The 12-lead ECG shown
in Figure-1 was obtained from
a 51-year old man with new-onset
chest pain. The patient has diabetes, and he continues to smoke.
- How would you interpret this ECG?
- What is the likely “culprit” artery?
 |
| Figure-1: 12-lead ECG obtained from a 51-year old man with new-onset chest pain. What is the likely “culprit” artery? |
Although there is much
artifact (especially in leads II and III)
— this does not prevent appreciation of the obvious abnormalities on this
tracing:
- The rhythm is sinus tachycardia at a rate just over 100/minute. The PR and QRS intervals are normal — but the QT appears to be prolonged. The axis is normal. There is no chamber enlargement.
- Q-R-S-T Changes: There are small and narrow q waves in most infero-lateral leads. R wave progression is normal, with transition occurring between leads V2-to-V3. There are dramatic ST-T wave changes. There is over 10mm of J-point ST segment depression in several anterior leads. All lateral leads show marked ST segment elevation, which nearly attains 10mm in lead V6!
IMPRESSION: There is an obvious acute
STEMI (ST Elevation Myocardial Infarction). Localization of ST segment elevation
to the lateral leads strongly suggests acute occlusion of the LCx ( =
Left Circumflex
Artery). This is supported by the finding of several millimeters of ST
elevation in lead II, but virtually none in leads III and aVF. In contrast,
with acute RCA ( = Right Coronary
Artery) occlusion — ST elevation is localized to the inferior leads,
with the relative amount of ST elevation typically more in lead III compared to
lead II. The dramatic anterior ST depression strongly suggests acute posterior as well as lateral infarction. This distribution of
marked and acute infero-lateral wall
involvement is seen with acute occlusion of a dominant LCx artery.
Follow-Up: Fortunately, this large acute STEMI was
immediately recognized. Cardiac catheterization with prompt reperfusion of a dominant
LCx artery resulted in rapid resolution of virtually all ST-T wave abnormalities (Figure-2).
The “good news” about this case is that treatment was so promptly initiated,
that elevation of serum troponin was minimal. Together with resolution of ST-T
wave abnormalities and lack of QRS
amplitude loss or development of new Q waves — it is likely that almost all
jeopardized myocardium was salvaged with minimal longterm damage from this
event. That said, cardiac catheterization revealed severe multi-vessel underlying coronary disease — such that longterm
prognosis remains guarded even if the patient completely stops smoking. If he
doesn’t, his days are likely to be
numbered ...
 |
| Figure-2: Follow-up ECG obtained after reperfusion of the acutely occluded LCx artery. Virtually all ST-T wave abnormalities that were seen in Figure-1 have resolved! |
PEARLS: This case provides a wonderful clinical
example of how prompt recognition and treatment of acute STEMI, with
reperfusion of the “culprit” artery may result in life-saving myocardial
salvage. Localization of the ST-T wave abnormalities in this case facilitated
prediction of a dominant LCx artery
as the source of the acute insult.
- The dramatic and extensive amount of the ST-T wave changes seen in Figure-1 is most probably attributable to the acute insult of LCx occlusion on top of severe underlying multi-vessel disease.
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Acknowledgment: — My thanks to Mustafa
Alwan (from Amman, Jordan) for his
permission allowing me to use this case and ECG.
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