A 60-year-old male with a past medical history of hypertension, coronary artery disease status post stenting of the left anterior descending (LAD) artery and right coronary artery (RCA) in 2023 presents to the emergency department (ED) with a chief complaint of left-sided chest pain that started one hour prior to arrival. A triage ECG (Figure 1) is obtained:
Figure 1. Index ECG.
Interpretation:
Rate: 52 bpm; Rhythm: sinus bradycardia; Axis: normal axis (I: pos., II:pos., aVF: pos) Intervals: PR: 131, normal; QRS: 113, normal; QT: 385, normal; P-Waves: present; QRS Complex: normal, normal R wave progression; ST Segment/T-waves: T waves normal, 0.5-1mm ST depressions in leads I, aVL, 0.5mm ST depression in leads V2-V4, and 1mm STE in lead aVR and lead III
The patient was brought back immediately to the ED from triage. A repeat ECG (Figure 2) was obtained after the cardiac monitor alerted for ventricular tachycardia:
Figure 2. Repeat ECG after cardiac monitoring alerted for ventricular tachycardia.
Interpretation:
Rate: 96 bpm; Rhythm: salvos of non-sustained regular wide-complex rhythm, several visible native beats; Axis: normal axis (I: pos., II:pos., aVF: pos) Intervals: PR: not present; QRS: 138, wide; QT: 420, prolonged; P-Waves: absent; QRS Complex: wide complex, native beats are narrow; ST Segment/T-waves: from the single visible native beat in limb leads, Q waves with associated ST elevation in III, aVF borderline STE with hyper-acute T-wave, reciprocal 1-2mm ST depressions in leads I, aVL, 1-2mm ST depression in leads V2-V6, and 1.5mm STE in lead aVR
A point-of-care ultrasound (POCUS) echocardiogram was performed, which demonstrated a regional wall motion abnormality along the posterior aspect of the left ventricle in parasternal short axis view, which is in the RCA vascular territory. The cath lab was emergently activated, and the patient was taken for percutaneous coronary intervention (PCI), which showed 100% thrombotic stenosis of the RCA just proximal to the previously placed mid-vessel stent. The final angiogram demonstrated good angiographic result after PCI in the RCA. The patient had an uneventful Cardiac ICU stay and was ultimately discharged two days status post PCI.
Discussion:
The initial ECG (Figure 1) does not meet any ST-Elevation Myocardial Infarction (STEMI) criteria but does show findings of an acutely occluded coronary artery, also referred to as an occlusion myocardial infarction (OMI). There is a 0.5mm depression in lead I and 1mm depression in lead aVL. There is also reciprocal ST elevation in lead III. These findings raise concern for an inferior wall myocardial infarction. The next step, if there is concern for an inferior occlusion, is to look at V2 for ST depression. While not always present with RCA occlusions, when there is simultaneous ST depression in V2, this virtually confirms an inferior-posterior RCA occlusion.
When the patient began to experience runs of non-sustained ventricular tachycardia (NSVT), he remained hemodynamically stable, but only a single native beat was visible on two consecutive ECGs (Figure 2). The single beat was enough to show signs of progressive myocardial injury with a Q-wave and ST elevation in lead III, hyperacute T-wave in lead aVF, and reciprocal ST depression in leads I, aVL and V2-V4. This correlated with the troponin returning at an elevated level of 0.105 ng/mL.
We often see ventricular tachycardia (VT) as the presenting rhythm for a patient in cardiac arrest, but this case offers a unique view of VT as the end-point arrhythmia pointing to an OMI with initial ECG changes but normal sinus rhythm, progression to short runs of hemodynamically stable VT, and ultimately type I OMI with a positive troponin requiring PCI.
When coronary oxygen supply to myocardium is disrupted, coagulation necrosis and cell death occurs in cardiac myocytes, which results in rapid electrophysiologic changes to the myocardium. These changes can result in electrical disturbances and induce ventricular arrhythmias such as VT. Additionally, as the infarcted tissue heals, scar tissue forms, increasing the risk for the development of future ventricular arrhythmias due to abnormal electrical conduction in the scar tissue of the infarcted myocardium (1,2). This patient has two above risk factors for development of VT: 1) re-occlusion of the RCA causing acute ischemia for more than one hour prior to PCI (coagulation necrosis onset within 30-45 min of occlusion), and 2) previous OMI with scar tissue in the RCA distribution.
The development of VT in the setting of OMI increases the patient’s risk of in-hospital mortality, so prompt recognition of OMI and cath lab activation is critical to improving patient outcomes. One study of 670 patients suffering from confirmed myocardial infarctions who were hospitalized in France in 2005 demonstrated that in-hospital mortality was significantly higher among VT patients (adjusted OR 7.38, 95% CI 4.27-12.75, P < 0.001) with an overall survival rate at 5 years of 74.4% (95% CI 72.8-76.0) (3). Another study of 2148 patients diagnosed with STEMI and discharged alive from a hospital in Sweden demonstrated that patients with a ventricular arrhythmia (VA) at index OMI (N=151) were eight times more likely to have VA at re-occlusion OMI than patients without VA at index OMI (33.3% vs. 3.9%, P < 0.001) (4).
Take Away Points:
Patients with a history of VA with OMI remain at high risk for recurrent arrhythmic complications in case of repeated ischemic events.
Classic STEMI criteria can miss significant OMI events that still benefit from emergent cath and PCI. Use OMI criteria and, if suspicion is high in the absence of STEMI criteria, consult Cardiology urgently to activate the cath lab.
When a patient presents with an unexplained VA such as VT, consider OMI.
Authored by Michael Hohl, MD; Taylor Wahrenbrock, MD; and Ari Edelheit, MD.
References:
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Thygesen, K., Alpert, J. S., White, H. D., & Joint ESC/ACCF/AHA/WHF Task Force for the Redefinition of Myocardial Infarction (2007). Universal definition of myocardial infarction. European heart journal, 28(20), 2525–2538. https://doi.org/10.1093/eurheartj/ehm355
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