ST-Elevation Myocardial Infarction: Diagnosis and Electrocardiographic Criteria

Definition and Pathophysiology

Acute coronary syndromes (ACS) encompass a spectrum of clinical conditions characterized by a recent change in symptoms or signs, with or without electrocardiographic changes, and with or without acute elevations in cardiac troponin concentrations. Based on the presenting electrocardiogram (ECG) and the presence of troponin elevation, ACS are classified into unstable angina (UA), non-ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI). While the incidence of STEMI is decreasing and the incidence of NSTEMI is increasing, STEMI remains a critical clinical entity requiring immediate reperfusion therapy.

The pathophysiology of myocardial infarction injury involves the overlapping of vulnerable plaque and thrombogenic blood, which are critical determinants for infarction occurrence and extension. Plaque rupture or erosion leads to thrombus formation and subsequent coronary occlusion. Plaque rupture typically involves a thin, collagen-poor fibrous cap overlying a large lipid core with many macrophages, resulting in a red, fibrin-rich thrombus. In contrast, plaque erosion tends to occur in vessels with little or no lipid core, rich proteoglycans, and many smooth muscle cells, leading to a white, platelet-rich thrombus.

Myocardial vulnerability, largely driven by coronary microvascular dysfunction, also contributes to the extension and severity of ischemic injury. In its most severe form, known as no-reflow, structural and functional impairments sustain vascular obstruction. Endothelial dysfunction triggers leukocyte and platelet activation, while thrombotic debris may worsen the obstruction. Furthermore, cardiomyocyte swelling, interstitial edema, and tissue inflammation promote extravascular compression, exacerbating myocardial injury.

Clinical Presentation and Symptoms

In up to one-half of STEMI cases, a precipitating factor such as vigorous physical exercise, emotional stress, or a medical or surgical illness is present before the event. Although STEMI may occur at any time, circadian variations have been reported, with clusters occurring in the morning within a few hours of awakening.

Pain is the most common presenting complaint. The pain is deep and visceral, frequently described as heavy, squeezing, and crushing, though it may occasionally be reported as stabbing or burning. It resembles the discomfort of angina pectoris but typically occurs at rest, is more severe, and lasts longer. The pain usually involves the central portion of the chest or the epigastrium and occasionally radiates to the arms. Less common sites of radiation include the abdomen, back, lower jaw, and neck. The pain may radiate as high as the occipital area but does not radiate below the umbilicus. It is often accompanied by sweating, nausea, vomiting, anxiety, and a sense of impending doom. When pain begins during exertion, it does not usually subside with cessation of activity, distinguishing it from angina pectoris.

The location of the pain beneath the xiphoid and epigastrium, combined with patient denial, often leads to a mistaken impression of indigestion. STEMI pain can simulate pain from acute pericarditis, pulmonary embolism, acute aortic dissection, costochondritis, and gastrointestinal disorders. Radiation of discomfort to the trapezius ridge is not seen in STEMI and suggests pericarditis instead.

Pain is not uniformly present. The proportion of painless or silent STEMIs is greater in patients with diabetes mellitus and increases with age. STEMI may present as sudden-onset breathlessness. Other less common presentations, with or without pain, include sudden loss of consciousness, a confusional state, profound weakness, the appearance of an arrhythmia, evidence of peripheral embolism, or an unexplained drop in arterial pressure. Silent or unrecognized infarction occurs more often in patients without antecedent angina and in those with diabetes and hypertension. Of these unrecognized infarctions, approximately half are truly silent, while the other portion of patients can recall an event characterized by symptoms compatible with acute MI in response to leading questions after ECG or imaging abnormalities are found. The prognosis of patients with silent and symptomatic manifestations of STEMI appears quite similar.

Evaluation and Physical Examination

Prompt assessment of vital signs is recommended at first medical contact (FMC), concurrent with the acquisition of an initial ECG. In patients presenting with suspected ACS, physical examination is useful both to eliminate differential diagnoses and to identify very high-risk and high-risk ACS features. This is particularly relevant for patients presenting with cardiac arrest, signs of cardiogenic shock, and hemodynamic or electrical instability.

A focused physical examination should include checking for the presence of all major pulses, measurement of blood pressure in both arms, auscultation of the heart and lungs, and assessing for signs of heart failure or circulatory compromise. If the patient has a large area of myocardial ischemia, physical findings can include diaphoresis; pale, cool skin; sinus tachycardia; a third and/or fourth heart sound; basilar rales; hypotension; and in severe cases, cardiogenic shock. An important goal of the physical examination is to identify potential alternative life-threatening diagnoses, such as pulmonary embolism, aortic dissection, and cardiac tamponade, given the vastly different treatment plans required.

Diagnostics: Electrocardiogram Criteria

The ECG remains a key test for the diagnosis and management of acute and chronic coronary syndromes. The waveform findings vary considerably depending on the duration of the ischemic process (acute, evolving, or chronic), severity (ischemia with or without infarction), extent (size and degree of transmural involvement), topography (anterior, inferoposterolateral, or right ventricular), and the presence of other underlying abnormalities such as prior infarction, left bundle branch block (LBBB), Wolff-Parkinson-White (WPW) patterns, or electronic pacemaker patterns.

For patients with suspected ischemic chest discomfort, an ECG should be obtained within 10 minutes after arrival. It should also be acquired as rapidly as possible for patients with a history of chest discomfort consistent with ACS but whose discomfort has resolved by the time of evaluation, so that patients who might benefit from immediate reperfusion therapy can be identified. Obtaining a prehospital ECG decreases door-to-diagnosis time and, for STEMI, door-to-balloon time without prolonging scene or transport times. The availability of a previous ECG improves diagnostic accuracy and reduces admission rates for patients with abnormal baseline tracings. Serial ECG tracings improve the ability to diagnose acute MI, especially if the patient remains symptomatic and particularly if combined with serial measurement of cardiac biomarkers.

STEMI Criteria and ECG Findings

A critical clinical distinction is between STEMI and non-STEMI syndromes. ST-segment elevation ≥1 mm in ≥2 contiguous leads is generally consistent with the diagnosis of STEMI. However, the ST threshold may vary depending on the lead and sex. ST-segment depression as little as 0.5 mm is suggestive of ischemia. T wave inversions of at least 2 mm can also indicate ischemia but are less specific. Patients with left circumflex or right coronary occlusions with posterior ischemia may be "electrically silent" and require right-sided leads for identification. Posterior leads can be useful for identifying ischemia in the territory supplied by the circumflex coronary artery, which is otherwise relatively silent on standard ECGs.

During the initial stage of STEMI, total occlusion of an epicardial coronary artery produces ST-segment elevation. Most patients initially presenting with ST-segment elevation ultimately evolve Q waves on the ECG. Q waves in the leads overlying the infarct zone may vary in magnitude and appear only transiently, depending on the reperfusion status of the ischemic myocardium and restoration of transmembrane potentials over time. A small proportion of patients presenting with ST-segment elevation will not develop Q waves when the obstructing thrombus is not totally occlusive, obstruction is transient, or a rich collateral network is present. Contemporary studies using magnetic resonance imaging suggest that the development of a Q wave is more dependent on the volume of infarcted tissue rather than the transmurality of infarction. Terms such as Q-wave MI, non-Q-wave MI, transmural MI, and nontransmural MI have been replaced by the STEMI and NSTEMI classification.

Likelihood Ratios for ECG Findings

The ECG aids in both diagnosis and prognosis. Patients with normal or nearly normal ECG findings have a better prognosis than those with clearly abnormal ECGs at initial evaluation. A normal ECG has a negative predictive value of 80% to 90% for ACS, regardless of whether the patient was experiencing chest pain at the time the ECG was obtained. The likelihood ratios for ACS with various ECG findings are detailed below.

Differential Diagnosis on the ECG

Diffuse ST-segment elevation and PR-segment depression suggest pericarditis. Right-axis deviation, right bundle branch block, T wave inversions in leads V1 to V4, and an S wave in lead I with a Q wave and T wave inversions in lead III suggest pulmonary embolism. Patients with an initial ECG revealing ST-segment depression and/or T wave inversion without ST-segment elevation are not considered candidates for immediate reperfusion therapy unless a posterior or inferobasal injury current is suspected. If the initial ECG is nondiagnostic (no ST-segment deviation or T wave inversion) in a patient with a clinical history suggestive of STEMI, serial tracings should be obtained. Emergency department staff can seek the sudden development of ST-segment elevation by periodic visual inspection of the bedside monitor, continuous ST-segment recording, or auditory alarms when ST-segment deviation exceeds programmed limits.

Biomarkers and Laboratory Findings

The diagnosis of NSTEMI is established if a patient with ischemic features develops evidence of myocardial necrosis, as reflected in abnormally elevated levels of circulating troponin, in the absence of another explanation. Patients with STEMI will typically sustain myocardial necrosis and troponin elevation, fulfilling the criteria for MI, though MI will not be the final diagnosis in all patients with a working diagnosis of STEMI.

High-sensitivity cardiac troponins (hs-cTn) are sensitive, relatively specific, and the preferred markers of myocardial necrosis. In NSTEMI, there is a characteristic temporal rise of the plasma concentration, peaking at 12 to 24 hours after onset of symptoms and gradually decreasing thereafter. A direct relationship exists between the degree of troponin elevation and mortality. A 1-hour rapid rule-out MI algorithm, defined by no abnormal elevation of hsTn at 0 or 1 hour after presentation, has been recommended by recent practice guidelines.

It is important to distinguish myocardial injury from myocardial necrosis. Myocardial injury is defined by elevations of cTn >99th percentile of the upper reference limit in patients without a clear clinical history or ECG features of acute myocardial ischemia. Myocardial injury may be caused by a variety of noncardiac and cardiac conditions other than MI.

Treatment and Management

Prehospital Care and Logistics

Individuals experiencing acute chest pain in the community represent an undifferentiated population. If the first responding medical professional suspects ACS, a 12-lead ECG should be acquired and analysed as soon as possible. All medical and paramedical personnel caring for ACS patients within the emergency medical service (EMS) setting should have access to defibrillation equipment and be trained in basic cardiac life support. Patients with suspected ACS are categorized based on the 12-lead ECG into two pathways: one for STEMI (persistent ST-segment elevation or equivalent patterns) and one for suspected non-ST-segment elevation ACS (NSTE-ACS).

An initial diagnosis of suspected STEMI portends a higher risk of immediate, life-threatening complications such as ventricular fibrillation (VF), warranting initiation of an emergency reperfusion strategy and direct transfer to a centre with 24/7 percutaneous coronary intervention (PCI) capabilities. Patients without ST-segment elevation but with ongoing ischemic symptoms should undergo pre-hospital triage in accordance with STEMI protocols due to immediate risks including ventricular arrhythmias.

At a national level, an EMS with an easily recalled, well-publicised unique medical dispatching number is important to speed up system activation. Parallel circuits that bypass the EMS should be avoided. Ambulances must be equipped with ECG recorders, defibrillators, telemetry devices, and at least one person trained in advanced life support. Ambulance personnel must be trained to recognize ischemic symptoms, secure intravenous access, relieve pain, administer fibrinolysis when indicated, and provide basic life support.

The greatest delay in STEMI care usually occurs between symptom onset and the patient's decision to call for help. This delay can be reduced by healthcare professionals educating the public on the significance of chest discomfort. Regular office visits with patients who have a history of, or risk for, ischemic heart disease serve as important teachable moments.

Emergency Department Management

When evaluating patients in the emergency department (ED), physicians must rapidly identify patients who require urgent reperfusion therapy, triage lower-risk patients appropriately, and avoid unnecessary admissions while preventing inappropriate discharges. Because lethal arrhythmias can occur suddenly, all patients should have bedside ECG monitoring and intravenous access.

The presence of ST-segment elevation suggests thrombotic occlusion of an epicardial coronary artery and should trigger a rapid assessment for reperfusion. Critical factors in selecting a reperfusion strategy include the time elapsed since symptom onset, the risk associated with STEMI, the time required to initiate an invasive strategy, and the risk related to administering a fibrinolytic.

Reperfusion Strategies and Time Goals

Reperfusion can be accomplished by pharmacologic (fibrinolysis) or catheter-based (primary PCI) approaches. The overall system goal is to maintain a network of transportation and destination hospitals so that total ischemic time is kept under 120 minutes. Specific time objectives include:

• If EMS has fibrinolytic capability and the patient qualifies, prehospital fibrinolysis should be started within 30 minutes of EMS arrival on scene.

• For patients transported to a non-PCI-capable hospital for fibrinolysis, the first medical contact (FMC)-to-needle time should be ≤30 minutes.

• If transported to a PCI-capable hospital, the FMC-to-device time should be ≤60 minutes.

• For patients transferred to a PCI hospital, the FMC-to-PCI time should be ≤90 minutes.

• European guidelines suggest initiation of fibrinolytic times of ≤10 minutes after diagnosis, while North American guidelines recommend FMC-initiation of ≤30 minutes.

Emergency interhospital transfer to a PCI-capable hospital for mechanical revascularization is appropriate if fibrinolysis is contraindicated, PCI can be initiated promptly (anticipated FMC-to-device time ≤120 minutes), or if fibrinolysis is unsuccessful (rescue PCI). Secondary non-emergency interhospital transfer should occur for routine invasive evaluation 2 to 24 hours after fibrinolysis. In areas remote from PCI centers, fibrinolytic therapy may be administered prehospital if there is ability to transmit 12-lead ECGs, trained personnel present, and online medical command available.

Indications for Revascularization

For patients with STEMI and ischemic symptoms with symptom onset <12 hours, primary PCI is indicated if PCI is feasible. If symptom onset is ≥12 hours, primary PCI is indicated for cardiogenic shock or heart failure, ongoing ischemia, heart failure, or electrical instability, and if a large area of myocardium is at risk. Coronary artery bypass grafting (CABG) may be considered in certain scenarios. If a totally occluded infarct artery is found >24 hours after symptom onset and the patient has no symptoms or severe ischemia, PCI provides no benefit.

Assessment for Electrical Instability

After STEMI, patients have the greatest risk for development of sudden cardiac death (SCD) from malignant ventricular arrhythmias in the first 1 to 2 years. Multiple techniques may stratify patients into those at increased risk, including measurement of QT dispersion, ambulatory ECGs (Holter or patch monitoring), invasive electrophysiologic testing, signal-averaged ECG, and measurement of heart rate variability or baroreflex sensitivity.

However, none of these approaches has proved sufficiently useful to recommend routine use after STEMI. The low positive predictive value (<30%) of noninvasive screening tests limits their usefulness when viewed in isolation. Although combining several tests improves predictive value, the therapeutic implications of an increased risk profile remain uncertain. The reductions in mortality achievable with general use of revascularization, beta blockers, RAAS inhibition, lipid-lowering therapy, and antiplatelet therapy, coupled with concerns about the efficacy and safety of antiarrhythmic drugs and the cost of implanted defibrillators, leave considerable uncertainty about the therapeutic implications of an abnormal noninvasive test result for electrical instability in an asymptomatic patient. Management of patients with sustained, hemodynamically compromising arrhythmias is a separate clinical priority.

Prognosis and Follow-Up

Both short-term and long-term survival after STEMI depend on three major factors: resting left ventricular (LV) function, residual potentially ischemic myocardium, and susceptibility to serious ventricular arrhythmias. The most important of these factors is the state of LV function. The second most important factor is how the severity and extent of obstructive lesions in the coronary vascular bed perfusing residual viable myocardium affect the risk for recurrent infarction and serious ventricular arrhythmias. Thus, survival relates to the quantity of myocardium that has become necrotic and the portion remaining in ischemic jeopardy. The third risk factor, susceptibility to serious arrhythmias, is reflected in ventricular ectopic activity and other indicators of electrical instability, such as reduced heart rate variability, reduced baroreflex sensitivity, and abnormal findings on a signal-averaged ECG. All these factors identify patients at increased risk for death.

The prognosis in STEMI in the era of primary PCI is largely related to the occurrence of electrical complications (arrhythmias) and mechanical complications (pump failure). Most out-of-hospital deaths from STEMI result from the sudden development of ventricular fibrillation. The vast majority of deaths due to ventricular fibrillation occur within the first 24 hours of the onset of symptoms, and of these, over half occur in the first hour. Women and men receive equal benefit from invasive and non-invasive management strategies and, in general, should be managed similarly.