Letter to the Editor: Culprit coronary occlusion as a stronger short-term prognostic marker over electrocardiographic pattern in acute myocardial infarction

Abstract

Kos et al recently published a study in World Journal of Cardiology report that an acute myocardial infarction patient’s outcome is more strongly determined by whether the culprit artery is totally occluded than by the initial electrocardiographic presentation. In this Letter, we highlight the clinical significance of their finding that ST-segment elevation on electrocardiogram was not an independent predictor of 30-day mortality, underscoring the importance of angiographic occlusion status. We discuss the utility and caveats of using troponin levels as a surrogate for infarct size, the observed protective association of chronic statin therapy with lower likelihood of occlusion, and the need for earlier detection of occlusions. We share the authors’ view that integrating culprit vessel patency into acute myocardial infarction risk assessment is essential and that an “occlusion myocardial infarction” approach may improve triage decisions and outcomes.

Key Words: Infarct-related artery occlusion; Electrocardiographic presentation; Acute myocardial infarction; Troponin; Statin therapy

Core Tip: This letter discusses the study by Kos et al and emphasizes that in acute myocardial infarction, the presence of a totally occluded culprit artery drives short-term mortality risk more than the electrocardiogram classification (ST-segment elevation vs non-ST segment elevation). We also note troponin as a practical, but imperfect, surrogate for infarct size and urge cautious interpretation. Finally, the association between previous statin use and a lower likelihood of presentation with total occlusion suggests plaque stabilizing effects of statins that merit further investigation.

TO THE EDITOR

We read with great interest the recent study by Kos et al[1] published in World Journal of Cardiology. This large prospective study of 2483 acute myocardial infarction (AMI) patients found that a completely occluded culprit coronary artery was associated with markedly worse 30-day survival[1]. In fact, the presence of an occlusion increased the risk of short-term mortality approximately threefold[1]. Importantly, this prognostic effect was independent of the initial electrocardiographic presentation - whether an AMI manifested as ST-segment elevation on the electrocardiogram (ECG) or not did not itself predict 30-day mortality after adjusting for occlusion status.

Kos et al[1] demonstrate that relying on ECG criteria alone may overlook high-risk occlusions. Indeed, prior studies have shown up to 25%-30% of patients labeled non-ST-elevation myocardial infarction (NSTEMI) harbor a complete vessel occlusion on angiography[2]. Such “hidden” occlusions, if not promptly opened, can lead to larger infarcts and worse outcomes comparable to classic ST-elevation myocardial infarction (STEMI) cases[3]. These data have supported the call for a new paradigm of occlusion myocardial infarction vs non-occlusion myocardial infarction, emphasizing the presence of an occluded culprit vessel as the key determinant of emergent care[2,3].

A key point in the study is the use of cardiac troponin levels as a surrogate for infarct size. Numerous studies have shown that the extent of troponin elevation correlates with the infarct size as measured by cardiac imaging[4]. This makes troponin an attractive and practical surrogate for infarct size in large clinical studies such as Kos et al[1], where direct imaging of infarcts in thousands of patients would be impractical. However, we also recognize important limitations in using troponin as a stand-in for infarct size. Troponin release dynamics can be influenced by biological and clinical factors[5]. Timing of presentation and reperfusion therapy will also affect peak levels as an early reperfused occlusion may result in a lower peak troponin despite a large area at risk whereas a late-presenting patient might have a very high troponin from prolonged occlusion. Additionally, baseline patient characteristics can confound interpretation. Thus, while troponin remains an indispensable and validated proxy for infarct size, one must be cautious in over-relying on its absolute values. We encourage continued efforts to refine such surrogate measures - perhaps by combining biomarkers with imaging or considering patient-specific factors (e.g. left ventricular mass).

Using ST-segment elevation alone to guide reperfusion decisions or predict myocardial infarction prognosis is outdated. Clinical presentation, refractory pain, hemodynamic status, age, comorbidities, and ventricular arrhythmias must all inform the urgency and type of reperfusion. Although many services already apply this broader approach, minimizing the severity of myocardial infarction solely because ST elevation is absent is an unsafe and outdated practice.

An intriguing finding by Kos et al[1] is the association between chronic statin therapy and lower likelihood of presenting with an occluded infarct-related artery. In their cohort, patients who were on statins prior to the myocardial infarction had a significantly higher chance of arriving with a patent (non-occluded) culprit vessel. This observation aligns with the known benefits of statins in coronary artery disease. Clinical data support this mechanism: For example, Ndrepepa et al[6] analyzed 12989 patients with a history of coronary artery disease undergoing coronary angiography and found that patients with prior statin use more frequently presented with unstable angina and non-STEMI and less often present with STEMI, suggesting that plaques were more stable, and any thrombosis was more limited. The findings by Kos et al[1] provide clinical corroboration that statins may prevent total occlusions during an AMI, likely by mitigating the extent of thrombus formation or by promoting collateral blood flow. While this was an observational association and not proof of causation, it adds to the substantial body of evidence for the beneficial role of statins in acute coronary syndrome outcomes. We encourage future research on how prior statin use influences thrombotic occlusion severity.

In conclusion, these findings suggest that promptly recognizing an infarctrelated occlusion should be a central goal in managing AMI, irrespective of the initial ECG pattern. We commend the authors for bringing attention to the prognostic importance of identifying a totally occluded infarct-related artery. By detecting and treating occlusions early - even in the absence of classic STEMI criteria - we stand to improve short-term survival and outcomes for our patients with AMI.