This ECG is from a 54-year-old woman who had an M.I. one week prior to this tracing.  She did not receive interventional treatment, as it was not available where she lived when this happened years ago.  Her ECG shows the signs of healing injury, as well as probable permanent damage. 

Where was this M.I.?      The affected leads are all of the precordial leads (V1 through V6), as well as I and aVL.   The precordial leads reflect the anterior and low lateral walls of the heart, and Leads I and aVL show us the high lateral wall.  This area is perfused by the left coronary artery, and she had a proximal lesion. 

What ST and T wave changes are present?    All of the leads listed above show a flattening of the ST segments.  While they are no longer elevated (the acute injury is over), they are flat and almost convex upward.  This shape is usually abnormal, and it has persisted even though the acute injury is subsiding.  The T waves in the anterolateral leads are all inverted.  This represents reperfusion of the injured tissue.  Whether the offending clot is removed by invasive procedure, thrombolytic drugs, or natural degradation, the tissue that is still alive will reperfuse. 

This ECG was obtained from a 49-year-old man who was a patient in an Emergency Dept.  We do not know his presenting complaint, only that he had a history of insulin-dependent diabetes mellitus (IDDM).  It was noted by the donor of the ECG that the patient had no chest pain, no shortness of breath, and no other cardiac symptoms.  We do not know his hydration or electrolyte status.  There are quite a few interesting abnormalities on this ECG, and the exact interpretation would, of course, depend upon the patient's clinical status.  It would definitely help to be there!

First, we note a sinus tachycardia at a rate of 118 bpm.  This could be due to very many causes, including but not limited to:  dehydration, pain, anxiety, high or low blood glucose, fever, or CHF.  The PR and QT intervals are within normal limits.  The QRS complexes are narrow.  The axis is normal at 0 degrees.  The QRS voltage in the lateral leads is on the high side of normal, but we do not know this patient's body type.  Voltage as read by the ECG can be influenced by a thin chest (making voltage look larger) or a large chest (making voltage lower).

There are T wave abnormalities in the lateral leads:  I, aVL, V5 and V6.  The T waves are inverted, which can have many meanings.  However, when inverted T waves are in the lateral leads, as opposed to the inferior or right chest leads, it is often a sign of ischemia.  The flat, horizontal ST segments can also signify coronary artery disease (CAD).  This patient denied cardiac symptoms, but his age and history of IDDM make it probably that CAD is a factor.  The leads with T wave inversion also have a small amount of ST segment depression.  The right precordial leads, V1 and V2, have a small amount of ST elevation,  This possibly represents a reciprocal change to the ST depression in V5 and V6.

Because we are not at the bedside of this patient, there are many details we do not know.  But these inverted T waves could be ischemic T waves, and this requires that the patient be further evaluated.

As always, we welcome comments, as this ECG probably has more to say!

REFERENCES:  Dr. Ken Grauer,  Life In The Fast Lane, World Journal of Cardiology 

This ECG is the last in a series of 6 that were donated by Jenda Enis Štros showing the evolutionary changes of an M.I. from onset, through spontaneous reperfusion, angioplasty, re-occlusion by thrombus, and recovery.  This ECG shows deep precordial T wave inversions, an expected evolutionary change after reperfusion of an occluded artery - in this case, the left anterior descending.  The patient has lost some of his QRS amplitude (viable heart muscle), but has not developed pathological Q waves.  Pathological Q waves would indicate full-thickness necrosis of the wall, which is usually a permanent injury.  

The patient was discharged home with a 45% ejection fraction (60% is ideal), and he had akinesis of part of his anterior wall.  This can be permanent or temporary, and followup studies would be needed to evaluate the ongoing health and function of the left ventricle.

Here are links to all six ECGs from this series:

http://www.ecgguru.com/ecg/teaching-series-1113-ecg-1-6-acute-anterior-wall-mi

http://www.ecgguru.com/ecg/teaching-series-1113-ecg-2-6-acute-anterior-wall-mi

http://www.ecgguru.com/ecg/teaching-series-1113-ecg-3-6-acute-anterior-wall-mi

http://www.ecgguru.com/ecg/teaching-series-1113-ecg-4-6-acute-anterior-wall-mi

http://www.ecgguru.com/ecg/teaching-series-1113-ecg-5-6-acute-anterior-wall-mi

http://www.ecgguru.com/ecg/teaching-series-1113-ecg-6-6-acute-anterior-wall-mi

During our summer break, we are reprising a few of the best ECGs from our archives, to give you a chance to comment or to ask questions.

This ECG was taken from a 52 year old man who was complaining of chest pain, with a history of severe multi-vessel disease. He has a history of M.I. and states he has five coronary stents.

His pain was partially relieved by Ntg., and he was given aspirin in the field, and then IV Ntg., Integrelin, and morphine before being sent to the cath lab. This ECG shows T wave inversions with coved upward ST segments, but no ST elevation in the lateral leads: I and aVL, and the anterior-lateral leads, V3 through V6. This represents the territory covered by the left coronary artery, and points to a lesion in the proximal portion of the artery. Also in this ECG are pathological Q waves in right side leads, III, V1 and V2.

In the cath lab, he was discovered to have a ruptured plaque in the proximal LAD, with some blood getting through a very narrow channel. He was referred for coronary artery bypass surgery the next day.