The Fourth Universal Definition of Myocardial Infarction (MI) defines pathologic ST-segment elevation (STE) as J-point elevation in two contiguous leads of ≥1 mm, except in leads V2–V3, where the thresholds are >2 mm in men ≥40 years, >2.5 mm in men <40 years, and > 1.5 mm in women regardless of age [1]. The requirement for STE in two contiguous leads is widely accepted but originates more from intuition than robust empirical evidence. In the pivotal Fibrinolytic Therapy Trialists' (FTT) meta-analysis, which led to the modern STEMI/non-STEMI paradigm, only 4 of the 9 included randomized-controlled trials (RCTs) provided a definition for STE, each using different criteria and measurement techniques, and only one trial mandated the presence of STE in two contiguous leads. [2] This two‑lead criterion was then formally adopted in the First Universal Definition of MI [3], referencing the study by Menown et al [4]. That study applied logistic regression to identify optimal STE thresholds for various leads and proposed ≥2 mm in at least one of V1–V4 or ≥ 1 mm in any other lead. Notably, it was not designed to distinguish STEMI from non-STEMI and did not require two contiguous leads. Nonetheless, this definition has been perpetuated across successive guideline iterations [5].

More recently, several studies have demonstrated that the topographic correlation between the leads showing STE and the actual location of the infarct may be unreliable [6], and that rigidly assigning lead groups to specific myocardial territories may result in misclassification of infarct location [[7], [8], [9]]. Furthermore, the two-contiguous‑lead requirement may decrease the sensitivity for detecting STEMI in certain patterns [10,11] and might obscure recognition of novel electrocardiographic (ECG) presentations of acute coronary occlusion.

We previously described a new ECG pattern, now referred to as Aslanger's pattern, characterized by inferior STEMI superimposed on diffuse subendocardial ischemia, which results in STE limited to a single lead [5,12]. The net ST-vector in this scenario is more rightward than in typical inferior MI due to the additive effect of two vectors: the inferior MI vector directed inferiorly and often rightward, and the subendocardial ischemia vector pointing toward aVR, independent of coronary territory. Their resultant vector aligns nearly perpendicular to aVF, pointing toward lead III (STE) and lead aVR (also often with STE), while showing ST depression in leads I and II and an isoelectric ST segment in aVF [12] (Fig. 1A).

We hypothesized that a similar vectorial mechanism could produce a reverse pattern, in which lateral wall MI, when combined with widespread subendocardial ischemia, generates an average ST-vector directed superiorly (Fig. 1B). This resultant vector projecting solely onto the positive pole of lead aVL while remaining isoelectric in the contiguous lead I, fails to meet the standard STE in two contiguous leads criterion. Though likely rarer than the inferior variant, this pattern may signal a more complex and prognostically adverse ischemic substrate. Here, we present an illustrative case that exemplifies this atypical ECG pattern.