The 12-lead ECG in the figure below was obtained from a 50-year-old man with chest discomfort. How would you interpret this ECG? Are the ECG findings suggestive of early repolarization or something else? Clinically, what might be done to clarify the situation?
In view of the limited history provided, assessment of this ECG is challenging. Practically speaking, a definitive answer to the question of whether this tracing represents a normal repolarization variant or early anterior ST elevation myocardial infarction (STEMI) is not forthcoming from an interpretation of this single tracing. The rhythm is sinus, with slight variability in rate (sinus arrhythmia). All intervals and the mean QRS axis are normal. Although QRS amplitudes are somewhat difficult to discern, because of overlap of complexes in some of the chest leads, voltage criteria for left ventricular hypertrophy are not satisfied.
At first glance, assessment of Q-R-S-T changes appears unremarkable. There are no Q waves. The point of transition in the chest leads is normal (occurs between V3 to V4). There is no more than minimal ST elevation in leads I and V2. All T waves are upright (except in aVR), and there is no ST depression. The shape of the upsloping segment of T waves in leads V2-V6 is concave up (i.e., “smiley”-configuration), as is usual with normal repolarization variants.
A more discriminating assessment of Q-R-S-T changes suggests a different conclusion. The patient is a 50-year-old man with chest discomfort. This fact alone calls for far greater scrutiny in assessing Q-R-S-T changes than would be the case if the patient was asymptomatic.
Although Q waves are absent and transition occurs normally between V3 to V4, r wave amplitude is decidedly reduced in leads V1, V2, and V3. In this context, the T waves seen in leads V2 and V3 appear to be disproportionately tall and peaked, with a rounder (fatter) T wave peak in V2 than should be expected given the relatively low amplitude rS complex in this lead. Closer scrutiny of the limb leads reveals that they are not completely “normal” as was initially suggested on superficial assessment. Instead, the ST segments in leads III and aVF appear flattened (despite the presence of upright T waves in these leads), and the subtle-but-real 0.5 mm J-point ST elevation in lead I might be relevant.
All the above findings are subtle. Admittedly, they may mean nothing. But in a 50-year-old man with new chest discomfort, they could be harbingers of an important acute event about to evolve. One cannot be certain from this single ECG about whether or not the subtle abnormalities noted are clinically significant. In a patient with new-onset chest discomfort, further evaluation is needed. This might include repeating the ECG to look for serial changes, comparison with any prior ECGs that may have been performed on this patient, and/or obtaining an echocardiogram during symptoms to look for wall motion abnormality. In this case, repeating the ECG just a short time later revealed dramatic new precordial lead ST segment elevation, confirming that the ECG in the figure was an early harbinger of acute anterior STEMI.
NOTE: Please see http://tinyurl.com/KG-Blog-115 for additional details on this case.
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