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Background An understanding of inflammation following myocardial infarction may be of importance in the development of novel therapeutics to limit the development of heart failure following myocardial injury. However, the quantification of inflammation in this setting continues to be challenging. Hybrid FDG PET/MR may offer a non-invasive in vivo solution through intrinsic registration of these complementary modalities. This study sought to validate its use in a canine model of myocardial infarction (MI).

Background The clinical application of stem cell therapy for myocardial infarction will require the development of methods to monitor treatment and pre-clinical assessment in a large animal model, to determine its effectiveness and the optimum cell population, route of delivery, timing, and flow milieu. Objectives To establish a model for a) in vivo tracking to monitor cell engraftment after autologous transplantation and b) concurrent measurement of infarct evolution and remodeling. Methods We evaluated 22 dogs (8 sham controls, 7 treated with autologous bone marrow monocytes, and 7 with stromal cells) using both imaging of 111Indium-tropolone labeled cells and late gadolinium enhancement CMR for up to12 weeks after a 3 hour coronary occlusion. Hearts were also examined using immunohistochemistry for capillary density and presence of PKH26 labeled cells. Results In vivo Indium imaging demonstrated an effective biological clearance half-life from the injection site of ~5 days. CMR demonstrated a pattern of progressive infarct shrinkage over 12 weeks, ranging from 67–88% of baseline values with monocytes producing a significant treatment effect. Relative infarct shrinkage was similar through to 6 weeks in all groups, following which the treatment effect was manifest. There was a trend towards an increase in capillary density with cell treatment. Conclusion This multi-modality approach will allow determination of the success and persistence of engraftment, and a correlation of this with infarct size shrinkage, regional function, and left ventricular remodeling. There were overall no major treatment effects with this particular model of transplantation immediately post-infarct.

Introduction: Reperfusion injury in myocardial infarction leads to microvascular obstruction, which can occur with or without gross reperfusion hemorrhage. The incidence and implications of reperfusion hemorrhage are not well investigated. A recently described in vivo imaging approach using T2*-weighted cardiovascular magnetic resonance can help investigate the pathophysiology of reperfusion hemorrhage in vivo. Hypothesis: We hypothesized that hemorrhage reflects a severer from of reperfusion injury and therefore occurs with larger infarct size and worse LV function as compared to reperfusion injury without hemorrhage. Methods: In 14 female mongrel dogs, myocardial infarction was induced by ligation of the left anterior descending coronary artery for 2–4 hours, followed by reperfusion. On day 3 ± 1, a cardiovascular magnetic resonance study was performed in vivo to (1) assess presence of microvascular obstruction, defining reperfusion injury (2) assess presence of reperfusion hemorrhage (3) quantify left ventricular end-diastolic volume, ejection fraction and cardiac output and (4) quantify infarct size with late enhancement. An independent-samples t-test was performed to compare these parameters in dogs with and without hemorrhage in reperfusion injury. Results: From 14 dogs, 9 had microvascular obstruction, and 4/9 had reperfusion hemorrhage in addition to microvascular obstruction. Dogs with hemorrhagic infarcts had significantly larger infarct size (26.1 ± 6.6 g vs. 5.5 ± 3.9 g, p < 0.05), lower LV ejection fraction (28 ± 7% vs. 53 ± 12%, p < 0.05), and lower cardiac output (1.9 ± 0.2 l/min vs. 2.8 ± 0.5 l/min, p < 0.05). There were no differences in LV end-diastolic volume and LV mass. Discussion and conclusion: In this dog model of ischemia/reperfusion injury, gross hemorrhage was associated with significantly larger infarct size and worse LV functional parameters. This supports the hypothesis that hemorrhage may occur with advanced, severe ischemic tissue injury only.

Background: Reduced myocardial perfusion has been speculated as a potential mechanism for the development and/or propagation of myocardial fibrosis in hypertrophic cardiomyopathy (HCM). This study aims to evaluate the prevalence, distribution and extent of stress-induced perfusion abnormalities and their relationship to underlying fibrosis in patients with HCM using magnetic resonance imaging. Methods: 15 patients with echocardiographically diagnosed HCM have been enrolled. Cine imaging, first-pass stress perfusion imaging using vasodilator stress (Dipyridamole), and delayed gadolinium enhancement imaging were performed. Stress hypoperfusion and delayed enhancement images were assessed both quantitatively and visually using a 16-segment model. Conversion of segmental visual scoring to % of LV by volume was achieved for both hypoperfusion (HP) and late enhancement (LE) using a standardized scoring system. For quantitative assessment prospectively defined cut-offs for LE and HP were used. Results: Maximal wall thickness ranged from 13 to 22 mm (mean 17 ± 2.6 mm). Non-ischemic pattern LE was present in 70% of patients. Perfusion abnormalities were identified on stress perfusion images in 80% of patients using visual analysis and 87% of patients using quantitative analysis. Perfusion abnormalities were predominantly subendocardial, and were regionally associated with segments containing LE (p < 0.01). Mean percent HP and mean percent LE were 17 ± 8.4% and 10 ± 9.3%, respectively by visual estimation and 20.0 ± 12.1% and 14.0 ± 7.4%, respectively by quantitative assessment. Figure 1. Conclusion: These preliminary results suggest that patients with HCM have a high prevalence of stress-induced myocardial hypoperfusion as represented by reduced first-pass gadolinium enhancement during vasodilator stress. This hypoperfusion appears to extend beyond regions of established LE suggesting a potential contribution of ischemia in the development and/or propagation of myocardial fibrosis in patients with HCM.

Background and objectives Patients with Dilated Cardiomyopathy (DCM) and Hypertrophic Cardiomyopathy (HCM) frequently demonstrate non-ischemic pattern myocardial fibrosis (MF) on delayed enhancement magnetic resonance imaging (DE-MRI). The clinical significance of this finding with respect to impact on Quality of Life (QOL) is poorly understood. In this study we identify the prevalence of MF in patients with HCM and DCM and assess its relationship with standardized measures of QOL. Methods One-hundred and seven consecutive patients with either DCM (n=50) or HCM (n=57) referred for MRI evaluation were identified. DCM was defined as a LVEF 3SD above reference myocardium) using validated commercial software. Results