Robert Miller and George Veenhuyzen EKG and U - Atrial Flutter Imitating Inferior ST-Elevation Robert Miller MD and George Veenhuyzen MD

About the Authors: The authors are with the Libin Cardiovascular Institute of Alberta, University of Calgary, Calgary, Alberta, Canada. Correspondence may be directed to [email protected]

George Veenhuyzen

Case minute, her detailed cardiovascular examination was unremarkable. A 73-year-old woman presented to the emergency department for 3 She was normotensive. The electrocardiogram (EKG) in Figure 1 hours of and a feeling of “heaviness all over” including was interpreted as showing an inferior ST-elevation myocardial chest heaviness. Her past medical history was significant for paroxysmal infarction. Because the cardiac catheterization laboratory was not atrial flutter managed with amiodarone and oral anticoagulation, immediately available to perform primary coronary intervention, , and asthma. Apart from a of 100 beats per the patient was treated with intravenous thrombolysis.

Figure 1. Initial 12-lead EKG. While the flutter wave makes the inferior ST-segments difficult to interpret, lack of consistent reciprocal changes argues against acute infarction.

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EKG Interpretation Discussion The rhythm is atrial flutter with 2:1 AV block at a rate of 98 beats This case demonstrates that atrial flutter waves can mimic ST per minute. There are prominent flutter waves in the inferior segment changes, which has been described previously.1 After leads, the timing of which permits every other flutter wave to electrical with confirmation of sinus rhythm, mimic ST segment elevation. While the atrial flutter cycle- Figure 2, the patient’s symptoms resolved and serial cardiac length is somewhat long for atrial flutter (300 ms), this could markers were normal. Luckily, the patient did not develop be explained by the patient’s use of amiodarone, which slows significant bleeding following thrombolysis. Her female sex conduction velocity in atrial muscle. The QRS axis is normal and older age are risk factors for intracranial hemorrhage, with no Q-waves and normal R-wave progression. There is no although she did not have hypertension or low body mass reciprocal ST segment depression in the high lateral leads, though index.2 She was discharged uneventfully from hospital without every other atrial flutter wave does mimic subtle ST segment recurrence of atrial flutter. depression in lead aVL (but not lead I).

Figure 2. Follow-up 12-lead EKG, following electrical cardioversion. The patient is now in sinus rhythm, with no evidence of ischemic EKG changes.

Conflict of Interest 2. Gurwitz JH, Gore JM, Goldberg RJ, et al. Risk for intracranial hemorrhage after tissue plasminogen activator treatment for acute myocardial infarction. None. Participants in the National Registry of Myocardial Infarction 2. Ann Int Med 1998 Oct 15;129(8):597–604. References 1. Antonis Manolis IK. Atrial flutter mimicking acute myocardial infarction. Hospital Chronicles 2015;10(4):1–3.

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