At a Glance

Represents
The ST segment (J point to T start) is the plateau after the QRS. The T wave is ventricular repolarization. Deviation signals injury (elevation) or subendocardial ischemia (depression).
Normal (Adult)
Isoelectric at the J point; no horizontal or downsloping depression; T waves upright in I, II and V3–V6, inverted in aVR.
Measure It
Measure the ST deviation at the J point against the TP (or PR) baseline in each lead. Compare contiguous leads and the prior ECG.
Abnormal → Think
  • STE in contiguous leads: STEMI by territory
  • Depression V1–V3: posterior MI until V7–V9 say otherwise
  • STE aVR with diffuse depression: left main or multivessel disease
Red Flags
New STE meeting criteria or a STEMI equivalent (de Winter sign, hyperacute T, posterior pattern, Sgarbossa criteria). Do not wait for classic STE.
Bedside Action
Serial 12-leads every 15–30 min in ongoing symptoms; V4R and V7–V9 when indicated; notify the PCI center per protocol. Avoid stress testing in Wellens pattern.

Physiology & What It Represents

The ST segment runs from the J point, where the QRS ends, to the start of the T wave. Think of it as the plateau. In phase 2 of the ventricular action potential, every ventricular myocyte is depolarized at once. No net current flows, so the lead reads flat.

The T wave is ventricular repolarization (phase 3). That is the recovery back to resting membrane potential. Recovery is where the trouble shows up, so the ST segment and T wave react to injury, ischemia and metabolic change:

  • Acute ischemia or injury: the most urgent cause of ST-T change
  • Electrolytes: Potassium and calcium both reshape the T wave and the ST segment.
  • Conduction and pacing: Bundle branch block and ventricular pacing change the order in which the ventricles repolarize.
  • Drugs and structural disease: digoxin, pericarditis, and hypertrophy

A shifted segment is not automatically ischemic. Measure every shift from the same baseline, every time. Injury current shows as ST elevation in the leads facing the injured myocardium. Subendocardial ischemia shows as ST depression in the leads facing the non-injured wall.

Key concept: The ST segment should sit flat at the J point, measured against the TP (or PR) baseline. A deviation in either direction counts only when its shape, distribution and evolution fit a cause.

Normal Values & How to Measure

ST and T-wave reference values
ParameterAdult NormalPediatric NoteWhere / How to Measure
J point and baseline
J point at the TP (or PR) baseline in most leads
Repolarization varies with age and heart rate; use age-matched norms
Mark the J point (end of QRS) and the TP baseline before judging the ST segment
ST elevation (ischemia)
Abnormal (STEMI): ≥1 mm at the J point in 2 contiguous leads (≥2 mm V2–V3 in men ≥40 y; ≥2.5 mm in men <40 y; ≥1.5 mm in women)
Pediatric ST elevation is usually non-ischemic; use age-based references
Read at the J point in each lead; compare with the TP baseline
ST depression (ischemia)
Abnormal (ischemic): ≥0.5 mm at the J point in 2 or more contiguous leads (horizontal or downsloping)
Rate-related and physiologic ST depression is more common with tachycardia
Confirm morphology and distribution; upsloping depression is less specific
T wave
Upright in I, II and V3–V6; inverted in aVR; variable in III, aVL and V1
Pediatric T-wave pattern varies with age; age-based norms apply
Judge amplitude and symmetry in the same leads as the ST segment
  1. Identify the J point in each lead as the end of the QRS, using a 12-lead with ECG paper at 25 mm/s.
  2. Set the baseline at the TP segment, or the PR segment when the TP is not usable.
  3. Measure the ST deviation at the J point. Some protocols also read at a fixed point after the J point (protocol-dependent).
  4. Compare contiguous leads to define the territory and check reciprocal depression.
  5. Check the shape: convex (tombstone), concave (smiley), horizontal or downsloping.
  6. Compare with the prior ECG and repeat the tracing when symptoms continue.
Measurement pitfall: Tremor, a wandering baseline or a wrong TP reference can fake an ST change or hide a real one. Don't act on a small deviation until you've re-measured it on a clean lead.

ST Elevation & STEMI Criteria

ST elevation is a current of injury. Injured muscle on the epicardial side sits at a different voltage from normal tissue during the plateau. The fourth universal definition of MI sets millimeter criteria for STEMI. Those criteria pick out who needs emergent reperfusion. They are not perfectly sensitive or specific.

ECG Criteria

  • New ST elevation at the J point in 2 contiguous leads: ≥1 mm in all leads except V2–V3
  • V2–V3, men ≥40 years: ≥2 mm
  • V2–V3, men <40 years: ≥2.5 mm
  • V2–V3, women: ≥1.5 mm
  • Reciprocal ST depression: in leads opposite the territory; it adds specificity but is not always present

Causes

  • Ischemic: STEMI from coronary occlusion
  • Non-ischemic: acute pericarditis, early repolarization, left ventricular hypertrophy, left bundle branch block, Brugada pattern, ventricular aneurysm, and takotsubo cardiomyopathy

Clinical Significance

  • Regional, convex or straight ST elevation with reciprocal depression? Treat it as STEMI until proven otherwise.
  • Diffuse, concave ST elevation with no reciprocal change points to a non-ischemic cause. Chest pain plus risk factors still means you exclude ischemia.
Non-ischemic look-alikes: Pericarditis and early repolarization can clear the millimeter thresholds. Shape, distribution and change over serial tracings are what separate them from STEMI. Check the Differential section before you decide.

STEMI Territories & Culprit Arteries

Elevation tells you which wall is at risk. Reciprocal depression shows the wall across from it. Localize the territory before the cath lab team asks.

STEMI territories
TerritoryST Elevation LeadsReciprocal DepressionTypical Culprit
Anterior
V1–V4
II, III, aVF
Proximal or mid LAD
Lateral
I, aVL, V5–V6
III, aVF
Circumflex or first diagonal branch of the LAD
Inferior
II, III, aVF
I, aVL
RCA (right-dominant) or circumflex (left-dominant)
Posterior
V7–V9 (posterior leads)
V1–V3 (ST depression is the mirror image)
RCA or circumflex
Right ventricular
V3R–V6R (right-sided leads); V4R ≥0.5 mm (≥1 mm in men <30 years)
Variable
Proximal RCA
  • Inferior STEMI: Record V4R and V7–V9. You are checking for right ventricular and posterior involvement.
  • Posterior STEMI: ≥0.5 mm of ST elevation in V7–V9 confirms the posterior wall. No sex or age modifier applies.
  • Right ventricular infarction: ST elevation in V4R with an inferior STEMI is the sign. These patients depend on preload.

STEMI Equivalents & Occlusion MI

Not every occlusion meets the classic millimeter criteria. Some patterns point to one anyway. The 2022 ACC Expert Consensus Decision Pathway treats posterior STEMI, left bundle branch block or paced rhythm with Sgarbossa criteria, de Winter sign and hyperacute T waves as STEMI equivalents. A growing body of work on occlusion MI (OMI) says the STEMI criteria miss many occlusions. Inconclusive ECG and high suspicion? Repeat the tracings and add a posterior and right-sided lead set.

De Winter Sign

  • Pattern: upsloping ST depression >1 mm at the J point in the precordial leads, with tall, prominent, symmetric T waves
  • Significance: described in proximal LAD occlusion. It counts as a STEMI equivalent and can occur without ST elevation.
  • Action: Activate cardiology or the cath lab right away, per protocol. Don't wait for ST elevation.

Hyperacute T Waves

  • Pattern: broad, asymmetric or peaked T waves early in STEMI, often before ST elevation appears; the ECDP wording is broad, asymmetric, peaked
  • Action: Repeat the ECG at short intervals. Treat it as a possible occlusion when the clinical picture agrees.

Posterior Pattern

  • Standard ECG: horizontal ST depression in V1–V3, dominant R wave (R/S >1) in V2, and upright T waves in the anterior leads
  • Confirmation: posterior leads V7–V9 with ST elevation ≥0.5 mm

Occlusion MI (OMI) and Non-Occlusion MI (NOMI)

  • Concept: OMI is defined by the occlusion itself, not by millimeter thresholds. NOMI is injury without occlusion, and it is often diffuse.
  • Bedside tools: 2026 reviews report higher sensitivity than STEMI criteria for some signs. Those signs don't yet replace guideline activation criteria.
Do not wait for STE: Hyperacute T waves, de Winter sign and posterior ST depression can show before classic ST elevation. Keep repeating the 12-lead every 15–30 minutes while symptoms last. A concordant clinical picture gets treated as possible occlusion.

ST Depression & NSTE Patterns

ST depression usually means subendocardial ischemia. The inner myocardium has the highest oxygen demand and the least perfusion. So it is the first to suffer. Horizontal or downsloping depression in two or more contiguous leads (≥0.5 mm at the J point) suggests ischemia.

Morphology

  • Horizontal: the most specific shape for ischemia when it appears in contiguous leads.
  • Downsloping: also points to ischemia, most of all with a convex ST segment.
  • Upsloping: the least specific. It is common with tachycardia and digoxin effect. Use context and serial ECGs.

Causes

  • NSTE-ACS: subendocardial ischemia. It is the most important cause.
  • Reciprocal change: the mirror image of ST elevation when an occlusion is present.
  • Posterior MI: what you see as ST depression in V1–V3 is posterior ST elevation seen from the front.
  • Digoxin effect: sagging ST depression with a reverse-tick shape
  • Hypokalemia and LVH strain: Read the potassium and hypertrophy pages for the detail.
  • Rate-related: demand ischemia or physiologic depression with tachycardia

ST Elevation in aVR With Diffuse ST Depression

  • Pattern: ST elevation in aVR with multilead ST depression in I, II, V4–V6 and no contiguous STE elsewhere
  • Significance: the 2022 ECDP files this under ischemia findings, not STEMI equivalents. It most often comes from diffuse subendocardial ischemia with left main or multivessel disease.
  • Threshold: ST elevation in aVR, commonly ≥1 mm, with multilead ST depression
  • Action: Take the high-risk NSTE pathway. Get urgent cardiology review and serial ECGs.
Depression in V1–V3 is a posterior MI until proven otherwise: Isolated ST depression in V1–V3, with no ST elevation elsewhere, can be a posterior STEMI. Record V7–V9 before you label it NSTEMI.

Wellens Pattern

Wellens pattern is a T-wave signature of a critical proximal LAD stenosis. It shows up after recent angina, usually once the pain has settled and the ECG looks close to normal. Treat it as a high-risk NSTE finding. It is not an active occlusion. The original de Zwaan and Wellens series describes it.

ECG Criteria (2022 ECDP)

  • Biphasic or deeply inverted, symmetric T waves in V2–V3 (may extend to V6)
  • ST segment: isoelectric or minimally elevated (under 1 mm); troponin normal or minimally elevated
  • Recent angina with pain resolved or minimal
  • No pathologic Q waves in the same leads

Causes and Significance

  • Cause: a critical proximal LAD stenosis. The T-wave change reflects myocardium that is reperfused but still ischemic.
  • Risk: without urgent evaluation and revascularization, extensive anterior infarction is highly likely.
  • Action: Get urgent cardiology review under the NSTE pathway. Don't discharge from the ED without that review.
Avoid stress testing and discharge without review: A Wellens pattern is not a routine negative chest pain workup. Avoid exercise stress testing until cardiology has reviewed the patient. Confirm against your local pathway.

ST Changes in LBBB & Paced Rhythm

In LBBB and ventricular paced rhythm, the ST-T changes run opposite the QRS. That is expected, and it is called discordant. Standard STEMI criteria do not apply. The modified Sgarbossa criteria were built to catch the concordant changes that suggest occlusion.

Smith-Modified Sgarbossa Criteria

  • Concordant ST elevation: ≥1 mm in leads with a positive QRS
  • Concordant ST depression: ≥1 mm in V1–V3
  • Discordant ST elevation: ≥1 mm at the J point and ≥25% of the preceding S-wave depth

Causes and Significance

  • New or presumed-new LBBB alone is not a STEMI equivalent. Apply the criteria to the tracing.
  • Paced rhythm: the same criteria apply to ventricular pacing.
  • Compare with a prior ECG when you have one. A previous LBBB changes how you read this tracing.
Concordance is the signal: Discordant ST elevation is expected in LBBB, so it is not the signal. The modified criteria test for concordant patterns and the ST/S ratio.

Differential Diagnosis & Mimics

Acute pericarditis and early repolarization are the main look-alikes for ST elevation. Both can clear the millimeter thresholds. Use the table below to split them from STEMI at the bedside.

STEMI, pericarditis and early repolarization
FeatureSTEMIAcute PericarditisEarly Repolarization
ST elevation distribution
Regional (one vascular territory)
Diffuse, in most leads
Lateral or inferior leads, often symmetric
ST morphology
Convex (tombstone) or straight
Concave up (smiley face)
Concave up with J-point notch or slur
Reciprocal depression
Present in the opposite territory
Absent (except aVR)
Absent
PR segment
Normal; PR elevation in aVR may occur
PR depression in most leads; PR elevation in aVR
Normal
Q waves
May develop
Absent
Absent
Evolution
Rapid over hours; Q waves and T inversion
Evolves over days to weeks: ST normalizes, then T inversion may develop
Stable on serial ECGs

Early repolarization means a J-point elevation (Jp) of ≥0.1 mV with an end-QRS notch or slur. You don't need ST elevation to meet that definition. Features that raise the risk: a J-point elevation of 0.2 mV or more, inferior or inferolateral leads, and a horizontal or descending ST segment. Pericarditis is a clinical call, with the ECG as one of several features (2015 ESC guideline).

Other STEMI Mimics

  • LVH: high voltage with discordant ST elevation in V1–V3
  • Brugada pattern: coved ST elevation of 2 mm or more with a negative T wave in V1–V2
  • Ventricular aneurysm: persistent ST elevation with Q waves that does not evolve
  • Takotsubo: wide-territory ST change after stress; a wall-motion abnormality that crosses coronary territories on echo
  • Hyperkalemia: peaked, narrow-based T waves and a widening QRS. It can mimic a de Winter pattern, so check potassium.
  • SAH or stroke: diffuse deep T-wave inversion with a long QT and no coronary occlusion
  • Tricyclic toxicity: wide QRS with a tall R wave in aVR (3 mm or more)

Artifact & Lead Misplacement

  • Limb-lead reversal: it shifts the axis and can make lead I or aVR look changed.
  • Precordial electrodes placed too high: they can fake ST elevation in V1–V2.
  • Tremor, shivering or motion: they can fake ST deviation and VT or VF.
  • Transport vibration: it can make the baseline unreadable. Stop and re-record.
Chest pain with ST elevation is ischemia until proven otherwise: When chest pain and risk factors are both present, pericarditis and early repolarization are diagnoses of exclusion. Repeat the ECG and bring in medical direction before you dismiss the STE.

Bedside Management & Escalation

Your ECG picks the pathway. STEMI or a STEMI equivalent means reperfusion. A high-risk NSTE pattern means urgent cardiology review. Every drug and threshold below runs through local protocols and online medical direction.

Stability and roles
SituationBLS (EMT)ALS (AEMT / Paramedic / RN)Critical Care / Transport
Unstable (hypotension, shock, pulmonary edema, ongoing pain)
Call ALS now; oxygen if SpO₂ <90% (or per local protocol); 12-lead acquisition and transmission where allowed
12-lead; notify the PCI center; IV access; hold nitrates if SBP <90 mmHg or 30 mmHg or more below baseline; treat per protocol
Continuous monitoring; serial 12-leads; transport to a PCI-capable center; manage shock
Stable with ischemic-pattern ST change
12-lead acquisition and transmission where allowed; oxygen if SpO₂ <90% (or per local protocol); notify ALS
12-lead; aspirin 162–325 mg chewed and nitroglycerin per protocol; repeat the 12-lead; notify the receiving center
Serial 12-leads every 15–30 min in ongoing symptoms; cath lab team on arrival
Pulseless or in arrest
Start CPR and use the AED; a 12-lead does not delay CPR or shocks
Follow the cardiac arrest protocol; treat the rhythm
Post-ROSC 12-lead; reperfusion decision per protocol
Therapy by ECG pattern
TherapyAdultPediatricKey Notes
Aspirin (suspected ACS)
162–325 mg PO loading dose, chewed (non-enteric-coated tablet)
Not established for ACS in children: specialist use only
Give unless truly allergic or actively bleeding; chewing speeds absorption
Nitroglycerin (chest pain)
ACS: 0.4 mg SL every 5 min, max 3 doses (nitroglycerin)
Not established in children: specialist use only
Contraindicated with PDE-5 inhibitors: avanafil within 12 h, sildenafil or vardenafil within 24 h, tadalafil within 48 h; also contraindicated with riociguat. Hold for SBP <90 mmHg or 30 mmHg or more below baseline, and in suspected RV infarction; heart-rate limits per protocol
Morphine (pain unrelieved by nitrates)
2.5–5 mg IV every 10 min, titrate to effect (morphine)
Off-label: 0.05–0.1 mg/kg IV/IO/IM slowly (max initial 10 mg; some protocols 2 mg/dose); specialist direction in ACS
High-alert Opioid for pain that persists after nitrates and other anti-ischemic therapy; may delay oral P2Y12 absorption; avoid with hypotension or RV infarction; watch respiratory rate and BP
Unfractionated heparin (ACS)
60 units/kg IV bolus (max 4,000 units), then 12 units/kg/hr (max 1,000 units/hr) (heparin)
Not established for ACS in children: specialist use only
High-alert Anticoagulant; follow the protocol and the cath lab plan
Clopidogrel (P2Y12 inhibitor)
ACS: 300–600 mg PO load (600 mg before PCI), then 75 mg daily. With fibrinolysis: 300 mg load if age 75 or younger; 75 mg with no load if older than 75 (clopidogrel)
Not established in children: specialist or medical-control use only
Agent and timing set by the cath lab and protocol; with a lytic, use the fibrinolysis dose (no 600 mg load)
Tenecteplase (STEMI, PCI >120 min away)
30–50 mg IV single bolus by weight band; at age 75 or older bleeding risk is higher and some protocols reduce the dose, so confirm locally (fibrinolytics)
Systemic lytics not established in children
High-alert Give when FMC-to-device time is expected to exceed 120 min. Absolute contraindications include prior intracranial hemorrhage, known intracranial neoplasm or AVM, ischemic stroke within 3 months, active bleeding and suspected aortic dissection. Heparin adjunct per protocol. Follow local transfer protocol
Oxygen
Give for SpO₂ below 90%; no routine oxygen when SpO₂ is normal; 88–92% if hypercapnia risk (oxygen)
Titrate to age-specific target
Avoid hyperoxia (SpO₂ above 98%, or above 92% with hypercapnia risk). Some EMS protocols still use a 94% threshold; follow local protocol
Nitrates and preload in RV infarction: Inferior STEMI with hypotension may be RV infarction. Hold nitrates and preload reducers, give fluids per protocol and get a V4R.

Doses vary by protocol; follow local protocols and medical direction.

Pediatric & Special Populations

Pediatrics

  • Pattern: Repolarization changes shift with age and heart rate. Use age-based pediatric ECG references.
  • Cause: In children, ST changes are more often non-ischemic (myocarditis, pericarditis, early repolarization). Ischemia is uncommon. When it is suspected, think about coronary anomalies and Kawasaki-related coronary disease.
  • Action: Call pediatric cardiology or medical direction early for a new ST change with symptoms. For rate and BP norms, see the pediatric vital signs reference.
  • Drugs: Pediatric dosing for nitrates, fibrinolytics and antiplatelet agents is not established. Use the weight-based dosing reference and specialist input.

Other Populations

  • Older adults and women: often present atypically. ST depression may be the only finding.
  • Pacemaker or ICD: paced rhythms call for the Sgarbossa criteria. Get a prior ECG to compare.
  • Heart transplant: denervated hearts can show abnormal ST-T patterns and blunted symptoms. Compare with prior tracings.
  • Pregnancy: ST-T changes can be normal in pregnancy. A true STEMI in pregnancy or the peripartum period is often spontaneous coronary artery dissection (SCAD). Fibrinolysis is generally avoided. It can extend the dissection, so PCI or conservative therapy is preferred. Bring in cardiology, obstetrics and the PCI center early. Follow medical direction for antithrombotics.

Monitoring & Transport Considerations

Monitoring and transport
IssueWhat to Do
Monitoring lead
Use the lead that shows the abnormality on the 12-lead; V2–V5 are common choices for anterior and lateral ischemia
Serial 12-leads
Repeat every 15–30 min in ongoing chest pain or symptoms, and transmit each tracing where allowed
Prehospital 12-lead
Obtain and transmit the 12-lead early; the guideline target is an ECG within 10 min of first medical contact, with pre-arrival notification to the PCI center
Posterior and right-sided leads
V7–V9 for suspected posterior MI; V4R for suspected RV infarction in inferior STEMI
Artifact
Stop, check electrodes and limb placement, and re-record before acting on an ST change from vibration or shivering
Transport ECG
Place limb electrodes on the torso to limit movement artifact, and record with the patient still where possible
Before moving an unstable patient
Place anterior-posterior pads for transcutaneous pacing or defibrillation when bradycardia or unstable tachycardia is present
Arrhythmia surveillance
Continuous rhythm monitoring with defibrillation readiness; treat VF or pulseless VT per the arrest protocol

Quiet the stretcher and cut the motion before you record. In transport, a clean tracing is the only reliable input for a diagnosis.

Step-by-Step Approach & Pitfalls

  1. Identify the J point and TP baseline in each lead before reading any shape.
  2. Measure the ST deviation at the J point and note its shape: convex, concave, horizontal or downsloping.
  3. Map the distribution to a territory, and check reciprocal leads.
  4. Check the STEMI equivalents: de Winter sign, hyperacute T waves, posterior ST depression, Sgarbossa criteria in LBBB or paced rhythm.
  5. Check the mimics: diffuse concave STE with PR depression (pericarditis), early repolarization, LVH, and artifact.
  6. Decide the pathway: STEMI or equivalent to reperfusion; high-risk NSTE (STE in aVR with diffuse depression, Wellens) to urgent cardiology review.
  7. Repeat and compare: serial ECGs and the prior tracing, and document each change with a time stamp.

Common Pitfalls

  • Don't wait for classic ST elevation when a de Winter sign or posterior pattern is present.
  • Don't label isolated V1–V3 ST depression as NSTEMI without posterior leads.
  • Don't use STEMI thresholds in LBBB or a paced rhythm. Use the Sgarbossa criteria.
  • Don't give nitrates to a hypotensive patient with inferior changes without checking V4R.
  • Don't order an exercise stress test for a Wellens pattern.

ECG Examples

Clinical Pearls

Morphology matters more than millimeters: Convex (tombstone) or straight elevation should raise your concern for STEMI. Concave (smiley) elevation is more often non-ischemic. Shape usually tells you more than the number, so read it first.
Reciprocal change strengthens the call: Reciprocal depression in the opposite territory makes ST elevation more specific for occlusion. Pericarditis and early repolarization usually lack it.
Serial ECGs are the safety net: Symptoms still going? A non-diagnostic first ECG does not rule out occlusion. Repeat the 12-lead every 15–30 min, and any time the symptoms change.
Check aVR with diffuse depression: Watch aVR. ST elevation there with diffuse depression in I, II and V4–V6 points to left main or multivessel disease. That puts the patient on the high-risk NSTE pathway.
The posterior MI trap: Isolated depression in V1–V3 with a dominant R in V2 can hide a posterior STEMI. Record V7–V9 before you accept an NSTEMI label.
Right ventricular infarction: In inferior STEMI, V4R elevation means the RV is involved. Those patients depend on preload, so avoid nitrates and preload reducers and give fluids per protocol.

References

  1. Rao SV, O'Donoghue ML, Ruel M, et al. 2025 ACC/AHA/ACEP/NAEMSP/SCAI guideline for the management of patients with acute coronary syndromes. J Am Coll Cardiol. 2025;85(22):2135-2237. https://doi.org/10.1016/j.jacc.2024.11.009
  2. Thygesen K, Alpert JS, Jaffe AS, et al. Fourth universal definition of myocardial infarction (2018). Circulation. 2018;138(20):e618-e651. https://doi.org/10.1161/CIR.0000000000000617
  3. Kontos MC, de Lemos JA, Deitelzweig SB, et al. 2022 ACC Expert Consensus Decision Pathway on the evaluation and disposition of acute chest pain in the emergency department. J Am Coll Cardiol. 2022;80(20):1925-1960. https://doi.org/10.1016/j.jacc.2022.08.750
  4. de Winter RJ, Verouden NJ, Wellens HJ, Wilde AA. A new ECG sign of proximal LAD occlusion. N Engl J Med. 2008;359(19):2071-2073. https://doi.org/10.1056/NEJMc0804737
  5. de Zwaan C, Bär FW, Wellens HJ. Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J. 1982;103:730-736 (landmark study). https://doi.org/10.1016/0002-8703(82)90480-x
  6. Smith SW, Dodd KW, Henry TD, Dvorak DM, Pearce LA. Diagnosis of ST-elevation myocardial infarction in the presence of left bundle branch block with the ST-elevation to S-wave ratio in a modified Sgarbossa rule. Ann Emerg Med. 2012;60(6):766-776. https://doi.org/10.1016/j.annemergmed.2012.07.119
  7. Macfarlane PW, Antzelevitch C, Haissaguerre M, et al. The early repolarization pattern: a consensus paper. J Am Coll Cardiol. 2015;66(4):470-477. https://doi.org/10.1016/j.jacc.2015.05.033
  8. Adler Y, Charron P, Imazio M, et al. 2015 ESC guidelines for the diagnosis and management of pericardial diseases. Eur Heart J. 2015;36(42):2921-2964. https://doi.org/10.1093/eurheartj/ehv318
  9. McLaren JTT, Nunes de Alencar J, Smith SW. Diagnosis of occlusion myocardial infarction. Curr Opin Crit Care. 2026;32(3):230-238. https://doi.org/10.1097/MCC.0000000000001359
  10. Hayes SN, et al. Spontaneous coronary artery dissection: current state of the science. A scientific statement from the American Heart Association. Circulation. 2018;137(19). https://doi.org/10.1161/CIR.0000000000000564

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