Beyond ST-elevation: A Case of Occlusion MI Confounded by ECG Criteria for Left Ventricular Hypertrophy

The current paradigm for emergency reperfusion therapy in acute coronary syndromes relies heavily on the presence of ST-segment elevation MI (STEMI) criteria on the 12-lead ECG. While this approach has been instrumental in improving outcomes, it is now understood that a significant subset of patients with acute coronary occlusion does not meet these classic criteria, leading to potential delays in treatment and increased myocardial injury.¹

To address this limitation, the occlusion MI (OMI) paradigm has been proposed, shifting the focus from ST-elevation to the direct angiographic or ECG evidence of an occluded artery, regardless of whether STEMI criteria are met.² However, identifying OMI can be exceptionally challenging when the ECG is confounded by underlying conditions. Left ventricular hypertrophy (LVH) is a prominent example because its characteristic secondary repolarisation abnormalities, including tall anterior T waves and lateral ST depressions, can effectively mimic or mask the subtle signs of acute ischaemia.

This report presents a compelling case of an acute left anterior descending (LAD) artery occlusion that progressed to cardiogenic shock. The initial ECG was non-diagnostic for OMI, with subtle T wave abnormalities confounded by underlying LVH. This case underscores the critical importance of maintaining a high index of clinical suspicion, using rapid serial ECGs, and looking beyond rigid STEMI criteria – which are often formally inapplicable in the setting of LVH – to ensure timely diagnosis and intervention in these diagnostically challenging scenarios.

Case Report

A 57-year-old man with a history of hypertension presented to another hospital with a chief complaint of epigastric pain. His initial ECG was performed at 10 am (Figure 1A). It showed a sinus rhythm with prominent, symmetric T waves in the precordial leads V2–V4, without meeting standard ST-elevation criteria for acute MI. However, no previous ECG was available for comparison. Critically, the ECG also demonstrated high QRS voltage meeting criteria for LVH, which significantly confounded the interpretation of the T wave abnormalities. As the patient’s symptoms were atypical and the ECG was considered non-ischaemic, he was managed conservatively.

Approximately 12 hours later, the patient’s condition acutely worsened with the onset of cold sweats and hypotension. He was subsequently transferred to our emergency room, arriving at 11.30 pm. Upon arrival, he was in cardiogenic shock with a blood pressure of 80/50 mmHg, despite vasopressor support initiated during transfer. A repeat ECG was obtained at 11.45 pm (Figure 1B). This ECG showed a subtle but critical evolution from the initial tracing, with the ST-segment elevation in leads V2 and V3 now measuring 2 mm, meeting the formal criteria for anterior STEMI in a male patient over 40 years old.

An emergent bedside echocardiogram revealed severe hypokinesis of the anterior wall and apex, with an estimated left ventricular ejection fraction of only 20%. Given the clinical picture of cardiogenic shock and the evolving ECG findings, the patient was taken immediately to the cardiac catheterisation laboratory.

Coronary angiography revealed a 99% thrombotic occlusion of the proximal LAD artery (thrombolysis in MI 2 flow) as shown in Figure 2. A successful percutaneous coronary intervention (PCI) was performed with the implantation of a drug-eluting stent, restoring blood flow to the vessel (thrombolysis in MI 3 flow). An intra-aortic balloon pump was placed for haemodynamic support. A post-PCI ECG showed resolution of the ST-segment changes; however, notably, there were no reperfusion T wave inversions in the anterior leads (Figure 1C). The patient was subsequently transferred to the intensive care unit for further management. Interestingly, on the post-PCI ECG, the loss of myocardial tissue resulted in a reduction of precordial R wave and S wave amplitudes, such that the tracing no longer met voltage criteria for LVH.

Discussion

The primary teaching point of this case is the significant diagnostic challenge posed by an acute coronary occlusion in the presence of confounding ECG findings from LVH. Our patient presented with an OMI that was initially missed due to a non-diagnostic ECG, leading to a critical delay in reperfusion and subsequent cardiogenic shock. This highlights a crucial limitation of the traditional STEMI paradigm, where the absence of clear ST-segment elevation can result in clinical inertia.¹

The initial ECG was particularly challenging because it was equivocal, falling into a diagnostic grey area. As expert reviewers have noted, the ECG does not fit an easy classification. On one hand, the high QRS voltage raises the possibility that the T wave abnormalities are secondary repolarisation changes of LVH. On the other hand, the T wave morphology is not typical for a simple ‘strain’ pattern and is highly suspicious for ischaemia. Without a prior ECG for comparison, it is nearly impossible to definitively differentiate true hyperacute T waves from the baseline pattern of LVH or – less likely given the lateral ST depression – benign early repolarisation.^3,4 This diagnostic uncertainty was further underscored by a sophisticated artificial intelligence algorithm (Queen of Hearts, PMCardio), which, despite being trained to identify subtle OMI, did not flag the ECG as ischaemic, likely due to the confounding high-voltage features.⁵

The diagnostic challenge presented by this ECG is further highlighted by a crucial concept in ECG: the distinction between prospective and retrospective interpretation. When presented with such a tracing in isolation, even expert interpreters would likely classify it as ‘non-diagnostic but highly suspicious’, withholding definitive judgement without a prior ECG for comparison. However, with the benefit of hindsight – knowing the patient’s catastrophic clinical decline and the angiographic finding of a 100% LAD occlusion – these subtle T wave changes can be confidently re-interpreted, in retrospect, as the initial sign of the ischaemic event. This underscores the reality that in real-time clinical practice, the decision to act often cannot wait for definitive certainty but must be based on a high index of suspicion.

This case powerfully illustrates that OMI is ultimately a clinical, not purely ECG, diagnosis.⁶ In a patient presenting with cardiogenic shock and a regional wall motion abnormality on bedside echocardiography, there is compelling clinical evidence of OMI that necessitates emergent angiography, regardless of the ECG findings.⁷ The ECG, in this context, serves as a supportive tool rather than a gatekeeper. An equivocal, but as one expert reviewer termed it, “very suspicious” ECG in a critically ill patient should therefore lower the threshold for immediate catheterisation laboratory activation, because every minute of delayed reperfusion results in irreversible myocardial loss.

Given this initial diagnostic uncertainty, the most critical intervention would have been the acquisition of rapid serial ECGs. Had tracings been performed every 15–30 minutes, the subtle evolution of ST segments, which ultimately met STEMI criteria 12 hours later, would have been detected far earlier.

This case powerfully illustrates that a single, static ECG is merely a snapshot in time. In a patient with ongoing symptoms suspicious for acute coronary syndrome, any dynamic change on serial ECGs should be considered evidence of an active ischaemic process warranting immediate action.³

Furthermore, the ECG pattern bears a superficial resemblance to the precordial swirl pattern. However, as noted by Goss et al., a key exclusion criterion is LVH. Moreover, the ECG does not meet the specific quantitative definition for this sign, which requires a V2 T wave amplitude to S wave amplitude ratio >0.40; in our patient, this ratio was 10/28 ≈ 0.36. This nuance captures the essence of the diagnostic challenge: the ECG was highly suspicious and nearly met criteria for a known OMI pattern, yet it remained formally non-diagnostic, reinforcing that the dominant feature was its ambiguity.⁸

Recent literature has increasingly highlighted the failure of standard STEMI criteria to identify all acute coronary occlusions. A recent study by Meyers et al. showed that nearly 40% of acute LAD occlusions did not present with diagnostic ST-elevation, yet many had subtle hyperacute T waves that could be identified with quantitative formulas.¹ While our patient’s ECG was confounded by LVH, the case aligns with the broader finding that a significant number of OMIs are missed by current protocols. The failure to recognise the evolving ECG changes, even when they met formal STEMI criteria on the second tracing, speaks to the need for greater awareness of the diverse and often subtle ECG manifestations of OMI.

Conclusion

This case demonstrates that in patients with LVH, an acute coronary occlusion can present with non-diagnostic T wave changes that fall outside the classic STEMI paradigm. It serves as a critical reminder that clinical judgement and a high index of suspicion must prevail over rigid ECG criteria. For patients with concerning symptoms and a confounded ECG, serial tracings are not just advisable—they are essential for unmasking an evolving OMI and preventing catastrophic delays in life-saving reperfusion.