|There is sinus rhythm. There is high voltage in aVL and typical "hockey stick" appearance of the ST-T complex (LVH with repolarization abnormalities. This also results in reciprocal ST elevation in inferior leads.|
Later review of old records showed this to be her baseline ECG.
Without an old ECG to compare, one would be very suspicious of inferior STEMI. One should know that not all reciprocal ST depression is due to STEMI. Inferior LV aneurysm, WPW, LVH, and LBBB may all have inferior ST elevation with reciprocal ST depression in aVL.
Here is an example of this in LV aneurysm:
Had the treating physicians known this, they might have looked for the previous ECG and realized that the patient was not having a STEMI.
Conversely, absence of any reciprocal ST depression of any amount almost completely rules out inferior STEMI. We presented this research in Boston June 2011 SAEM. Here is the abstract:
In acute inferior STEMI, Reciprocal ST depression in aVL and T-wave inversion in aVL are both more sensitive than ST elevation criteria and appear earlier in the course of STEMI
Stephen W. Smith
Background: A previous study found that reciprocal ST depression (rSTD) is present in only 82% of inferior ST elevation (STE) acute myocardial infarction (MI). However, we believe that changes in lead aVL are far more sensitive. Objectives: To find the incidence of any rSTD or T-wave inversion (TWI) in angiographically proven inferior STEMI. Methods: We searched the catheterization laboratory database for all cases coded as acute Inferior STEMI from January 2002 through March 2008. All cases were reviewed and the presenting ECG, as well as the first ECG that was used for diagnosis of acute STEMI, were analyzed. “True STEMI” was defined as 100% occlusion or as a culprit lesion with maximum troponin I (trop) > 10 ng/ml. STE was measured in leads II, III, aVF; aVL was scrutinized for any rSTD or TWI. TWI was defined as a T-wave mostly down, or a biphasic T-wave that is first down, then up (not up then down, which is associated with lateral AMI). Reperfusion criteria were defined as STE of at least 1 mm in 2 of 3 of inferior leads II, III, aVF. Results: There were 160 unique cases. 107 had 100% occlusion, and 35 had < 100% occlusion, but had a maximum trop > 10 ng/ml, for 142 true STEMI; 18 (11%) had < 100% occlusion and a max trop < 10 ng/ml. 85% of the diagnostic ECGs of true STEMI, and 84% of all cases, met STE criteria. No true STEMI had absence of reciprocal depression in lead aVL. Of the 107 with 100% occlusion, 100 (93%) had at least 0.5 mm of rSTD; the remainder had rSTD of < 0.5 mm. Even among those without true STEMI, 94% had some rSTD in aVL. Additionally, in 44 cases (28%), there was no STE whatsoever on the presenting (first) ECG; all of them had either rSTD or TWI. See Table. Conclusion: STE criteria for inferior STEMI are insensitive, especially on the presenting ECG. Changes in aVL, both some amount of rSTD and also TWI, are more sensitive than STE criteria in the diagnosis of inferior STEMI and are nearly universally present in inferior STEMI. These changes also appear earlier than STE.