The diagnosis of acute ST-segment elevation myocardial infarction (STEMI) is crucial in the emergency department for the rapid initiation of reperfusion therapy. But many situations of non-coronary obstruction can mimic the ECG findings of a STEMI. These features are confused with myocardial infarction (MI) on the 12-lead ECG, and lead to inappropriate activation of catheterization labs or thrombolytic therapy. In this report, we describe a case of STEMI mimicry produced by prominent atrial flutter waves.
case report:
A 45-year-old man with no previous medical history presented to the emergency department of a primary care hospital with palpitations and chest heaviness. Initial ECG showed narrow-complex tachycardia at 170 bpm with infero-lateral ST-segment elevation (Figure 1).
He received dual antiplatelet therapy (DAPT), unfractionated heparin, analgesics, oral Bisopolol and intravenous Amiodarone. The pre-hospital dispatch center was alerted to a STEMI. The emergency physician found a conscious patient with systolic blood pressure at 120 and diastolic at 80 mm Hg, tachycardia at 180 bpm and polypnoea with crepitants at the base of the lungs. He was treated with 40 mg furosemide, titrated with nitrate and transferred to the cardiac catheterization laboratory. The coronary angiography was performed and revealed normal coronaries.
On discharge, the patient presented with hypotension and exacerbation of pulmonary edema with persistent arrhythmia. The diagnosis was mal tolerated flutter, requiring electrical cardioversion and then a return to sinus rhythm after cardioversion. The ECG showed sinus rhythm with an aspect of early repolarization
Atrial flutter mimicking ST-elevation myocardial infarction: A case reports
Haifa BRADAÏ, Rabeb Mbarek, Sondes Laajimi, Dorra Loghmari, Mounir NAIJA.
Emergency Medical Service (SAMU 03), Sahloul University Hospital, Sousse, Tunisia
The diagnosis of acute ST-segment elevation myocardial infarction (STEMI) is crucial in the emergency department for the rapid initiation of reperfusion therapy. But many situations of non-coronary obstruction can mimic the ECG findings of a STEMI. These features are confused with myocardial infarction (MI) on the 12-lead ECG, and lead to inappropriate activation of catheterization labs or thrombolytic therapy. In this report, we describe a case of STEMI mimicry produced by prominent atrial flutter waves.
case report:
A 45-year-old man with no previous medical history presented to the emergency department of a primary care hospital with palpitations and chest heaviness. Initial ECG showed narrow-complex tachycardia at 170 bpm with infero-lateral ST-segment elevation (Figure 1).
He received dual antiplatelet therapy (DAPT), unfractionated heparin, analgesics, oral Bisopolol and intravenous Amiodarone. The pre-hospital dispatch center was alerted to a STEMI. The emergency physician found a conscious patient with systolic blood pressure at 120 and diastolic at 80 mm Hg, tachycardia at 180 bpm and polypnoea with crepitants at the base of the lungs. He was treated with 40 mg furosemide, titrated with nitrate and transferred to the cardiac catheterization laboratory. The coronary angiography was performed and revealed normal coronaries.
On discharge, the patient presented with hypotension and exacerbation of pulmonary edema with persistent arrhythmia. The diagnosis was mal tolerated flutter, requiring electrical cardioversion and then a return to sinus rhythm after cardioversion. The ECG showed sinus rhythm with an aspect of early repolarization. (Figure 2 A, Figure 2 B)
After electrical cardioversion with confirmation of sinus rhythm, the patient’s symptoms resolved and serial cardiac markers were normal.
Discussion :
The 12-lead surface electrocardiogram (ECG) is the cornerstone of the prompt diagnosis and management of Acutes coronaries syndromes. (ACS) particularly ST-elevation Myocardial Infarction (STEMI). The rapid and accurate diagnosis of this critical illness can lead to prompt reperfusion, and it enables the reduction of cardiac ischemic damage and results in improved subsequent outcomes.
However, a variety of other conditions aside from STEMI can cause ST-segment elevation on the ECG. Somes studies reported that the prevalence of false-positive cardiac catheterization laboratory activations was between 9.2-14%(1)
the ECG remains an imperfect diagnostic tool. Some patients present with classic symptoms and findings; however, around 60-80% of patients with ST-segment elevation on ECG are ultimately found not to be associated with STEMI (1, 2).
Atrial flutter waves, particularly 2:1 atrial flutter, can distort the ST segment in such a way as to mimic a lesion on the electrocardiogram. Flutter waves can mimic ST-segment elevation or depression (3).
However, there have been no previous reports of atrial flutter masking ST-segment elevation. Atrial flutter has not been included or considered as a mimic or confounder of acute myocardial infarction(4,5,6).
Apparently, the prominent flutter waves distorted the ST segment in this patient and misled physicians into initially considering an inferior STEMI. However, the absence of reciprocal ST-segment changes (ST depression) in the precordial leads could have been a clue. The second ECG ruled out q waves, but created further confusion by showing greater ST-segment elevation in precordial leads (V2-V4).
The third ECG confirmed that these changes already existed, although it is still debatable whether there is an additional component of early repolarization changes in the precordial leads contributing to the appearance of a myocardial infarction mimic.
This case demonstrates that atrial flutter waves can mimic ST segment changes, which has been described previously (7)
Conclusion:
Patients with atrial flutter may present with STEMI due to flutter waves coinciding with ST segments and Q waves. Repeat ECG with slower atrioventricular conduction during flutter can reveal the diagnosis.
Références:
3.Bruce M, Spodick D. Atypical elec. Sreeram N, Cheriex EC, Smeets J Gorgels AP, Wellens HJ. Value of the 12-lead electrocardiogram at hospital admission in the diagnosis of pulmonary embolism. Am J Cardiol 1994; 73:298–303.
Hospital Chronicles 2015;10(4):1–3.