ST-Segment Elevation Myocardial Infarction: Diagnosis and ECG Criteria

Definition and Pathophysiology

ST-segment elevation myocardial infarction (STEMI) is an acute coronary syndrome characterized clinically by acute myocardial ischaemic symptoms or equivalent presentations together with persistent ST-segment elevation, or an equivalent electrocardiographic pattern, suggesting acute coronary occlusion. Most patients with this working diagnosis subsequently develop myocardial necrosis and cardiac troponin elevation, although not every patient with an initial STEMI pattern has myocardial infarction as the final diagnosis.

The underlying process usually involves acute thrombotic obstruction of an epicardial coronary artery. A vulnerable atherosclerotic plaque and thrombogenic blood interact to initiate and extend thrombosis. Plaque vulnerability is influenced by inflammation, plaque morphology and location, comorbidities, environmental factors and genetic background. Thrombotic susceptibility is likewise affected by inflammation and other systemic influences.

The severity of myocardial injury is determined not only by the epicardial obstruction but also by the vulnerability of the myocardium and coronary microcirculation. Endothelial dysfunction promotes leukocyte and platelet activation and interaction. Thrombotic debris may worsen microvascular obstruction, while cardiomyocyte swelling, interstitial oedema and tissue inflammation produce extravascular compression. In the most severe form, termed no-reflow, structural and functional microvascular impairment persists despite restoration of epicardial flow.

The electrocardiographic appearance depends on several interacting factors:

• The stage of the ischaemic process: acute, evolving or chronic

• The severity of ischaemia and whether infarction has occurred

• The extent and degree of myocardial involvement

• The anatomical territory, including anterior, inferoposterolateral or right ventricular involvement

• Pre-existing abnormalities such as prior infarction, left bundle branch block, Wolff–Parkinson–White patterns or ventricular pacing

STEMI and non-ST-segment elevation myocardial infarction (NSTEMI) are contemporary clinical and electrocardiographic categories. Earlier terms such as Q-wave, non-Q-wave, transmural and non-transmural infarction are no longer considered reliable descriptors of pathological extent. Magnetic resonance imaging findings indicate that Q-wave development relates more closely to infarct volume than to transmurality.

Clinical Presentation and Symptoms

Typical presentation

Pain is the most frequent presenting symptom. It is generally deep and visceral, often described as heavy, squeezing or crushing, although stabbing or burning descriptions may occur. The discomfort resembles angina but is commonly more severe, occurs at rest and lasts longer.

The usual location is the central chest or epigastrium. Radiation may occur to one or both arms and less commonly to the abdomen, back, neck or lower jaw. Discomfort may extend superiorly as far as the occipital region but typically does not radiate below the umbilicus. Epigastric or subxiphoid pain may be mistaken for indigestion.

Associated manifestations include:

• Sweating

• Nausea and vomiting

• Anxiety

• A sense of impending doom

When STEMI begins during exertion, the symptoms generally do not resolve simply with cessation of activity, unlike typical exertional angina.

A precipitating factor is identifiable in up to one-half of cases. Reported precipitants include vigorous physical activity, emotional stress, and an intercurrent medical or surgical illness. Events may occur at any time, although clustering in the morning within several hours of awakening has been described.

Atypical and painless presentations

Pain is not universal. Painless STEMI is more frequent in people with diabetes and becomes more common with advancing age. Presentations without pain may include:

• Sudden breathlessness

• Syncope or sudden loss of consciousness

• Confusion

• Profound weakness

• An arrhythmia

• Peripheral embolism

• An otherwise unexplained fall in arterial pressure

Silent or unrecognized infarction may be discovered on a later ECG or imaging study, or at postmortem examination. Some patients recall a compatible episode only after directed questioning. Such infarctions may manifest as new regional wall-motion abnormalities, fixed perfusion defects or pathological Q waves. Silent STEMI is more frequent in patients with diabetes or hypertension and in those without preceding angina. The prognosis of silent and symptomatic STEMI appears similar.

Differential diagnosis

STEMI symptoms may overlap with those of:

• Acute pericarditis

• Acute aortic syndromes

• Pulmonary embolism

• Musculoskeletal disorders

• Gastrointestinal disease

• Costochondritis

Pain radiating to the trapezius is not characteristic of STEMI and may favour pericarditis. Nevertheless, symptom characteristics alone cannot reliably establish or exclude myocardial infarction.

Evaluation and Physical Examination

Initial assessment

The initial assessment combines:

• Clinical history and symptoms

• Vital signs

• Focused physical examination

• Immediate 12-lead ECG

• High-sensitivity cardiac troponin testing

A focused examination is particularly important when cardiac arrest, cardiogenic shock, heart failure, haemodynamic instability or electrical instability is present. It should include assessment of all major pulses, blood pressure measurement in both arms, cardiac and pulmonary auscultation, and examination for heart failure or circulatory compromise.

The examination also serves to identify alternative life-threatening diagnoses, particularly pulmonary embolism, aortic dissection and cardiac tamponade.

Physical findings

Many patients appear anxious and restless and may repeatedly change position in an attempt to relieve discomfort. Pallor, sweating and cool extremities are common. Persistent substernal pain lasting more than 30 minutes together with diaphoresis strongly supports STEMI.

During the first hour, pulse and blood pressure may remain normal. Autonomic findings can vary with infarct location:

• Anterior infarction may produce sympathetic activation, including tachycardia or hypertension.

• Inferior infarction may produce parasympathetic activation, including bradycardia or hypotension.

The precordium is often quiet, and the apical impulse may be difficult to detect. Findings suggesting ventricular dysfunction include:

• A third or fourth heart sound

• Reduced intensity of the first heart sound

• Paradoxical splitting of the second heart sound

• A reduced-volume carotid pulse, reflecting diminished stroke volume

• Basilar pulmonary rales

• Hypotension

A transient midsystolic or late systolic apical murmur may result from mitral apparatus dysfunction. A pericardial friction rub can occur during the course of a transmural STEMI. Temperature may rise to as much as 38 °C during the first week.

Diagnostics

Electrocardiogram

Timing and role

The resting 12-lead ECG is the first-line diagnostic investigation in suspected acute coronary syndrome. It should be recorded and interpreted as soon as possible at first medical contact, with a target of less than 10 minutes. In hospital, an ECG should be obtained within 10 minutes of arrival when myocardial ischaemia is suspected.

A prehospital ECG can shorten the time to diagnosis and, in STEMI, reduce the time to balloon deployment. It also facilitates direct triage to a percutaneous coronary intervention (PCI)-capable centre.

The ECG contributes to both diagnosis and prognosis. A normal or nearly normal initial tracing is associated with a better prognosis than a clearly abnormal ECG, but a normal ECG does not exclude acute coronary syndrome; its negative predictive value is approximately 80–90%.

Diagnostic ST-segment elevation criteria

The 2023 ESC criteria define STEMI by new ST elevation at the J point in at least two contiguous leads, using the following thresholds:

The criteria apply in the absence of left ventricular hypertrophy or left bundle branch block. In clinical practice, ST elevation of at least 1 mm in at least two contiguous leads is generally consistent with STEMI, although thresholds vary according to lead and sex.

Persistent ST-segment elevation in a patient with compatible ischaemic symptoms should trigger immediate assessment for reperfusion. It generally indicates acute epicardial coronary occlusion, although the final diagnosis may occasionally be another condition.

Other ECG manifestations

The ECG appearance evolves with the duration, severity, territory and extent of ischaemia.

• Initial total epicardial coronary occlusion commonly produces ST-segment elevation.

• Q waves frequently develop after initial ST elevation, but their size and duration vary.

• Q waves may be transient or absent when obstruction is incomplete or transient, or when collateral circulation is substantial.

• ST-segment depression, including depression as small as 0.5 mm, may suggest ischaemia.

• T-wave inversion of at least 2 mm can indicate ischaemia but is less specific.

• New conduction defects are associated with acute coronary syndrome.

• Patients initially without ST elevation may later develop a Q-wave infarction.

• ST-segment depression or T-wave inversion without ST elevation is not ordinarily an indication for immediate reperfusion unless posterior injury is suspected.

The diagnostic value of selected ECG findings is summarized below.

Additional leads and serial ECGs

Standard 12-lead ECG recording may fail to identify posterior ischaemia, particularly in left circumflex or right coronary occlusion. Additional leads are therefore recommended when inferior STEMI is present or when total coronary occlusion is suspected but the standard tracing is inconclusive:

• V3R

• V4R

• V7–V9

Posterior leads are especially useful for detecting ischaemia in the circumflex territory. Additional 12-lead ECGs should be obtained when symptoms recur or diagnostic uncertainty persists.

Serial tracings improve recognition of acute infarction, particularly when the patient remains symptomatic or the initial ECG is nondiagnostic. In the emergency department, serial recordings or continuous ST-segment observation may identify newly developing ST elevation.

ECG patterns suggesting alternative diagnoses

Some patterns may point toward other urgent diagnoses:

• Diffuse ST elevation with PR-segment depression suggests pericarditis.

• Right-axis deviation, right bundle branch block, T-wave inversion in V1–V4, and an S wave in lead I with a Q wave and T-wave inversion in lead III suggest pulmonary embolism.

These patterns must be interpreted in clinical context.

Continuous monitoring and defibrillation capability

Continuous ECG monitoring should begin as soon as possible in suspected or confirmed STEMI. Defibrillation capability must be immediately available because ventricular fibrillation may develop abruptly. Ambulances and receiving hospitals should have ECG recording, monitoring and resuscitation facilities, with personnel trained in advanced cardiac life support.

Biomarkers and Laboratory Findings

Cardiac troponins are central to confirming myocardial necrosis and distinguishing STEMI from other acute coronary syndromes. High-sensitivity cardiac troponin I or T is the preferred biomarker.

In suspected acute coronary syndrome:

• High-sensitivity troponin should be measured immediately after presentation.

• Results should be available within 60 minutes of blood sampling.

• Serial measurements should follow an algorithmic 0-hour/1-hour or 0-hour/2-hour pathway.

• If the first two measurements are inconclusive and no alternative diagnosis explains the presentation, further testing after 3 hours is recommended.

The characteristic biomarker pattern in NSTEMI is an early dynamic rise, with concentrations typically peaking 12–24 hours after symptom onset and then declining. The magnitude of elevation is directly related to mortality. In patients with ischaemic symptoms but no ST-segment elevation, troponin elevation indicating myocardial necrosis establishes NSTEMI when another explanation is absent.

Troponin elevation alone does not establish myocardial infarction. Myocardial injury is defined by a concentration above the 99th percentile upper reference limit without a clear clinical history or ECG evidence of acute myocardial ischaemia. Cardiac and non-cardiac conditions other than infarction can produce myocardial injury.

Imaging

Emergency transthoracic echocardiography is recommended when suspected ACS presents with cardiogenic shock or possible mechanical complications. The source material does not provide a detailed echocardiographic protocol or specific imaging thresholds.

Routine early coronary computed tomography angiography is not recommended in the initial assessment of suspected acute coronary syndrome.

Electrophysiology and Electrical Instability

After STEMI, the risk of sudden cardiac death from malignant ventricular arrhythmias is greatest during the first 1–2 years. Potential risk-stratification methods include:

• QT dispersion

• Ambulatory ECG monitoring, including Holter or patch monitoring

• Invasive electrophysiological testing

• Signal-averaged ECG

• Heart-rate variability

• Baroreflex sensitivity

None of these methods has demonstrated sufficient clinical usefulness to support routine use after STEMI. Their positive predictive value when used individually is below 30%. Although combining tests can improve predictive performance, the implications for treatment remain uncertain in asymptomatic patients. Consequently, management decisions based solely on abnormal non-invasive electrical-instability testing should await clearer outcome data.

The most clinically important immediate electrical risk is ventricular fibrillation, which accounts for most out-of-hospital deaths from STEMI. Most such deaths occur within the first 24 hours, with more than half occurring during the first hour after onset.

Treatment and Management

Immediate triage and reperfusion strategy

Patients with a working diagnosis of STEMI should be triaged immediately for emergency reperfusion. The principal objective is to restore coronary flow as rapidly as possible while maintaining continuous monitoring and resuscitation capability.

Prehospital systems should:

• Obtain and interpret or transmit a 12-lead ECG promptly.

• Categorize patients into STEMI and non-ST-elevation pathways.

• Transfer suspected STEMI directly to a PCI-capable centre when feasible.

• Avoid unnecessary transfer through non-PCI hospitals.

• Provide defibrillation and advanced life-support capability.

• Establish intravenous access and provide initial treatment.

• Administer fibrinolysis when appropriate and supported by local systems.

• Record and audit delays throughout the care pathway.

Patients with ongoing ischaemic symptoms despite an ECG without ST elevation may still face immediate risks, including ventricular arrhythmias, and should be triaged according to local protocols.

Primary PCI

Primary PCI is the preferred immediate reperfusion strategy when it can be delivered without unacceptable delay. PCI-capable centres should provide continuous 24/7 service and perform primary PCI without delay. Patients transferred for primary PCI should bypass the emergency department and intensive or coronary care admission processes and proceed directly to the catheterization laboratory.

System targets include:

• First-medical-contact-to-PCI of 60 minutes or less for patients presenting to a PCI-capable centre

• First-medical-contact-to-PCI of 90 minutes or less for patients requiring transfer to a PCI-capable hospital

• A total ischaemic time goal of less than 120 minutes

Emergency transfer to a PCI-capable centre is also appropriate when fibrinolysis is contraindicated, when PCI can be initiated promptly, or when fibrinolysis has failed and rescue PCI is required.

Fibrinolysis

Fibrinolysis is an alternative reperfusion strategy when timely PCI cannot be achieved and the patient is eligible. In a non-PCI-capable hospital, concurrent evaluation should address both transfer for PCI and contraindications to fibrinolytic treatment.

Relevant time objectives include:

• Initiation of prehospital fibrinolysis within 30 minutes of EMS arrival when the system is capable and the diagnosis is confirmed.

• First-medical-contact-to-needle time of 30 minutes or less when fibrinolysis is administered in a non-PCI-capable hospital.

• European guidance cited in the source material also identifies initiation within 10 minutes after diagnosis as a quality benchmark.

After fibrinolysis, routine non-emergency transfer for invasive assessment should occur within 2–24 hours. Rescue PCI is indicated when fibrinolysis is unsuccessful, although specific criteria for failed fibrinolysis are not provided in the source material.

Timing and outcome

Delay to reperfusion is associated with worse outcomes. Mortality rises progressively with increasing delay to fibrinolytic treatment, and mortality also increases as door-to-balloon time lengthens. System organization should therefore focus on reducing delay from symptom onset and first medical contact through diagnosis, transport and reperfusion.

Supportive acute care

All patients with STEMI should receive bedside ECG monitoring and have intravenous access. EMS personnel should be capable of recognizing ischaemic symptoms, providing analgesia when required, administering oxygen when indicated, and performing basic and advanced life support.

Oxygen is recommended when oxygen saturation is below 90%. Routine oxygen therapy is not recommended when saturation exceeds 90%.

The early management priorities are rapid recognition, immediate ECG diagnosis, continuous monitoring, defibrillation readiness, assessment for haemodynamic or mechanical complications, and expeditious reperfusion.

Guideline Recommendations

The principal recommendations for diagnosis and initial management are summarized below.

Prognosis and Follow-up

Short- and long-term survival after STEMI is determined principally by three domains:

• Resting left ventricular function

• The amount of residual myocardium at risk from potentially ischaemic coronary disease

• Susceptibility to serious ventricular arrhythmias

Left ventricular function is the most important of these factors. Prognosis also depends on the severity and extent of obstructive coronary disease supplying viable myocardium, because this influences recurrent infarction and ventricular arrhythmia risk. Overall survival reflects both the amount of myocardium that has been lost and the amount that remains vulnerable to ischaemia.

Electrical instability may be reflected by ventricular ectopy, reduced heart-rate variability, impaired baroreflex sensitivity or abnormal signal-averaged ECG findings. However, routine screening with these methods is not recommended because predictive accuracy is limited and the therapeutic consequences of abnormal results in asymptomatic patients remain uncertain.

The risk of malignant ventricular arrhythmia and sudden cardiac death is particularly high during the first 1–2 years after STEMI. Immediate monitoring is therefore essential during the acute phase, when ventricular fibrillation may occur suddenly. Long-term follow-up should include reassessment of ventricular function, residual ischaemic risk and clinically apparent arrhythmias, although the source material does not specify a particular follow-up schedule or detailed secondary-prevention medication regimen.