The differential diagnosis for this patient’s EKGs includes acute MI, historical MI with left ventricular aneurysm, reperfusion effects, and acute neurological catastrophe with catecholaminergic stress pattern.
On the left is a normal (80%) Right-Dominant coronary system showing the PDA branching from the RCA. On the right is a volume rendered CT image demonstrating a Left-Dominant system with the PDA (arrowhead) and a posterolateral branch (white arrow) arising from the circumflex (black arrow). 
Inferolateral STEMI secondary to Left-Dominant LCx occlusion showing reciprocal depressions across the anterior leads.
A proximal occlusion of a wraparound LAD resulting in an “inferoanterior” STE pattern could also be hypothesized, perhaps with greater similarity to the case study EKGs, and a good case report of this phenomenon with angiographic evidence can be found in Akdemir et al. (2005). The graphic bellow illustrates the interpretive advantages of such a theory.
Note that the inferior elevations in both this case from Akdemir et al. and in the title EKGs are most apparent in aVF. Given that aVF views the inferior apical region, elevation seen here might be considered contiguous and consistent with elevations in V2-5 looking at the anterior wall. The territory of infarction can then be seen as a continuous band, reaching down the path of the wraparound LAD, down the anterior wall, and curling under the heart to the inferior wall.
Ultimately the diagnosis of STEMI would command greater credence here were there clearly pronounced reciprocal changes in corresponding leads. While in the first EKG one can imagine a fraction of a millimeter of ST depression in aVL, there are no explicit reciprocal depressions and the global T-wave inversions cannot be accorded any significance in this regard. Rather, if committed to the diagnosis of STEMI, the T-wave inversions might be considered a Wellenoid feature, perhaps suggesting a prodrome of isolated T inversions which has subsequently evolved into acute STE. Lastly, the case for AMI is supported by the prolonged QT interval, although this remains a non-specific factor.
On consultation with Tom Bouthillet of EMS 12-Lead, it was suggested that a reperfusion T-wave pattern might help to explain some of what is seen here. This view is attractive from a morphological standpoint and can perhaps be best explicated via comparison with an exemplar case as seen below.
This EKG represents post-reperfusion of a 100% occluded wraparound LAD; Dr Smith (2011) states, “There are “reperfusion” T-waves in V1-V6 and I, aVL. There is a QS-wave in V2, and QR-wave in aVL, and poor R-wave progression in V3 and V4, all diagnostic of anterolateral MI, subacute.”
As in this EKG from Dr. Smith, the QS complexes and obliteration of R-wave progression from the case study tracings raises suspicion of a subacute or chronic pathology. In conjunction with the concave downward ST segment morphology, an extinction of anterior electrical forces with deep pathologic Q-waves suggests the possibility of persistent ST elevation due to prior MI and LV aneurism. Dr. Smith (2005) has proposed a formula for the differentiation of anterior STEMI from persistent STE secondary to historical MI premised on the ratio of the T-wave to the QRS amplitude; qualitatively, AMI should present with large T-wave amplitude relative to the QRS, while LV aneurysm should demonstrate a comparatively lower T/QRS ratio. Smith states, “the T/QRS ratio in any one of leads V1-V4 was almost always higher than 0.36 in acute MI, and almost always lower in LV aneurysm. Better was a T amplitude (V1+V2+V3+V4) / QRS amplitude (V1+V2+V3+V4) <> 0.22.”
Applying this rule to the initial case study EKG, (V1-1.5mm, V2-2mm, V3-3mm, V4-4.5mm) / (10mm, 23mm, 21mm, 12mm) = 0.16. Biphasic or inverted T-waves are unlikely in AMI, yet they are not uncommon in LVA. Observe the ST morphology and T-wave inversions in the EKG below.
In their 2008 case study, Biyik et al. captured this EKG, stating, “Thirty days after myocardial infarction, echocardiography revealed an akinetic apical aneurysm, anterolateral hypokinesia of the left ventricle, and decreased ejection fraction (45%).”
Both the results from the Smith formula and comparison with the EKG above point away from AMI and more toward a historical MI w/ LVA. It has been suggested, however, that a tall R-wave in aVR may be correlated with aneurysm; the absence of this finding here is of unclear significance but perhaps counts against the mounting argument for LVA.
Lastly, global, deep symmetric T-wave inversions transgressing multiple territories of coronary perfusion have long been documented in the setting of acute neurological catastrophe. Inferoanterior ST elevation and prolonged QT have also been described in this context, specifically with regard to Takotsubo syndrome, and can be seen below.
A patient with Takotsubo cardiomyopathy demonstrating ST elevation in anterior and inferior leads. 
Top represents a pt’s baseline EKG with QTc of 407; bottom is the same pt., now with echocardiographic evidence of Takotsubo syndrome, showing diffuse T-wave inversions and a prolonged QTc calculated at 519. 
The mechanism of these neurogenic EKG manifestations is believed to result from an autonomicaly mediated catecholamine surge leading to transient coronary vasospasm and myocardial ischemia. The case study, “Status post arrest, now with transtentorial herniation,” from September 2010 of The Jarvik 7 discusses this issue at greater length, and it should be noted that the ST deflections in the 2010 case are comparably global in distribution, again showing incongruity with traditional zones of coronary perfusion.
Returning, however, to Biyik’s 2008 case, it is not surprising to find a correlation between LV aneurysm morphology and neurogenic stress cardiomyopathy. An LVA electrocardiographic overlay may reflect the physiological reality that Takotsubo syndrome is partly characterized by a “ballooning” or temporary aneurysm of the apical region of the left ventricle. In this case, Biyik reports of a 35yr male presenting with intense agitation following a narrowly avoided attempt on his life. Future inquiry and systematic literature review may yield confirmation of this relationship and further insight into the mechanisms involved.
In the absence of clinical context or additional test results, these EKGs present a challenging electrocardiographic differential diagnosis. By morphological as well as mathematical criteria, the anterior leads are suggestive of LVA, yet the limb leads betray additional findings which demand a more inclusive pathophysiology. In light of the arguments explored above—principally the suspiciously non-localized ST and T-wave abnormalities coupled with the morphological elements of the T inversions—the case for an ischemic stress pattern may carry the most persuasive weight.
As always, comments and additional observations are welcome. I am indebted to both Tom Bouthillet and Dr. Steven Smith for consultation on this case.
Smith, S. (2011). Hyperacute T-waves, missed by computer, short DTB, but large myocardial infarction. Dr. Smith’s EKG Blog. Retrieved from http://hqmeded-ecg.blogspot.com/2011/01/hyperacute-t-waves-missed-by-computer.html.
 Tomich et. al.
 Wong, A. et al. (2010). Preoperative takotsubo cardiomyopathy identified in the operating room before induction of anesthesia. Anesthesia & Analgesia, 110(3), 712-715. doi: 10.1213/ane.0b013e3181b48594