Critical Pathways in Cardiology •  Volume 13, Number 4, December 2014 www.critpathcardio.com  |  135 ORIGINAL ARTICLE Abstract: Patients with presumed ST-elevation myocardial infarction (STEMI) have no clear culprit artery in approximately 10–15% of cases. We examined the value of cardiac magnetic resonance (CMR) for diagnosis in patients with “no culprit” STEMI. Data from a comprehensive prospective registry of STEMI patients were reviewed from March 2003 to December 2009. “No culprit” patients were followed for diagnosis and clinical outcome. CMR was performed at the discretion of the attending cardiologist. Of 2728 consecutive presumed STEMI patients, 412 (15%) had no clear culprit artery. Of these, 202 (49%) had abnormal cardiac biomarkers with a definitive diagnosis in 157 (78%). Diagnoses in this group included myocardial infarction without a culprit lesion (24%), myopericarditis (22%), and stress cardiomyopathy (21%). In 210 (51%) patients with normal biomarkers, only 84 (40%) received a definitive diagnosis. Diagnoses in this group included myopericarditis (27%), noncardiac causes (21%), and cardiomyopathy (14%). CMR was performed in 123 (30%) “no culprit” patients. Patients who had CMR were more likely to have a definitive diagnosis than those who did not (95/123 [77%] vs. 144/289 [50%]; P = 0.01). In particular, “no culprit” patients with abnormal biomarkers were more likely to have a definitive diagnosis with CMR. CMR led to a diagnosis different from the presumptive clinical diagnosis in 53% of all cases. CMR is a valuable diagnostic tool to improve diagnostic accuracy in patients with “no culprit” STEMI. Key Words: cardiac magnetic resonance imaging, ST-elevation myocardial infarction, cardiac biomarkers (Crit Pathways in Cardiol 2014;13: 135–140) E lectrocardiographic ST-elevation initiates emergent diagnosis and therapy for patients with suspected ST-elevation myocardial infarction (STEMI). 1–4 However, 10–15% of patients with electro- cardiographic ST-elevation have no clear culprit coronary artery at coronary angiography. 5 Serious conditions other than acute plaque rupture may cause ST-elevation with abnormal cardiac biomarkers, including coronary artery spasm, coronary artery embolism, stress cardiomyopathy, myocarditis/pericarditis, and pulmonary embo- lism. 6,7 Causes of ST-elevation with no clear culprit artery and nor- mal cardiac biomarkers may be no less severe, including malignant arrhythmias and acute aortic dissection. 5,6 Definitive diagnosis can be challenging in patients presenting with presumed STEMI and no clear culprit artery. Cardiac magnetic resonance (CMR) imaging offers potential diagnostic advantages, with the ability to distinguish myocardial fibrosis, myocardial infarc- tion (acute and chronic), and tissue edema. 8–15 We examined patients presenting emergently with electrocardiographic ST-elevation and no clear culprit artery by coronary angiography to determine the utility of CMR for diagnosis. METHODS The Level 1 Myocardial Infarction program of the Minneapolis Heart Institute at Abbott Northwestern Hospital (Minneapolis, MN) is a regional STEMI system using a standardized protocol and rapid transfer of STEMI patients for percutaneous coronary intervention (PCI).The design and clinical results of the program have been pre- viously published. 4,5,16 Detailed past medical history, cardiovascular risk factors, clinical presentation, time to treatment, laboratory, elec- trocardiogram (ECG), angiographic, and follow-up data to 5 years are entered in a comprehensive prospective database. We examined the Level 1 myocardial infarction (MI) database to determine the util- ity of CMR for diagnosis in patients presenting with STEMI and no clear culprit artery from March 2003 to December 2009. Definitions A culprit artery was defined as an acute total or subtotal coro- nary occlusion or a lesion with visible thrombus. 5 ST-elevation was defined as J-point elevation in 2 or more contiguous leads, with a cutoff of greater than or equal to 0.2 mV in leads V1, V2, or V3 and greater than or equal to 0.1 mV in other leads. Abnormal cardiac biomarkers were defined as CK-MB peak of greater than 8 ng/mL with CK total peak greater than 140 ng/mL and/or troponin-T peak of greater than 0.05 ng/mL. 17 The presumptive diagnosis was the initial clinical diagno- sis of the attending cardiologist. A definitive diagnosis was based on subsequent clinical developments or additional diagnostic tests, such as characteristic findings on CMR. Presumptive and definitive diagnoses (clinical and CMR) were separated into the following cat- egories: MI without coronary lesion (ie, spontaneous resolution of thrombus, embolism, or spasm), myocarditis/pericarditis, stress car- diomyopathy, cardiomyopathy, pulmonary embolism, cardiac arrest, presumed noncardiac, miscellaneous, and no diagnosis. No diagnosis was defined as nondiagnostic CMR in patients with normal or mild coronary artery disease, as well as patients with previous PCI, MI, or coronary artery bypass surgery (CABG), but no acute culprit lesion. MI without a coronary culprit was diagnosed by (1) character- istic CMR finding of MI in a discrete vascular distribution 8,9,15 and (2) clinical findings of spontaneous resolution of thrombus, embo- lism, or coronary spasm. Myocarditis was defined by characteristic CMR findings 10,18 or diagnostic ECG findings of pericarditis with elevated cardiac biomarkers. Pericarditis was defined by clinical and ECG findings with normal cardiac biomarkers. 6 Stress cardiomy- opathy was defined by (1) CMR without hyperenhancement, (2) the physician’s clinical diagnosis of typical apical or mid-ventricular bal- looning noted on left ventriculography, or (3) reversible left ventricu- lar systolic dysfunction without significant coronary disease. 11,12,19 Cardiomyopathy included chronic ischemic and nonischemic eti- ologies. Pulmonary embolism was identified by diagnostic CMR or computed tomographic pulmonary angiogram findings. Cardiac arrest included hemodynamically unstable ventricular tachycardia, “No Culprit” ST-Elevation Myocardial Infarction: Role of  Cardiac Magnetic Resonance Imaging Madeline M. Stark, BA,* Robert S. Schwartz, MD,* Daniel Satran, MD,† John R. Lesser, MD,* Scott W. Sharkey, MD,* Ross F. Garberich, MS,* Christopher J. Solie, BS,* Terrence F. Longe, MD,* Bjorn P. Flygenring, MD,* David Lin, MD,* David M. Larson, MD,* and Timothy D. Henry, MD*‡ Copyright © 2014 by Lippincott Williams & Wilkins ISSN: 1003-0117/14/1304-0135 DOI: 10.1097/HPC.0000000000000023 From the *Minneapolis Heart Institute Foundation, Abbott Northwestern Hospital, Minneapolis, MN; †Park Nicollet Heart and Vascular Center, St. Louis Park, MN; and ‡Cedars-Sinai Heart Institute, Los Angeles, CA. Reprints: Timothy D. Henry, MD, Cedars Sinai Heart Institute, 127 S. San Vicente Blvd., Suite A3100, Los Angeles, CA 90048. E-mail henryt@cshs.org.