In addition to the well-known convex ST-segment elevation myocardial infarction (STEMI) pattern associated with acute occlusive myocardial infarction (OMI), there are other cases that are recognized as OMI without fulfilling the established characteristic STEMI criteria. Over one-fourth of the patients initially classified as having non-STEMI can be re-classified as having OMI by recognizing other STEMI equivalent patterns. We report a case of a 79-year-old man with multiple comorbidities who was brought to the ED by paramedics with a two-hour history of ongoing chest pain. During transport, the patient suffered a cardiac arrest associated with ventricular fibrillation (VF) that required electric defibrillation and active cardiopulmonary resuscitation. Upon ED arrival, the patient was unresponsive, with a heart rate of 150 beats/min and ECG evidence of wide-QRS tachycardia that was misinterpreted as ventricular tachycardia (VT). He was further managed with intravenous amiodarone, mechanical ventilation, sedation, and unsuccessful defibrillation therapy. Upon persistence of the wide-QRS tachycardia and clinical instability, the cardiology team was emergently consulted for bedside assistance. On further review of the ECG, a shark fin (SF) OMI pattern was identified, indicative of an extensive anterolateral OMI. A bedside echocardiogram revealed a severe left ventricular systolic dysfunction with marked anterolateral and apical akinesia. The patient underwent a successful percutaneous coronary intervention (PCI) to an ostial left anterior descending (LAD) culprit occlusion with hemodynamic support but ultimately died due to multiorgan failure and refractory ventricular arrhythmias. This case illustrates an infrequent OMI presentation (<1.5%) formed by the fusion of the QRS, ST-segment elevation, and T-wave resulting in a wide triangular waveform, giving the appearance of an SF that can also potentially lead to ECG misinterpretation as VT. It also highlights the importance of recognizing STEMI-equivalent ECG patterns to avoid delays in reperfusion therapy. The SF OMI pattern has also been associated with a large amount of ischemic myocardium (such as with left main or proximal LAD occlusion) with a higher mortality risk from cardiogenic shock and/or VF. This high-risk OMI pattern should lead to a more definite reperfusion treatment, such as primary PCI and the possible need for backup hemodynamic support.

Acute aortic dissection (AD) involves the tearing of the aortic intima by shearing forces, resulting in a false lumen, which, depending on its location and extent, may lead to hemodynamic compromise, hypoperfusion of vital organs, or even rupture of the aorta. The classical presentation is a sudden chest or back pain described as sharp or ripping in quality. We present a 60-year-old male with a history of hypertension, Liddle’s syndrome, obstructive sleep apnea, and chronic cannabis use for insomnia who arrived at a non-PCI hospital complaining of severe retrosternal chest pain lasting several hours in evolution that started upon masturbation. The pain was ripping in character, starting retrosternally and radiating to his neck and back. After evidence of rising troponin values, he was initially diagnosed with non-ST segment elevation myocardial infarction (NSTEMI), managed with dual antiplatelet therapy with full anticoagulation, and subsequently transferred to our institution for further care. Shortly after his arrival at our hospital, he suddenly deteriorated with recurrent chest pain and hypotension, which triggered an emergent bedside echocardiogram evaluation. This revealed a hemodynamically significant pericardial effusion, moderate to severe aortic valve regurgitation (AR), and an intimal flap visualized on the ascending and descending aorta, suggestive of an extensive AD. A computerized tomographic angiogram confirmed the diagnosis of a Stanford type A AD that required an emergent surgical pericardiotomy, ascending aorta with partial arch replacement, and aortic valve repair. Often, AD may mimic an acute coronary syndrome (ACS) or even present with an acute myocardial infarction (AMI). The appropriate diagnostic imaging evaluation prior to the initiation of anticoagulation therapy should be done in patients with higher-risk clinical criteria for AD to reduce adverse treatment outcomes. The use of a simple three-step diagnostic algorithm for acute aortic syndromes (AAS) may decrease diagnostic delays, misdiagnosis, and inappropriate therapies.