A 59-year-old man without prior cardiac history presented with three hours of severe upper sternal chest pressure that radiated to his throat, which he described as “strangulating.”
An ECG was obtained, and is shown here. It demonstrates a sinus rhythm at rate of approximately 75 bpm. The PR and QT intervals are normal.
There is concerning 1 mm of ST-elevation in V5 and V6 with ST-segment depression in V2 and V3, suggestive of a posterior myocardial infarction.
The initial ECG was concerning for 1 mm of ST-elevation in V5 and V6 with ST-segment depression in V2 and V3. This is suggestive of a posterior myocardial infarction, prompting us to obtain a posterior ECG. This can be done by removing the leads for V4 thru V6 and placing them on the back at the same thoracic level. The lead for V7 is placed more posterior than V6, V8 is placed in line with the tip of the scapula, and V9 is placed in the left paraspinal region. The other leads remain the same. These leads generally record lower voltage levels because the distance to the heart is greater for them. The patient’s posterior ECG was obtained about 10 minutes after the initial ECG.
The QRS complex and T-wave does indeed have low voltage in leads V7 thru V9, but the T-wave is large in proportion to the R-wave. These hyperacute T-waves can be seen shortly after occlusion of an artery and after reperfusion. No ongoing ST-elevation of the posterior leads is present as was seen in V5 and V6. Interestingly, the ST-depression in V2-V3 is resolving. Dynamic ECG changes are consistent with an acute coronary syndrome. The initial troponin I was 0.659 ng/mL. Wall motions were difficult to visualize on bedside echocardiogram, but a formal echocardiogram with Definity contrast confirmed a large posterior wall motion abnormality.
This was considered a ST-segment elevation myocardial infarction (STEMI) based on the clinical history and ECG findings. The patient was given aspirin 81 mg PO, clopidogrel 600 mg PO, and started on a heparin infusion. The cardiac catheterization lab was activated for emergency PCI. A repeat ECG 45 minutes after the initial one interestingly showed further dynamic ST-segment changes in the precordial leads with resolution of the ST elevation and dynamic T-wave changes inferiorly.
This patient was found in the cath lab to have 99% stenosis in the proximal segment of the first obtuse marginal that gives rise to a good-sized lateral branch. He was also found to have a 90% ulcerated plaque in the proximal right circumflex artery. The left circumflex lesion underwent thrombectomy, and both lesions were stented with a drug-eluting stent. TIMI III flow (complete perfusion with normal flow which fills the distal coronary bed completely) was established.
This STEMI was picked up by ECG and immediate bedside echocardiogram, and the patient went to angiography and PCI. It is important to note that the second ECG shows evidence of reperfusion in facilities where this is not available in a timely manner. Thrombolytics would be contraindicated in that situation, but the patient should be treated with nitroglycerin, anticoagulation, and dual antiplatelet therapy (aspirin, thienopyridines, or a GP IIb/IIIa inhibitor) before transport for definitive treatment.