Dr. Smith at Dr. Smith’s ECG Blog has a great post about missed MI due to circumflex artery or obtuse marginal artery occlusion. Recall that the circumflex artery branches from the left main coronary artery and wraps around to the posterior wall, giving off first the obtuse marginal branch(es) and then the postero-lateral branches. This territory, the posterior wall is large, but classically is considered ‘electrically silent’. Now clearly the territory is not truly electrically silent, and ECG experts like Dr. Smith can pick up subtle findings that represent MI, but these findings are subtle and are still likely to be missed by the average emergency doctor.
Dr. Smith does a great job at educating the masses in emergency medicine about subtle and important ECG findings. I think it is also useful to consider what we actually mean when we call a myocardial infarction a STEMI (ST segment elevation myocardial infarction) or a NSTEMI (Non-ST segment elevation myocardial infarction).
Remember that the ECG as a test is a surrogate for what is actually going on anatomically and electrically with the heart. When we say an ECG shows a STEMI we are actually saying that the ECG predicts with reasonable certainty that there is an obstruction (thrombosis) of a fairly large blood vessel proximal in the vascular bed represented by the area of ST elevation on the ECG. It’s not perfect, remember that there are other causes of ST elevation, and causes of vascular obstruction besides thrombosis (vaso-spasm, dissection, emboli, etc.). This is important because we know that when we treat thrombosis causing ST segment elevation with thrombolysis or PCI (percutaneous coronary intervention) we can improve outcomes.
When we diagnose a patient with a NSTEMI we are saying that the patient has a myocardial infarction due to a reason other than the occlusion of the proximal portion of a cardiac vascular bed. NSTEMI is usually evidenced by patient presentation of ischemic type chest pain or equivalent plus positive biomarkers (troponin), possibly with non-STEMI ECG changes. This could be a type II MI, occlusion of the distal portion of a coronary vascular bed, or proximal occlusion of an ‘electrical silent’ area of the heart. Importantly NSTEMI is generally not treated with primary PCI.
In the example Dr. Smith gives of circumflex artery occlusion the patient is 39 years old and has a large area of myocardium at risk in spite of a non-STEMI ECG. Often the ECG is thought of as perfect, STEMIs go to the cath lab NSTEMs get medical management but reality is not nearly as simple, false positives and false negatives can both occur. In patients who have ischemic symptoms, no reason for type II MI, and no vasculopathy that would suggest small vessel infarction a through hunt for STEMI should be made. Serial ECGs, right sided and posterior leads can all help prove STEMI. It is also important to remember that ischemic chest pain in spite of maximal medical therapy (ASA, clopedigrel, nitroglycerin, heparin, beta-blockers, glycoprotein IIb IIIa inhibitors) also require urgent PCI.
When we see a patient who clinically appears to have pneumonia, but a non-diagnostic chest x-ray we don’t hesitate to seek more advanced testing, especially if the patient is unstable or deteriorating. Likewise, the ECG is simply one piece of the picture in the acute coronary syndrome. In patients who clinically appear to have ischemic chest pain and an unstable clinical picture, but a non-STEMI ECG we should hunt for STEMI and even when it is absent consult with our colleagues in interventional cardiology when the patient is symptomatic in spite of maximal therapy.