The clinical diagnosis of patients with non-obstructive coronaries and positive troponin remains a challenge. The concordance between CMR and clinical diagnosis is poor. CMR provides a diagnosis in majority of these patients.

BackgroundNo-reflow (TIMI < 3) during primary PCI (PCI) for STEMI occurs in 11–41% of cases, indicates poor myocardial tissue perfusion, and is associated with a poor outcome. We aimed to determine predictors and 12 month outcomes of patients who developed no-reflow.MethodsWe analysed the PCI database of The Canberra Hospital and identified 781 patients who underwent primary PCI during 2008–2012. Follow-up at 12 months was with letter, phone call and review of hospital records.ResultsNo-reflow was observed in 189 patients (25%) at the end of the procedure. Patients with no-reflow were older (64 vs. 61 years, p = 0.03). No-reflow patients were more likely to have initial TIMI flow < 3 (89% vs. 79%, p = 0.001), thrombus score ≥ 4 (83% vs. 69%, p = 0.0001), higher use of glycoprotein IIb/IIIa inhibitors (57% vs. 48%, p = 0.03) and longer median symptom to balloon time (223 min vs. 192 min, p = 0.004). No-reflow was an independent predictor of mortality (HR 1.95, CI 1.04-3.59, p = 0.037) during 12 month follow-up. On multivariate analysis, age > 60 years, thrombus score ≥ 4 and symptom to balloon time > 360 min were independent predictors of no-reflow. In 17% of cases of no reflow, it occurred only after stent insertion.ConclusionsNo-reflow occurred in 25% of STEMI patients undergoing primary PCI and was more likely with older age, high thrombus burden and delayed presentation. No-reflow was associated with a higher risk of death at 12 month follow-up.

BackgroundEgr‐1 is implicated in the pathogenesis of myocardial ischemia–reperfusion injury. The aim of this study was to ascertain the effectiveness of intracoronary delivery of DNAzyme targeting the transcription factor Egr‐1 at reperfusion following experimental myocardial ischemia.Methods and ResultsFunctional DNAzyme targeting Egr‐1 or a size‐matched scrambled control were delivered via the intracoronary route immediately on reperfusion after 60 minutes' balloon occlusion of the left anterior descending coronary artery in a pig model of myocardial I/R injury (n=7 per treatment group). Heart function and extent of myocardial infarction were determined following intervention by echocardiography and cardiac magnetic resonance imaging, respectively. Hearts were removed and examined for molecular and histological markers of inflammation and apoptosis. Administration of functional DNAzyme led to an overall decrease in the expression of inflammatory markers including intracellular adhesion molecule‐1, tissue factor, and complement 3, with associated decreases in the extent of neutrophil infiltration, oxidative damage, and subsequent apoptosis within the infarct border zone. Functional significance was indicated by an increase in salvaged left ventricular myocardium (P=0.012), ejection fraction (P=0.002), and fractional area change (P=0.039) in the functional DNAzyme–treated group compared with the control.ConclusionsEgr‐1 silencing through intracoronary delivery of a targeting DNAzyme at the time of reperfusion following acute myocardial ischemia decreases myocardial inflammation and apoptosis leading to improved cardiac function.

BackgroundQuantification of myocardial “area at risk” (AAR) and myocardial infarction (MI) zone is critical for assessing novel therapies targeting myocardial ischemia–reperfusion (IR) injury. Current “gold‐standard” methods perfuse the heart with Evan's Blue and stain with triphenyl tetrazolium chloride (TTC), requiring manual slicing and analysis. We aimed to develop and validate a high‐resolution 3‐dimensional (3D) magnetic resonance imaging (MRI) method for quantifying MI and AAR.Methods and ResultsForty‐eight hours after IR was induced, rats were anesthetized and gadopentetate dimeglumine was administered intravenously. After 10 minutes, the coronary artery was re‐ligated and a solution containing iron oxide microparticles and Evan's Blue was infused (for comparison). Hearts were harvested and transversally sectioned for TTC staining. Ex vivo MR images of slices were acquired on a 9.4‐T magnet. T2* data allowed visualization of AAR, with microparticle‐associated signal loss in perfused regions. T1 data demonstrated gadolinium retention in infarcted zones. Close correlation (r=0.92 to 0.94; P<0.05) of MRI and Evan's Blue/TTC measures for both AAR and MI was observed when the combined techniques were applied to the same heart slice. However, 3D MRI acquisition and analysis of whole heart reduced intra‐observer variability compared to assessment of isolated slices, and allowed automated segmentation and analysis, thus reducing interobserver variation. Anatomical resolution of 81 μm3 was achieved (versus ≈2 mm with manual slicing).ConclusionsThis novel, yet simple, MRI technique allows precise assessment of infarct and AAR zones. It removes the need for tissue slicing and provides opportunity for 3D digital analysis at high anatomical resolution in a streamlined manner accessible for all laboratories already performing IR experiments.