the coefficient of variance between rest MPS and stress MPS, was 6% for both the new method and QPS. Both the new algorithm and QPS systematically overestimated LVM in hearts with thin myocardium and underestimated LVM in hearts with thick myocardium. CONCLUSION: The new segmentation algorithm quantifies LVM with a significantly lower bias and variability than does the commercially available QPS software, when compared to manually segmented LVM by MRI. This makes the new algorithm an attractive method to use for estimating the size of the perfusion defect when expressing it as percentage of the left ventricle. This study shows that inaccurate estimation of wall thickness is the main source of error in automatic segmentation. (Less)

Background Cardiovascular-MR (CMR) is the gold standard for quantifying myocardial infarction using late gadolinium enhancement (LGE) technique. Both 2D- and 3D-LGE-sequences are used in clinical practise and in clinical and experimental studies for infarct quantification. Therefore the aim of this study was to investigate if image acquisitions with 2D- and 3D-LGE show the same infarct size in patients and ex vivo. Methods Twenty-six patients with previous myocardial infarction who underwent a CMR scan were included. Images were acquired 10-20 minutes after an injection of 0.2 mmol/kg gadolinium-based contrast agent. Two LGE-sequences, 3D-inversion recovery (IR) and 2D-phase-sensitive (PS) IR, were used in all patients to quantify infarction size. Furthermore, six pigs with reperfused infarction in the left anterior descending artery (40 minutes occlusion and 4 hours of reperfusion) were scanned with 2D- and 3D-LGE ex vivo. A high resolution T1-sequence was used as reference for the infarct quantification ex vivo. Spearman’s rank-order correlation, Wilcoxon matched pairs test and bias according to Bland-Altman was used for comparison of infarct size with different LGE-sequences. Results There was no significant difference between the 2D- and 3D-LGE sequence in left ventricular mass (LVM) (2D: 115 ± 25 g; 3D: 117 ± 24 g: p = 0.35). Infarct size in vivo using 2D- and 3D-LGE showed high correlation and low bias for both LGE-sequences both in absolute volume of infarct (r = 0.97, bias 0.47 ± 2.1 ml) and infarct size as part of LVM (r = 0.94, bias 0.16 ± 2.0%). The 2D- and 3D-LGE-sequences ex vivo correlated well (r = 0.93, bias 0.67 ± 2.4%) for infarct size as part of the LVM. The IR LGE-sequences overestimated infarct size as part of the LVM ex vivo compared to the high resolution T1-sequence (bias 6.7 ± 3.0%, 7.3 ± 2.7% for 2D-PSIR and 3D-IR respectively, p Conclusions Infarct quantification with 2D- and 3D-LGE gives similar results in vivo with a very low bias. IR LGE-sequences optimized for in vivo use yield an overestimation of infarct size when used ex vivo.

Background Automatic segmentation of the left ventricle (LV) is desirable to assess the cardiac parameters end-diastolic volume (EDV), end-systolic volume (ESV), ejection fraction (EF) and left ventricular mass (LVM) since manual segmentation is time consuming and observer dependent. A physiologically correct segmentation of the left ventricle requires careful consideration of the long axis displacement and the LV outflow tract which makes the myocardium non-circumferential in the basal slices. To detect the long axis displacement a constraint could be used to keep the LVM fairly constant over the cardiac cycle. However, in order to use this constraint, the error of the segmentation has to be low regarding both endocardial and epicardial borders in the non-basal part of the LV. Therefore, the purpose of this study was to improve and validate an automatic algorithm for LV segmentation in the non-basal part of the LV, as a first step towards fully automatic segmentation.

Aims Determination of the myocardium at risk (MaR) and final infarct size by cardiac magnetic resonance imaging (CMR) enables calculation of salvaged myocardium in acute infarction. T2-weighted imaging is performed prior to the administration of gadolinium, since gadolinium affects T2 tissue properties. This is, however, difficult in an ex vivo model since gadolinium must be administered for determination of infarct size by CMR. We aimed to test the ability of ex vivo T2-weighted imaging to assess MaR using myocardial perfusion single photon emission computed tomography (SPECT) as reference and to investigate whether MaR could be assessed by ex vivo T2-weighted imaging after injection of gadolinium. Materials and methods In 18 domestic pigs, the left anterior descending artery was occluded for either 30 or 40 min, followed by 4 h of reperfusion. After explantation of the hearts, myocardial perfusion SPECT and T2-weighted imaging were performed for determination of MaR, either with or without gadolinium. Infarct size was determined by T1-weighted imaging and by triphenyl tetrazolium chloride (TTC) staining. Results T2-weighted imaging agreed with myocardial perfusion SPECT, both with and without gadolinium ( r 2= 0.70, P < 0.01) with a bias of 2.6 ± 5.1% ( P = 0.04). Infarct size was 15.4 ± 5.3 and 22.1 ± 5.6% with TTC and T1-weighted imaging, respectively ( P = 0.008) in nine pigs who had both infarct measures. Conclusion T2-weighted CMR imaging can be used to determine MaR in an ex vivo experimental model, both with and without the presence of gadolinium. Thus, CMR alone can be used to assess myocardial salvage in experimental studies.

Background T2-weighted cardiovascular magnetic resonance (CMR) has been shown to be a promising technique for determination of ischemic myocardium, referred to as myocardium at risk (MaR), after an acute coronary event. Quantification of MaR in T2-weighted CMR has been proposed to be performed by manual delineation or the threshold methods of two standard deviations from remote (2SD), full width half maximum intensity (FWHM) or Otsu. However, manual delineation is subjective and threshold methods have inherent limitations related to threshold definition and lack of a priori information about cardiac anatomy and physiology. Therefore, the aim of this study was to develop an automatic segmentation algorithm for quantification of MaR using anatomical a priori information. Methods Forty-seven patients with first-time acute ST-elevation myocardial infarction underwent T2-weighted CMR within 1 week after admission. Endocardial and epicardial borders of the left ventricle, as well as the hyper enhanced MaR regions were manually delineated by experienced observers and used as reference method. A new automatic segmentation algorithm, called Segment MaR, defines the MaR region as the continuous region most probable of being MaR, by estimating the intensities of normal myocardium and MaR with an expectation maximization algorithm and restricting the MaR region by an a priori model of the maximal extent for the user defined culprit artery. The segmentation by Segment MaR was compared against inter observer variability of manual delineation and the threshold methods of 2SD, FWHM and Otsu. Results MaR was 32.9 ± 10.9% of left ventricular mass (LVM) when assessed by the reference observer and 31.0 ± 8.8% of LVM assessed by Segment MaR. The bias and correlation was, -1.9 ± 6.4% of LVM, R = 0.81 (p < 0.001) for Segment MaR, -2.3 ± 4.9%, R = 0.91 (p < 0.001) for inter observer variability of manual delineation, -7.7 ± 11.4%, R = 0.38 (p = 0.008) for 2SD, -21.0 ± 9.9%, R = 0.41 (p = 0.004) for FWHM, and 5.3 ± 9.6%, R = 0.47 (p < 0.001) for Otsu. Conclusions There is a good agreement between automatic Segment MaR and manually assessed MaR in T2-weighted CMR. Thus, the proposed algorithm seems to be a promising, objective method for standardized MaR quantification in T2-weighted CMR.

BACKGROUND: By gating image acquisition in myocardial perfusion SPECT (MPS) to ECG, left ventricular (LV) volumes and function can be determined. Several previous studies have shown that existing MPS software packages underestimate LV volumes compared to cardiac magnetic resonance (CMR). The aim of this study was therefore to develop a new LV segmentation algorithm for gated MPS using CMR as reference standard. METHODS AND RESULTS: A total of 126 patients with suspected coronary artery disease, who underwent both gated MPS and CMR were retrospectively included. The proposed LV segmentation algorithm (Segment) was trained in 26 patients, and tested in 100 patients in comparison to four commercially available MPS software packages (QGS, MyoMetrix, ECTb, and Exini) using CMR as reference standard. Mean bias ± SD between MPS and CMR was for EDV -5% ± 12%, -43% ± 8%, -40% ± 8%, -42% ± 9%, -32% ± 7%, for ESV 0% ± 17%, -41% ± 16%, -34% ± 15%, -54% ± 13%, -41% ± 10%, for EF -2% ± 13%, -1% ± 14%, -7% ± 15%, 17% ± 16%, 10% ± 17% for Segment, QGS, MyoMetrix, ECTb, and Exini, respectively, and for LVM 3% ± 18%, 33% ± 25%, 37% ± 24% for Segment, QGS, and ECTb, respectively. Correlation between MPS by Segment and CMR were for EDV R (2) = 0.89, for ESV R (2) = 0.92, for EF R (2) = 0.69, and for LVM R (2) = 0.72, with no difference compared to the correlation between the other MPS software packages and CMR (EDV R (2) = 0.86-0.92, ESV R (2) = 0.91-0.93, EF R (2) = 0.64-0.65, and LVM R (2) = 0.68-0.70). CONCLUSION: The Segment software quantifies LV volumes and EF by MPS with similar correlation and a low bias compared to other MPS software packages, using CMR as reference standard. Hence, the Segment software shows potential to provide clinically relevant volumes and functional values from MPS.

Background Polymorphonuclear neutrophils, stimulated by the activated complement factor C5a, have been implicated in cardiac ischemia/reperfusion injury. ADC-1004 is a competitive C5a receptor antagonist that has been shown to inhibit complement related neutrophil activation. ADC-1004 shields the neutrophils from C5a activation before they enter the reperfused area, which could be a mechanistic advantage compared to previous C5a directed reperfusion therapies. We investigated if treatment with ADC-1004, according to a clinically applicable protocol, would reduce infarct size and microvascular obstruction in a large animal myocardial infarct model. Methods In anesthetized pigs (42-53 kg), a percutaneous coronary intervention balloon was inflated in the left anterior descending artery for 40 minutes, followed by 4 hours of reperfusion. Twenty minutes after balloon inflation the pigs were randomized to an intravenous bolus administration of ADC-1004 (175 mg, n = 8) or saline (9 mg/ml, n = 8). Area at risk (AAR) was evaluated by ex vivo SPECT. Infarct size and microvascular obstruction were evaluated by ex vivo MRI. The observers were blinded to the treatment at randomization and analysis. Results ADC-1004 treatment reduced infarct size by 21% (ADC-1004: 58.3 ± 3.4 vs control: 74.1 ± 2.9%AAR, p = 0.007). Microvascular obstruction was similar between the groups (ADC-1004: 2.2 ± 1.2 vs control: 5.3 ± 2.5%AAR, p = 0.23). The mean plasma concentration of ADC-1004 was 83 ± 8 nM at sacrifice. There were no significant differences between the groups with respect to heart rate, mean arterial pressure, cardiac output and blood-gas data. Conclusions ADC-1004 treatment reduces myocardial ischemia-reperfusion injury and represents a novel treatment strategy of myocardial infarct with potential clinical applicability.

Exacerbation of ST elevation associated with reperfusion has been reported in patients with myocardial infarction. However, the cause of the "reperfusion peak" and relation of its magnitude to the size of myocardial damage has not been explored. The aim of our study was to assess the correlation between the ST-dynamics during reperfusion, the myocardium at risk (MaR), and the infarct size (IS).Infarction was induced in 15 pigs by a 40-minute-long balloon inflation in the left anterior descending coronary artery. Tetrofosmin Tc 99m was given intravenously after 20 minutes of occlusion, and ex vivo single photon emission computed tomography was performed to assess MaR. Maximal ST elevation in a single lead and maximal sum of ST deviations in 12 leads were measured before, during, and after occlusion from continuous 12-lead electrocardiographic monitoring. A gadolinium-based contrast agent was given intravenously 30 minutes before explantation of the heart. Final IS was estimated using ex vivo cardiac magnetic resonance imaging.All pigs developed an anteroseptal infarct with MaR = 42% ± 9% and IS = 26% ± 7% of left ventricle. In all pigs, reperfusion was accompanied by transitory exacerbation of ST elevation that measured 1300 ± 500 μV as maximum in a single lead compared with 570 ± 220 μV at the end of occlusion (P.001). The transitory exacerbation of ST elevation exceeded the maximal ST elevation during occlusion (920 ± 420 μV, P.05). The ST elevation resolved by the end of the reperfusion period (90 ± 30 μV, P.001). Exacerbation of ST elevation after reperfusion correlated with the final IS (r = 0.64, P = .025 for maximal ST elevation in a single lead and r = 0.80, P = .002 for sum of ST deviations) but not with MaR (r = 0.43, P = .17 for maximal ST elevation in a single lead and r = 0.49, P = .11 for sum of ST deviations). The maximal ST elevation in a single lead and the sum of ST deviations during occlusion did not correlate with either MaR or final IS.In the experiment, exacerbation of ST elevation is common during restoration of blood flow in the occluded coronary artery. The magnitude of the exacerbation of ST elevation after reperfusion in experimentally induced myocardial infarction in pigs is associated with infarct size but not with MaR.

Introduction In the situation of acute coronary occlusion, the myocardium supplied by the occluded vessel is subject to ischemia and is referred to as the myocardium at risk (MaR). It has previously been shown that cardiac magnetic resonance (CMR) imaging can be used for the assessment of MaR employing a T2-weighted edema sequence. Recently, it has been suggested that the endocardial extent of hyperenhancement as assessed by contrast enhanced CMR can also be used to quantify the MaR.

To assess reperfusion therapy, it is necessary to determine how much myocardium is salvaged by measuring the final infarct size in relation to the initial myocardium at risk (MaR) of the left ventricle (LV). T2 weighted MRI has recently been shown to be able to identify MaR but has not been validated against an independent method in humans.

A graphic method was developed for presentation of the location and extent of the myocardium at risk in patients with acute myocardial infarction (AMI). This method is based on a mathematical processing of ST-segment deviations of standard 12-lead electrocardiogram following the concept of Titomir and Ruttkay-Nedecky in their dipolar electrocardiotopographic method. The center of the location of the area at risk is given by the spatial orientation of the resultant spatial ST vector, and the extent of the area at risk is derived from the Aldrich score. The areas at risk are projected on a spherical image surface, on which a texture of the anatomical quadrants of the ventricular surface and its coronary artery supply are projected. The method was tested in 10 patients with AMI with single-vessel disease, including 6 patients with an occlusion in the proximal left anterior descending coronary artery (LAD), 3 patients with an occlusion in the right coronary artery, and one patient with occlusion in the left circumflex coronary artery. The estimated areas at risk were compared with myocardial perfusion single photon emission computed tomography. Eight (80%) patients of 10 were correctly localized according to the Aldrich decision rules for the location of AMI. The areas at risk in patients with LAD occlusion correctly localized by the Aldrich score were situated in the anteroseptal and anterosuperior quadrants. In the inferior AMI group, the area at risk was localized in the posterolateral and inferior quadrants. The visual comparison with myocardial perfusion single photon emission computed tomography (SPECT) showed best agreement in patients with LAD involvement. The initial testing showed that this method allows a graphic presentation of estimated area at risk using clinically defined diagnostic rules. The area at risk can be displayed in images that are familiar for clinicians and can be compared with or superimposed on results of other imaging methods used in cardiology.

Background: Accurate quantification of left ventricular mass (LVM) by single photon emission computed tomography (SPECT) is important when analysing LVM as such, but also when estimating the relative size of a perfusion defect. Existing algorithms for segmentation of LVM by SPECT have undergone limited validation. The aim of this study was to develop and validate a new segmentation algorithm for LVM by SPECT, and compare the new method to the commercially available software Quantitative Gated SPECT (QGS). Methods: 98 patients with known or suspected coronary artery disease underwent both rest and stress SPECT and MR. The new method was trained in 20 patients (40 studies) and tested in 78 patients (156 studies) by comparing LVM in both rest and stress SPECT with manually segmented LVM by magnetic resonance imaging (MRI) as the reference standard. The new method was compared to results from QGS. Results: The mean difference ±SD in LVM between SPECT and MRI was lower for the new method (6±15 %LVM) compared to QGS (18±19 %LVM) for both mean difference (p . Conclusion: The new method quantifies LVM with a significantly lower bias and variability compared to the commercially available QGS software, when compared to manually segmented LVM by MRI.

Background Knowledge of the size and location of ischemic myocardium during acute coronary occlusion could provide decision support before reperfusion therapy. Electrocardiogram (ECG) scores based on the number of leads and the sum of ST-segment elevation have been unreliable in quantifying ischemia. We aimed to develop a new method to graphically display ischemic myocardium from simulated ECGs (DIMS-ECG) associated with known ischemic regions. Methods Twenty-one patterns of ischemia based on normal coronary anatomy were programmed into the freely available program ECGSIM ( www.ecgsim.org ). Minor variations of these patterns and 5 levels of ischemia severity produced 45 455 ECGs; 1000 normal ECGs were also added. Given a de novo ECG (an ECG from a patient), ST-segment and T-wave measurements are compared with ECG measurements in the database. The closest 200 matches are selected, and the corresponding ischemic areas are “averaged” to create a graphical display of the ischemic myocardium. Results Three patients are presented who underwent elective coronary angioplasty with continuous ECG recording and scintigraphically defined ischemic myocardium. Based on ECG analysis, the program graphically displays the ischemic myocardium with close agreement to the scintigraphic images. The program's source code and the ECG database will be made freely available. Conclusions The DIMS-ECG method graphically displays ischemic myocardium from information contained in the 12-lead ECG based on a novel approach to use a large simulated database instead of rule- or score-based method. After further development and testing, the DIMS-ECG method could be used to risk stratify patients with acute myocardial infarction.

This study presents a new method for estimation and imaging of the area at risk (AaR) in myocardial infarction (MI). The values of the ST-segment deviations of 12-lead ECG signal were used as input parameters. Based on DECARTO model, the spherical surface was chosen as a reference surface to approximate the ventricular wall. On this surface, the spatial ST vector was projected. The center of AaR was defined as an intersection of the spatial ST vector with spherical surface; the size of the AaR was set to be proportional to the number of electrical leads with ST-segment deviations. The method was tested using data of 10 patients with acute MI. The visual comparison showed good agreement with the AaRECG estimates based originally on the Selvester QRS scoring as well as with a non-electrocardiographic imaging method (SPECT).

The aim of the present study was to test the hypothesis that perfusion SPECT, estimation of regional wall thickening using MRI and the distribution of ST changes on the admission ECG display similar localization of the MaR in patients with reperfused first-time MI. Eleven patients with first-time MI with ST-elevation underwent percutaneous coronary intervention (PCI), SPECT imaging within 3 hours of the PCI and Cardiac MRI the day after admission. All images were presented in polar plots and compared with polar plots generated from the initial ECG's, based upon ST-changes. Comparison of the displays reveals similarity of location of myocardium at risk by all three methods in 73% of the patients, between SPECT and ECG in 91% of the patients, and between SPECT and wall thickening by MRI in 73% of the patient.

Background Left ventricular function is altered during and after AMI. Regional function can be determined by cardiac magnetic resonance (CMR) wall thickening, and velocity encoded (VE) strain analysis. The aims of this study were to investigate how regional myocardial wall function, assessed by CMR VE-strain and regional wall thickening, changes after acute myocardial infarction, and to determine if we could differentiate between ischemic, adjacent and remote segments of the left ventricle. Methods Ten pigs underwent baseline CMR study for assessment of wall thickening and VE-strain. Ischemia was then induced for 40-minutes by intracoronary balloon inflation in the left anterior descending coronary artery. During occlusion, 99mTc tetrofosmin was administered intravenously and myocardial perfusion SPECT (MPS) was performed for determination of the ischemic area, followed by a second CMR study. Based on ischemia seen on MPS, the 17 AHA segments of the left ventricle was divided into 3 different categories (ischemic, adjacent and remote). Regional wall function measured by wall thickening and VE-strain analysis was determined before and after ischemia. Results Mean wall thickening decreased significantly in the ischemic (from 2.7 mm to 0.65 mm, p

Infarct quantification with 3D- and 2D-LGE gives similar results in vivo with a very low bias. IR LGE-sequences optimized for in vivo use yield an overestimation of infarct size ex vivo.

Background In the situation of acute coronary occlusion, the myocardium supplied by the occluded vessel is subject to ischemia and is referred to as the myocardium at risk (MaR). Single photon emission computed tomography has previously been used for quantitative assessment of the MaR. It is, however, associated with considerable logistic challenges for employment in clinical routine. Recently, T2-weighted cardiovascular magnetic resonance (CMR) has been introduced as a new method for assessing MaR several days after the acute event. Furthermore, it has been suggested that the endocardial extent of infarction as assessed by late gadolinium enhanced (LGE) CMR can also be used to quantify the MaR. Hence, we sought to assess the ability of endocardial extent of infarction by LGE CMR to predict MaR as compared to T2-weighted imaging. Methods Thirty-seven patients with early reperfused first-time ST-segment elevation myocardial infarction underwent CMR imaging within the first week after percutaneous coronary intervention. The ability of endocardial extent of infarction by LGE CMR to assess MaR was evaluated using T2-weighted imaging as the reference method. Results MaR determined with T2-weighted imaging (34 ± 10%) was significantly higher (p < 0.001) compared to the MaR determined with endocardial extent of infarction (23 ± 12%). There was a weak correlation between the two methods (r2 = 0.17, p = 0.002) with a bias of -11 ± 12%. Myocardial salvage determined with T2-weighted imaging (58 ± 22%) was significantly higher (p < 0.001) compared to myocardial salvage determined with endocardial extent of infarction (45 ± 23%). No MaR could be determined by endocardial extent of infarction in two patients with aborted myocardial infarction. Conclusions This study demonstrated that the endocardial extent of infarction as assessed by LGE CMR underestimates MaR in comparison to T2-weighted imaging, especially in patients with early reperfusion and aborted myocardial infarction.

Background In the situation of an acute coronary occlusion, the myocardium supplied by the affected artery becomes ischemic. This part of the myocardium is at risk of developing infarction unless reperfusion occurs, and is therefore referred to as the myocardium at risk (MaR). Myocardium at risk and infarct size can be used to calculate myocardial salvage when evaluating efficacy of interventional or cardioprotective therapies. Cardiovascular magnetic resonance (CMR) has been shown to enable quantification of MaR using T2-weighted CMR and has been validated for use in patients. There are few studies validating T2-weighted CMR for ex vivo quantification of MaR in experimental studies, especially with presence of a gadolinium-based contrast agent needed for assessment of infarct size. The purpose of this study was to test if the clinically validated T2-weighted short tau inversion recovery (T2-STIR) imaging sequence can be used to assess MaR with gadolinium present in an experimental ex vivo setting. Methods Acute ischemia was induced in 26 pigs for 40 minutes followed by 4 hours of reperfusion using a closed-chest, catheter-based experimental model. After explantation and preparation of the heart, T2-STIR CMR images were acquired for quantification of MaR. As reference standard for MaR, ex vivo myocardial perfusion SPECT was used. For assessment of infarct size, high resolution T1-weighted CMR images were acquired. Results A strong correlation between MaR by T2-STIR CMR imaging and myocardial perfusion SPECT was found (r2=0.81, p