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Description of Clinical Presentation:
55-year-old caucasian man with a 4 hour history of sub-sternal, non-radiating, and non-exertional chest pain and pressure.
Past medical history includes positive stress test and negative subsequent cath for atypical chest pain 10 years ago.
Clinical examination and vitals were unremarkable, negative initial troponin, baseline ECG showed borderline ST depressions in V4 and V5.Repeat troponins were abnormal and repeat EKG showed a new RBBB.
Patient was started on heparin infusion, aspirin, high dose statin and transferred to the CCU.
Emergent echocardiogram demonstrated basal and mid-septum akinesis/dyskinesis.
Catheter coronary angiography performed(Fig 1) and interpreted as mild non-obstructive coronary artery disease. Medical management was maximized.
Subsequently patient developed palpitations, nausea and vomiting; repeat ECG showed type 1 Mobitz heart block with intermittent 3rd degree heart block and troponins were increasing.
CMR was ordered suspecting a non-ischemic etiology including acute myocarditis due the negative catheterization, AV Block and rising troponins
Diagnostic Techniques and Findings:
Emergent CMR was obtained and Cine SSFP(Fig 9,10) showed normal thickness of LV myocardium with basal anterior, anteroseptal and septal walls akinesis. T2 darkblood(Fig 3,4) showed hyperintensity and delayed post contrast PSIR images(Fig 5,7,8) showed subendocardial pattern of very dark signal with near transmural extent and a thin peripheral rim of late hyper-enhancement of basal septal wall.
CMR findings were compatible with acute transmural myocardial infarction and associated extensive microvascular obstruction(MVO) (no reflow phenomenon). Corresponding magnitude IR images(Fig6) showed high signal of MVO due to a long T1 effect.
Findings of AMI and MVO were discussed with cardiology team and recatheterization was recommended to identify a culprit coronary vessel.
Coronary catheter angiography was repeated and a total occlusion of a large first obtuse marginal branch(Fig 1)-- with a very early take off from the left circumflex coronary artery-- was identified and successfully stented, the artery become widely patent(Fig2)
Patient’s  post procedural course was unremarkable and he was discharged two days later following a permanent pacemaker.
Learning Points from this Case:
Power of CMR in depicting acute myocardial infarction, which was missed clinically and also on the gold standard catheter angiography in our patient. 
T2 hyperintensity (edema), MVO, late hyperenhancement with normal wall thickness and systolic wall motion abnormality indicate AMI on CMR
MVO is a poor prognostic predictor due to the risk of future CV events such as fatal arrhythmia
MVO on TI dependent magnitude IR images may have patchy high signals due to long T1 effect of an acute thrombus, but will depict dark signal on non TI dependent PSIR sequence. 
It is important for cardiac imagers to recognize findings and pitfalls of acute myocardial infarction on CMR  in patients presenting with chest pain as clinical indication and traditional cardiac tests including catheter angiography can be occasionally misleading. 
Utility of CMR in detecting clinically and angiographically missed acute myocardial infarction
Edgar Karanjah, Eduardo Hernandez-Rangel, Teferi Mitiku*, Pranav Patel*, Mayil S. Krishnam
Department of Radiological Sciences and *Division of Cardiology
University of California Irvine , Orange County, USA
SCMR 2017
Washington, D.C 8 1 2
Fig8. PSIR-LVOT: MVO within a full thickness infarction of basal anteroseptum. 9
Fig 1: Coronary Catheter Angiogram: Occluded OMI barely seen.
Fig2. Repeat Coronary Catheter Angiogram: Stent placement within OMI, widely patent 4 3 5 6 7
Fig 9 Snapshot of Cine SSFP basal SA during diastole . 10
Fig 5 PSIR: MVO within a full thickness infarction of anteroseptal wall. of LV
T2 DB SA(Fig 3) and HLA(Fig 4) : Hyperintensity at basal septal and anteroseptal wall of LV
Fig 6. MGIR: High signal of MVO due to long T1 effect of clot
Fig 7: PSIR-HLA: MVO within a full thickness infarction of basal septum.
Fig 10. Snapshot of Cine SSFP basal SA during systole; note no systolic thickening of anteroseptal wall of LV .
Fig 11: Initial EKG showed borderline ST depression on
V4 and V5 leads
Fig 12. Subsequent EKG showed RBBB
Fig 13. Mobitz type 1 with junctional escape rhythm.