The ECG in the figure below was obtained from a 61-year-old man whom paramedics treated for new onset chest discomfort. How would you interpret this ECG? Is there evidence of acute ST elevation myocardial infarction (STEMI)?

There are a number of findings on this ECG that strongly suggest acute STEMI. Note the following:

  • The rhythm is sinus. Intervals are normal. The axis is slightly leftward (at about -15 degrees). Voltage for left ventricular hypertrophy (LVH) is satisfied by an R wave in lead aVL that clearly exceeds 12 mm in amplitude.
  • There is a Q wave in lead V1, a QS in V2, and no more than the tiniest of R waves in lead V3. Thus, R wave amplitude is clearly reduced in the anterior leads, and Q waves in V1, V2 could be consistent with septal infarction.
  • The T wave in leads V2-V5 looks like it may be hyperacute. T wave amplitude in lead V2 seems disproportionately tall compared to the QRS complex in this lead. Additionally, the amount of J-point elevation in leads V4 and V5 seems more than is normally expected in these leads, especially given relatively small R waves in V4 and V5.
  • There is ST elevation in lead aVL that looks to be the mirror image of lead III. There appears to be reciprocal change in the inferior leads.

Considering the above findings together, one must be concerned about the possibility of acute left anterior descending coronary artery occlusion in this 61-year-old man with new onset symptoms. That said, there are a number of features against this being an acute anterior STEMI. These include:

  • Probable Lead Malposition — It is surprising how frequently leads V1 and V2 are placed too high on the chest. Doing so may give the false impression of anterior infarction. Clues in this tracing that precordial leads were probably placed one (or even two) interspaces too high include: 1) a significant negative component to the P wave in both lead V1 and V2 and 2) the finding of an r’ deflection in lead V1. Perhaps lead V3 also is malpositioned? So maybe there is not loss of R wave (and development of Q waves) after all in the anterior leads?
  • Other Factors — The leftward axis might account for normal T wave inversion in predominantly negative limb leads III and aVF. Shape of the J-point ST elevation in limb leads I and aVL is concave up (i.e., “smiley”-configuration) with small, narrow septal Q waves and J-point notching. This has the appearance of early repolarization. Finally, LVH is present not only by meeting voltage criteria in lead aVL but also by the presence of a surprisingly tall R wave in lead V6, which partially is masked by overlap of QRS complexes from V5. LVH is notorious for producing a reciprocal “strain” pattern in anterior leads, and this could account for at least some of the suspicious T wave appearance in leads V2 and V3.

It is difficult to be certain from this single tracing if acute STEMI is evolving. One simply cannot always tell from the initial ECG. Depending on clinical circumstances one might either decide to repeat the ECG with an echocardiogram in the ED (looking for wall motion abnormality) or simply proceed to cardiac catheterization for definitive diagnosis. It turned out that this patient did not have acute infarction.

ECG Review 301