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After a reperfused myocardial infarction (MI), dynamic tissue changes occur (edema, inflammation, microvascular obstruction, hemorrhage, cardiomyocyte necrosis, and ultimately replacement by fibrosis). The extension and magnitude of these changes contribute to long-term prognosis after MI. Cardiac magnetic resonance (CMR) is the gold-standard technique for noninvasive myocardial tissue characterization. CMR is also the preferred methodology for the identification of potential benefits associated with new cardioprotective strategies both in experimental and clinical trials. However, there is a wide heterogeneity in CMR methodologies used in experimental and clinical trials, including time of post-MI scan, acquisition protocols, and, more importantly, selection of endpoints. There is a need for standardization of these methodologies to improve the translation into a real clinical benefit. The main objective of this scientific expert panel consensus document is to provide recommendations for CMR endpoint selection in experimental and clinical trials based on pathophysiology and its association with hard outcomes., (Copyright © 2019 The Authors. Published by Elsevier Inc. All rights reserved.)

Objectives: This study was designed to determine the diagnostic value of adenosine cardiac magnetic resonance (CMR) in troponin-negative patients with chest pain., Background: We hypothesized that adenosine CMR could determine which troponin-negative patients with chest pain in an emergency department have coronary artery disease (CAD) or future adverse cardiac events., Methods: Adenosine stress CMR was performed on 135 patients who presented to the emergency department with chest pain and had acute myocardial infarction (MI) excluded by troponin-I. The main study outcome was detecting any evidence of significant CAD. Patients were contacted at one year to determine the incidence of significant CAD defined as coronary artery stenosis >50% on angiography, abnormal correlative stress test, new MI, or death., Results: Adenosine perfusion abnormalities had 100% sensitivity and 93% specificity as the single most accurate component of the CMR examination. Both cardiac risk factors and CMR were significant in Kaplan-Meier analysis (log-rank test, p = 0.0006 and p < 0.0001, respectively). However, an abnormal CMR added significant prognostic value in predicting future diagnosis of CAD, MI, or death over clinical risk factors. In receiver operator curve analysis, adenosine CMR was a more accurate predictor than cardiac risk factors (p < 0.002)., Conclusions: In patients with chest pain who had MI excluded by troponin-I and non-diagnostic electrocardiograms, an adenosine CMR examination predicted with high sensitivity and specificity which patients had significant CAD during one-year follow-up. Furthermore, no patients with a normal adenosine CMR study had a subsequent diagnosis of CAD or an adverse outcome.

Objectives: The current study tested the hypothesis that gadolinium delayed enhancement assessment of infarct size correlates with clinical indices of myocardial infarction (MI) in humans. Acute infarct mass by cardiac magnetic resonance (CMR) was compared with peak troponin I, acute and chronic left ventricular (LV) systolic function, and chronic infarct mass in patients imaged after recent acute MI., Background: Cardiac magnetic resonance accurately determines myocardial viability in patients with chronic ischemic heart disease but is not well validated for recent MI., Methods: Patients with first acute MI (n = 33) or chronic MI (n = 10) underwent cine CMR followed by gadolinium delayed enhancement imaging. A follow-up CMR scan was performed on 20 of the 33 acute MI patients and all of the chronic MI patients., Results: In patients with acute percutaneous coronary intervention, acute MI mass correlated with peak troponin I (r = 0.83, p < 0.001, n = 23). In the 20 acute infarct patients with follow-up CMR scans, the acute infarct size correlated well with the follow-up LV ejection fraction (r = 0.86, p < 0.001). The transmural extent of delayed enhancement imaged acutely correlated inversely with wall thickening measured acutely (p < 0.001) and at follow-up (p < 0.001). Although chronic infarct size was reproducible (11 +/- 4% vs. 12 +/- 7%, p = NS), acute infarct size decreased from 16 +/- 12% to 11 +/- 9% (p < 0.003)., Conclusion: In humans imaged shortly after acute MI, gadolinium delayed enhancement acute CMR infarct size correlates with acute and chronic indices of infarct size but will appear to diminish in size on follow-up.