Recently, I evaluated a patient who presented as an acute coronary syndrome with some features that were puzzling to the house staff. Several teaching points can be made from this case.
Patient Presentation
This was a 68‐year‐old male who presented as a transfer from another hospital emergency department (ED) to our ED because of severe chest pain and an elevated troponin T. His chest pain was precipitated by biking and consisted of substernal discomfort accompanied by sweating and pain that radiated to the left arm and left jaw. When seen in our ED, it was obvious that this patient had classic symptoms for myocardial ischemia, and when combined with an elevated troponin of 3.25 and creatine kinase‐MB of 17.6, the patient was considered by the ED physician to have an acute coronary syndrome and probable myocardial infarction.
Electrocariogram (12 Lead)
Interestingly, the patient's 12‐lead electrocardiogram (ECG) was normal during chest pain. There was no evidence of ST segment depression, ST elevation, or T‐wave abnormalities. He was given sublingual nitroglycerin, and the pain resolved. The patient was admitted to an inpatient cardiology service as a non ST‐segment elevation myocardial infarction and treated with aspirin, β‐blocker, clopidogrel, and heparin.
A repeat 12‐lead ECG on admission, once again, was normal. The admitting house staff thought that the patient had a non‐ST segment elevation myocardial infarction, but were somewhat puzzled by the fact that the ECG showed no evidence for myocardial ischemia.
ECG (15 Lead)
When the patient was presented to me, I agreed with the admitting diagnosis of acute coronary syndrome presenting as acute myocardial infarction. I then asked the house staff to obtain a 15‐lead ECG (ie, adding V7, V8, and V9 to the usual 12‐lead ECG). My rationale was that perhaps the patient's main pathology producing the myocardial infarction was located principally in the obtuse marginal distribution of the circumflex coronary artery, and that area of the heart was not being seen by the precordial leads.
Despite resistance from the ECG technicians, who said they did not do 15‐lead ECGs, we eventually obtained one, and interestingly, there was moderate ST elevation in V7, V8, and V9. This prompted us to send the patient to the catheterization laboratory, and findings there revealed the following.
Angiography Findings
The left ventricular ejection fraction assessed in the right anterior oblique (RAO) projection was 55%.
A left anterior oblique (LAO) ventriculogram was not done.
In the RAO projection, there was normal chamber size and overall contraction, but there was mild hypokinesis of the anterolateral wall.
Because ventriculography was done only in the RAO projection, the lateral wall and septum were not visualized.
Selective coronary angiography revealed mild stenosis of the ostium of the left main coronary artery, 70% proximal left anterior descending stenosis, and 99% circumflex coronary artery stenosis just prior to a trifurcation of the obtuse marginal branches. There was a small 60% proximal right coronary artery (RCA) lesion.
Although I did not see anything to suggest a clot in this vessel, it is possible that it was initially occluded and reperfused spontaneously, resulting in a huge rise in the troponin T to 3.25, possibly due to washout.
Summary
This patient had significant coronary artery disease as well as a myocardial infarction principally of the lateral wall of the left ventricle, which did not manifest itself on a 12‐lead ECG. Because of the complex nature of the circumflex coronary pathology and its trifurcating branches, it was decided that this patient would be better suited for coronary artery bypass graft (CABG) surgery. Elective CABG was accomplished 5 days later, after clopidogrel had been stopped. During the washout of clopidogrel, the patient remained symptomless and comfortable. CABG consisted of internal thoracic artery to left anterior descending, saphenous vein graft (SVG) to RCA, and SVG to first and third obtuse marginal (OM1 and OM3). Although the diagnosis of acute myocardial infarction was clearly based on the history and the marked rise in cardiac markers, it was somewhat unusual in that the 12‐lead ECG was normal.
Teaching Points
This case illustrates a few teaching points that are worth remembering. First of all, if there is a good story as well as an increased troponin T, myocardial infarction has to be thought of and looked for even though the ECG is normal. Second, although patients who present with a good story and increased troponin T with a normal ECG are not common, it is possible that certain regions of the heart can be missed by the standard 12‐lead ECG. Third, the patient did have a mild regional wall motion abnormality in the RAO projection, which probably relates to the culprit area, but the LAO projection was not assessed so that the left ventricular free wall and septum were not evaluated. Cardiac ultrasound did reveal lateral left ventricular wall hypokinesis. Fourth, when this situation presents itself, a 15‐lead ECG is justified and should be obtained to solidify the diagnosis of a lateral wall infarction, particularly in the distribution of the obtuse marginal branches. Finally, although the patient does not represent silent myocardial ischemia or silent myocardial infarction, he does represent myocardial infarction with a silent 12‐lead ECG.