58 year old female with chief complaint of chest pain x2hours with PMH of type 2 diabetes mellitus, Hyperlipidemia, and hypertension. She is brought in via EMS still having active chest pain.
BP: 102/88 HR: 82 RR: 24 O2 Sat on 2L: 99% Temp 99.0
ECG obtained at arrival is shown…
Before reading on, try to come up with your own interpretation of this ECG before moving on to the final impression
- Rate: Ventricular rate 82
- Rhythm: Normal sinus rhythm
- Axis: normal axis
- QRS: narrow complex
- ST/T Waves: ST elevation in leads II, III, and aVF (inferior leads) and V3R – V6R (right sided leads); ST depression in leads I and aVL (high lateral leads)
- Final ECG Interpretation: Right Sided STEMI
There are several points to discuss on this ECG. First, lets focus on the inferior ST elevation and the reciprocal changes in the high lateral leads. Lead aVL is the closest thing on the ECG to a mirror image of the inferior leads. As a matter of fact it is exactly 150 degrees away from lead III (Reciprocal Changes in Lead aVL). If you take lead aVL and flip it upside down (shown below) it has a similar morphology as lead III (mirror images). Reciprocal changes in lead aVL and ST elevations in the inferior leads are typically seen in 70 – 97.2% of patients with a true inferior wall MI. [1][2]
Lead aVL Turned Upside Down (mirror image of inferior leads)
Next lets talk about the ST elevation in the inferior leads and anterolateral leads. In general, the right coronary artery is the culprit vessel in about 80 – 90% of inferior wall MIs. The left circumflex can also be the culprit vessel in some cases. There are a few clues that can help determine which vessel is involved in inferior myocardial infarction:
- If ST elevation in lead III > lead II and ST depression in leads I and aVL (> 1 mm), then RCA is the culprit artery with a sensitivity of 90%, specificity of 71%, and PPV of 94%. [3]
- If ST elevation in leads V3R and V4R, then RCA is the culprit artery with sensitivity of 100% and specificity of 87% [1]
- No ST depression in lead aVL, then LCx is the culprit vessel with sensitivity of 80% and specificity of 93%. [1]
In this ECG, ST elevation is greater in lead III vs lead II and there is > 1mm ST depression in lead aVL. Also, there is ST elevation in leads V3R and V4R pointing to an RCA occlusion. 3 options to consider with inferior STEMI are:
- Dominant RCA = ST elevation in leads II, III, & aVF + ST elevation < 2mm in V5 & V6 [4]
- Dominant LCx
- “Mega-artery” = ST elevation in leads II, III, & aVF + ST elevation > 2mm in V5 & V6 [4]
- Mega-artery = Large posterolateral branches (originating from the RCA or LCx arteries) and a small or medium LAD artery [5]
Case Conclusion: Cath showed a 100% proximal RCA occlusion with a “mega-RCA”
References:
- Birnbaum Y et al. the Electrocardiogram in ST Elevation Acute Myocardial Infarction: Correlation with Coronary Anatomy and Prognosis. Postgrad Med J 2003. PMID: 13679544
- Barrabes JA et al. Prognostic Significance of ST Segment Depression in Lateral Leads I, aVL, V5 and V6 on the Admission Electrocardiogram in Patients with a First Acute Myocardial Infarction Without ST Segment Elevation. JACC 2000. PMID: 10841229
- Zimetbaum PJ et al. Use of the Electrocardiogram in Acute Myocardial Infarction. NEJM 2003. PMID: 12621138
- Eskola MJ et al. How to Use ECG for Decision Support in the Catheterization laboratory. Cases with Inferior ST Elevation Myocardial Infarction. J Electrocardiol 2004. PMID: 15484153
- Assali AR et al. Comparison of Patients with Inferior Wall Acute Myocardial Infarction with Versus without ST-Segment Elevation in Leads V5 and V6. Am J Cardiol 1998. PMID: 9462612
