A 39-year old female presents to our emergency department with complaints of “worsening of heartburn”. The patient states that for several months she has had episodic indigestion and chest discomfort. She has been taking antacids for several weeks as prescribed by her family doctor without improvement. Today, she states the indigestion is constant and accompanied with mild shortness of breath with exertion. She rates the discomfort a 4 out of 10 on a visual analog scale. The patient has a history of multiple sclerosis but takes no medication. She has no family history of heart disease and does not smoke or use illicit drugs. She denies any recent illnesses. On presentation to the emergency department, she appears in no distress. Her vital signs were heart rate 104, respiratory rate 18, blood pressure 119/89 and, oxygen saturation of 100% on room air. Physical exam revealed a well developed 39-year old female in no distress. Her lungs were clear to auscultation bilaterally. The patient was mildly tachycardic but no murmurs appreciated. Her abdomen was unremarkable and, extremities without cyanosis or edema. Initially, the patient stated she felt mild relief when leaning forward. She was given aspirin 325 mg PO. There was no change in her discomfort after sublingual nitroglycerin.
Initial laboratory data revealed a normal complete blood count, normal basic metabolic panel, normal d-dimer and, a troponin I of 1.51 (normal reference less than 0.02.) Chest X-ray was normal in appearance. The initial EKG is shown below. What do you see? What should you do next?
To look at the EKG, it is very abnormal, not just aVR. So, one could easily be distracted by the ST-segment depression in leads I, aVL, V2-V6. So, are these changes ischemic only or perhaps, a Non-STEMI? Both are reasonable conclusions unless you look at aVR, the frequently forgotten lead. The ST-segment elevation in lead aVR indicates this is a STEMI and the ST depressions are likely reciprocal changes or even, perhaps early extension to the posterior wall. Only one lead showing ST-segment elevation is not an accurate reflection of the amount of myocardium involved. It is more a statement of the weakness of the 12-lead electrocardiogram.
Recently, Dr. Amal Mattu has again brought to light the importance of close inspection of lead aVR in the evaluation of patients with suspected acute coronary syndrome. His article published in Medscape Emergency Medicine Viewpoints in February 2009 points out several key studies that demonstrate the significance of ST-segment elevation in lead aVR. The take home point of his literature analysis is that STE in lead aVR in patients with ACS is associated with more ominous coronary occlusions. Likewise, those patients with LAD occlusions, LMCA occlusions; or triple vessel occlusions have a worse prognosis and require aggressive immediate therapy and often cardiac bypass surgery (1).
After initial review of the EKG the interventional cardiologist was called and came immediately to the bedside. The patient was taken for emergent cardiac catheterization. During the procedure, the patient became hypotensive requiring placement of an intra-aortic balloon pump. Cardiac catheterization revealed a 90% occlusion of a left main coronary artery and a left ventricular ejection fraction of 25%. There was no disease noted in any of the other coronary arteries. The left main coronary artery was stented to 0% with a drug eluding stent. The patient was transferred to the coronary intensive care unit. During the course of the patient’s hospitalization, she showed great improvement with restoration of normal cardiac function. She was discharged after having spent five days in the hospital.
1. Mattu A, Medscape Emergency Medicine Viewpoints, Lead aVR: Importance of the “Forgotten 12th Lead” in Patients with ACS, February 2009
Patrick Shannon, DO, Core Faculty, Conemaugh Emergency Medicine Residency.
Zach Patrick, DO, Resident, Conemaugh Emergency Medicine Residency
Cool! Yes, I, too, was so busy tsk-ing the other leads’ ST depressions that the ST elevation in aVR flew right by me.
Very interesting case but I disagree with the etiquette STEMI. STEMI is ST elevation in 2 or more contiguous leads (or mirror image true posterior with pronounced ST depression in V1-V2, which is not that frequent) and its pathophysiological substrate is an acute thrombotic occlusion. In the case described, there is none of this. The diffuse ST depression indicates diffuse subendocardial ischemia due to a severe left main. The ST elevation in aVR is reciprocal nothing more. This should not be called a STEMI.