From ST-Segment Elevation MI to Occlusion MI: The New Paradigm Shift in Acute Myocardial Infarction.

A generation ago thrombolytic therapy led to a paradigm shift in myocardial infarction (MI), from Q-wave/non-Q-wave to ST-segment elevation MI (STEMI) vs non-STEMI. Using STE on the electrocardiogram (ECG) as a surrogate marker for acute coronary occlusion (ACO) allowed for rapid diagnosis and treatment. But the vast research catalyzed by the STEMI paradigm has revealed increasing anomalies: 25% of "non-STEMI" have ACO with delayed reperfusion and higher mortality. Studying these limitations has given rise to the occlusion MI (OMI) paradigm, based on the presence or absence of ACO in the patient rather than STE on ECG. The OMI paradigm shift harnesses advanced ECG interpretation aided by artificial intelligence, complementary bedside echocardiography and advanced imaging, and clinical signs of refractory ischemia, and offers the next opportunity to transform emergency cardiology and improve patient care. This State-of-the-Art Review examines the paradigm shifts from Q wave to STEMI to OMI.

International evaluation of an artificial intelligence-powered electrocardiogram model detecting acute coronary occlusion myocardial infarction.

Aims: A majority of acute coronary syndromes (ACS) present without typical ST elevation. One-third of non-ST-elevation myocardial infarction (NSTEMI) patients have an acutely occluded culprit coronary artery [occlusion myocardial infarction (OMI)], leading to poor outcomes due to delayed identification and invasive management. In this study, we sought to develop a versatile artificial intelligence (AI) model detecting acute OMI on single-standard 12-lead electrocardiograms (ECGs) and compare its performance with existing state-of-the-art diagnostic criteria. Methods and results: An AI model was developed using 18 616 ECGs from 10 543 patients with suspected ACS from an international database with clinically validated outcomes. The model was evaluated in an international cohort and compared with STEMI criteria and ECG experts in detecting OMI. The primary outcome of OMI was an acutely occluded or flow-limiting culprit artery requiring emergent revascularization. In the overall test set of 3254 ECGs from 2222 patients (age 62 ± 14 years, 67% males, 21.6% OMI), the AI model achieved an area under the curve of 0.938 [95% confidence interval (CI): 0.924-0.951] in identifying the primary OMI outcome, with superior performance [accuracy 90.9% (95% CI: 89.7-92.0), sensitivity 80.6% (95% CI: 76.8-84.0), and specificity 93.7 (95% CI: 92.6-94.8)] compared with STEMI criteria [accuracy 83.6% (95% CI: 82.1-85.1), sensitivity 32.5% (95% CI: 28.4-36.6), and specificity 97.7% (95% CI: 97.0-98.3)] and with similar performance compared with ECG experts [accuracy 90.8% (95% CI: 89.5-91.9), sensitivity 73.0% (95% CI: 68.7-77.0), and specificity 95.7% (95% CI: 94.7-96.6)]. Conclusion: The present novel ECG AI model demonstrates superior accuracy to detect acute OMI when compared with STEMI criteria. This suggests its potential to improve ACS triage, ensuring appropriate and timely referral for immediate revascularization.

Beyond the ST-segment in Occlusion Myocardial Infarction (OMI): Diagnosing the OMI-nous.

The ST-segment elevation (STE) myocardial infarction (MI)/non-STEMI (NSTEMI) paradigm has been the central dogma of emergency cardiology for the last 30 years. Although it was a major breakthrough when it was first introduced, it is now one of the most important obstacles to the further progression of modern MI care. In this article, we trace why a disease with an established underlying pathology (acute coronary occlusion [ACO]) was unintentionally labeled with a surrogate electrocardiographic sign (STEMI/NSTEMI) instead of pathologic substrate itself (ACO-MI/non-ACO-MI or occlusion MI [OMI]/non-OMI [NOMI] for short), how this fundamental mistake caused important clinical consequences, and why we should change this paradigm with a better one, namely OMI/NOMI paradigm.

Considerations on the naming of myocardial infarctions.

The electrocardiogram is not only an indispensable tool for the diagnosis of myocardial infarction, but also helps in the prediction of its location and extent. However, there is a confusion regarding to the electrocardiographic nomenclature on the naming of infarcting left ventricular segments. This review briefly examines the sources of this confusion and gives some recommendations to avoid them.

Recognizing electrocardiographically subtle occlusion myocardial infarction and differentiating it from mimics: Ten steps to or away from cath lab.

It is increasingly evident that the ST-segment elevation (STE) myocardial infarction (MI)/non-STEMI paradigm that equates STEMI with acute coronary occlusion (ACO) is deceptive. This unfortunate paradigm, adhered to by the current guidelines, misses at least one-fourth of the ACOs, and unnecessarily over-triages a similar fraction of the patients to the catheterization laboratory. Accordingly, we have been calling for a new paradigm, the occlusion/nonocclusion MI (OMI/NOMI). Although this new OMI/NOMI paradigm is not limited to an electrocardiogram (ECG), the ECG will remain the cornerstone of this new paradigm because of its speed, repeatability, noninvasive nature, wide availability, and high diagnostic power for OMI. This review provides a step-by-step approach to ECG for the diagnosis of OMI.

Filtering electrocardiogram: Music, math, and ST-elevation myocardial infarction.

Clinicians should have a basic understanding of the working principle of the instruments they use to avoid potential pitfalls caused by post-processing of the acquired biological signals. An electrocardiogram (ECG) is no exception; many different errors can arise during the acquisition or the processing of the ECG data, which may result in dangerous misdiagnoses. We present a case where the use of an inappropriate high-pass filter led to a false diagnosis of ST-elevation myocardial infarction. In addition, this report discusses the basic mechanisms of this frequently overlooked phenomenon and methods to avoid it.

Time for a new paradigm shift in myocardial infarction.

The ST-elevation myocardial infarction (STEMI)/non-STEMI paradigm per the current guidelines has important limitations. It misses a substantial proportion of acute coronary occlusions (ACO) and results in a significant amount of unnecessary catheterization laboratory activations. It is not widely appreciated how poor is the evidence base for the STEMI criteria; the recommended STEMI cutoffs were not derived by comparing those with ACO with those without and not specifically designed for distinguishing patients who would benefit from emergency reperfusion. This review aimed to discuss the origins, evidence base, and limitations of STEMI/non-STEMI paradigm and to call for a new paradigm shift to the occlusion MI (OMI)/non-OMI.

STEMI: A transitional fossil in MI classification?

An important task in emergency cardiology is distinguishing patients with acute coronary occlusion (ACO), who will benefit from emergent reperfusion therapy, from those without ongoing myocyte loss who can be managed with medical therapy and for whom potentially harmful invasive interventions can be deferred. The electrocardiogram is critical in this process. Although the ST-segment elevation myocardial infarction (STEMI)/non-STEMI paradigm is well-established, with "STEMI" representing ACO, its evidence base is poor, and this can have dire consequences. The universally recommended STEMI criteria do not accurately diagnose ACO; in fact, they miss more than one-fourth of the patients with ACO, and also result in a substantial burden of unnecessary catheterization laboratory activations. We here discuss why we believe it is time to change the current STEMI/non-STEMI paradigm.

DIagnostic accuracy oF electrocardiogram for acute coronary OCClUsion resuLTing in myocardial infarction (DIFOCCULT Study).

BACKGROUND: Although ST-segment elevation (STE) has been used synonymously with acute coronary occlusion (ACO), current STE criteria miss nearly one-third of ACO and result in a substantial amount of false catheterization laboratory activations. As many other electrocardiographic (ECG) findings can reliably indicate ACO, we sought whether a new ACO/non-ACO myocardial infarction (MI) paradigm would result in better identification of the patients who need acute reperfusion therapy. METHODS: A total of 3000 patients were enrolled in STEMI, non-STEMI and control groups. All ECGs were reviewed by two cardiologists, blinded to any outcomes, for the current STEMI criteria and other subtle signs. A combined ACO endpoint was composed of peak troponin level, troponin rise within the first 24 h and angiographic appearance. The dead or alive status was checked from hospital records and from the electronic national database. RESULTS: In non-STEMI group, 28.2% of the patients were re-classified by the ECG reviewers as having ACO. This subgroup had a higher frequency of ACO, myocardial damage, and both in-hospital and long-term mortality compared to non-STEMI group. A prospective ACOMI/non-ACOMI approach to the ECG had superior diagnostic accuracy compared to the STE/non-STEMI approach in the prediction of ACO and long-term mortality. In Cox-regression analysis early intervention in patients with non-ACO-predicting ECGs was associated with a higher long-term mortality. CONCLUSIONS: We believe that it is time for a new paradigm shift from the STEMI/non-STEMI to the ACOMI/non-ACOMI in the acute management of MI. (DIFOCCULT study; ClinicalTrials.gov number, NCT04022668.).

Percutaneous coronary intervention increases microvascular resistance in patients with non-ST-elevation acute coronary syndrome.

AIMS: In the acute coronary syndrome setting, the interaction between epicardial coronary artery stenosis and microcirculation subtended by the culprit vessel is poorly understood. The purpose of the present study was to assess the immediate impact of percutaneous coronary intervention (PCI) on microvascular resistance (MR) in patients with non-ST-elevation myocardial infarction (NSTEMI). METHODS AND RESULTS: Thirty-eight patients undergoing PCI for NSTEMI were recruited consecutively. Culprit lesions were stented over a Doppler and pressure-sensor-equipped guidewire. In the presence of epicardial stenosis, MR was calculated by taking collateral flow, as measured by the coronary wedge pressure, into consideration. After removal of epicardial stenosis, MR was calculated simply as distal coronary pressure divided by average peak velocity. When collateral flow was incorporated into the calculation, MR increased significantly from 1.70 ± 0.76 to 2.05 ± 0.72 (p=0.001) after PCI in the whole population. Periprocedural changes (Δ) in absolute values of MR and troponin T correlated significantly (r=0.629, p=0.0001). In patients who developed periprocedural myocardial infarction, MR increased significantly after PCI (1.48 ± 0.73 versus 2.28 ± 0.71, p<0.001). Nevertheless, removal of the epicardial lesion did not change MR in patients without periprocedural MI (1.91±0.73 versus 1.81±0.67, p=0.1). CONCLUSIONS: When collateral flow is accounted for, removal of epicardial stenosis increases MR in patients with NSTEMI undergoing PCI.

Concurrent microvascular and infarct remodeling after successful reperfusion of ST-elevation acute myocardial infarction.

BACKGROUND: Connection between the course of microvascular and infarct remodeling processes over time after reperfused ST-elevation acute myocardial infarction has not been fully elucidated. The aim of this study is to investigate the association of temporal changes in hemodynamics of microcirculation in the infarcted territory and infarct size (IS) after primary percutaneous coronary intervention in patients with ST-elevation acute myocardial infarction. METHODS AND RESULTS: Thirty-five patients admitted with ST-elevation acute myocardial infarction undergoing primary percutaneous coronary intervention were enrolled in the study. Coronary flow reserve (CFR), index of microvascular resistance (IMR), and IS were assessed 2 days after primary percutaneous coronary intervention and at the 5-month follow-up. The predictors of the 5-month IS were the baseline values of IS (beta=0.6, P<0.001), IMR (beta=0.280, P=0.013), and CFR (beta=-0.276, P=0.017). There were significant correlations between relative change in IS and relative change in measures of microvascular function (IS and CFR [r=-0.51, P=0.002]); IS and IMR ([r=0.55, P=0.001]). In multivariate model, relative changes in IMR (beta=0.552, P=0.001) and CFR (beta=-0.511, P=0.002) were the only predictors of relative change in IS. In patients with an improvement in IMR >33%, the mean IS decreased from 32.3+/-16.9% to 19.3+/-14% (P=0.001) in the follow-up. Similarly, in patients with an improvement in CFR >41%, the mean IS significantly decreased from 29.9+/-20% to 15.8+/-12.4% (P=0.003). But in patients with an improvement in IMR and CFR, which were below than the mean values, IS did not significantly decrease during the follow-up. CONCLUSIONS: Improvement in microvascular function in the infarcted territory is associated with reduction in IS after reperfused ST-elevation acute myocardial infarction. This link suggests that further investigations are warranted to determine whether therapeutic protection of microvascular integrity results in augmentation of infarct healing.

Infarct remodeling process during long-term follow-up after reperfused acute myocardial infarction.

BACKGROUND: After acute myocardial infarction (AMI), the recovery of perfusion in infarct area may lead to significant spontaneous infarct size (IS) reduction during the subsequent period. The natural course of infarct-healing process after reperfusion therapy has not been fully elucidated. In this study, we investigated the time course of the spontaneous infarct-healing process in patients with reperfused AMI. METHODS AND RESULTS: Fifty-two patients with AMI who underwent primary percutaneous intervention were included. IS was measured with single-photon emission tomography using Bull's eye method at 4th day, at 5th, and at 10th months. IS was expressed as a percentage of the total myocardium. IS decreased by 33.6% at 5th month when compared with 4th day IS (from 26.3% +/- 18.8% to 17.5% +/- 12.9%, P < 0.001, n = 44). At 10th month, mean IS decreased by 21% when compared with 5th month IS (from 15.89% +/- 12.65% to 12.53% +/- 9.35%, P = 0.007, n = 31) and 49% when compared with 4th day IS (24.02% +/- 17.67% to 12.53% +/- 9.35%, P < 0.001). CONCLUSION: Significant endogenous recovery of perfusion in the infarct area occurs at the long term in patients with reperfused AMI. Infarct healing is a dynamic and ongoing process and decrease in IS continues long term after reperfused AMI.