Electrocardiographic Criteria for Differentiating Acute Ischemia, Infarction, and Prior Myocardial Injury

General Principles

• The American College of Cardiology states that the ECG distinguishes ischemia, necrosis, and old myocardial injury primarily through changes in the ST segment, T wave, and QRS complex [1][2].

Acute Myocardial Ischemia

• The American College of Cardiology defines acute myocardial ischemia by reversible ST‑T segment alterations without QRS abnormalities [2][3].
• ST‑segment elevation criteria – elevation ≥0.2 mV (2 mm) in leads V1‑V3, or ≥0.1 mV (1 mm) in any other leads, must be present in at least two contiguous leads [1][2][4][5].
• Hyperacute, tall, peaked T waves may appear in the earliest phase of ischemia [2][6].
• ST‑segment depression criteria – horizontal or downsloping depression ≥0.05 mV in two contiguous leads [1][5].
• Symmetric T‑wave inversion ≥0.1 mV in two contiguous leads with a prominent R wave or R/S > 1 also indicates ischemia [1][5].
• These ST‑T changes must be documented on two consecutive ECGs obtained several hours apart [2][3].
• Prolonged ST elevation lasting >20 minutes, especially with reciprocal ST depression, generally reflects acute coronary occlusion leading to necrosis [1][5].

Acute Myocardial Infarction (Necrosis)

• The American College of Cardiology identifies necrosis by the appearance of pathological Q waves on the QRS complex [2][3].
• Pathological Q in V2‑V3 – any Q wave ≥0.02 s or a QS complex in these leads satisfies the criterion [1][7]4.
• Pathological Q in other leads – Q wave ≥0.03 s and ≥0.1 mV deep, or a QS complex, must be present in at least two contiguous leads (e.g., I, II, aVL, aVF, V4‑V6) [1][7].
• Posterior MI pattern – R wave ≥0.04 s in V1‑V2 with R/S ≥ 1 and concordant positive T wave, in the absence of a conduction defect [1][7].
• A normal ECG does not exclude myocardial infarction; high‑sensitivity biomarkers can detect necrosis too small to produce QRS abnormalities [3][4].

Prior Myocardial Infarction (Old Lesion)

• A single ECG fulfilling pathological Q‑wave criteria is sufficient to indicate a prior infarction [2][4].
• Persistent pathological Q waves, as defined above, confirm an old lesion [1][7]4.
• The absence of acute ST‑segment elevation differentiates old infarction from an acute event [2][3].
• Q waves >30 ms accompanied by ST‑T depression may suggest infarction but require further confirmation [2][4].
• Pathological Q waves can also arise from myocardial fibrosis in non‑coronary diseases such as cardiomyopathies [1][5].

Practical Interpretation Algorithm

• Step 1 – Assess the ST segment (American College of Cardiology)
  
  • ST elevation → suspect ST‑segment elevation myocardial infarction (STEMI) or severe acute ischemia [1][5].
  • ST depression or T‑wave inversion → consider non‑ST‑elevation acute coronary syndrome (NSTE‑ACS) or ischemia [1][5].
  • Normal ST segment → does not rule out ischemia; obtain serial ECGs [1][8].
• Step 2 – Evaluate the QRS complex 3
  
  • New pathological Q waves plus ST elevation → evolving acute MI [2][6].
  • Pathological Q waves without ST elevation → old MI [2][4].
  • Normal QRS with ST‑T changes → ischemia without transmural necrosis [2][3].
• Step 3 – Use additional leads when indicated 4
  
  • Leads V7‑V9 for circumflex‑territory ischemia (ST elevation ≥0.05 mV) [1][7].
  • Leads V3R‑V4R for right‑ventricular MI (ST elevation >0.05 mV) [1][7].
  • ST depression in V1‑V3 may suggest inferobasal (posterior) MI [1][7].

Confounders and Non‑Ischemic Causes of ST Elevation

• QRS‑related confounders that invalidate Q‑wave criteria include bundle‑branch block, left ventricular hypertrophy, and Wolff‑Parkinson‑White syndrome [2][3]4.
• Non‑ischemic conditions that can produce ST elevation are acute pericarditis, left ventricular hypertrophy, left bundle‑branch block, Brugada syndrome, stress (Takotsubo) cardiomyopathy, and early repolarization pattern [1][5][4][6].

Serial ECG Monitoring and Temporal Dynamics

• The American College of Cardiology recommends that symptomatic patients with a nondiagnostic initial ECG undergo repeat recordings every 15–30 minutes [1][5]8.
• Dynamic ST‑T changes during acute ischemic episodes necessitate multiple ECGs to capture evolution [1][5].
• Greater magnitude of ST depression or widespread T‑wave inversion involving multiple territories correlates with more extensive ischemia and a poorer prognosis [1][5]8.

All statements are based on evidence and recommendations from the American College of Cardiology.

Electrocardiographic Criteria for Acute Myocardial Infarction

Diagnostic Thresholds

• The European Society of Cardiology (ESC) defines acute MI on a 12‑lead ECG when ST‑segment elevation meets sex‑ and age‑specific thresholds: ≥2.5 mm in leads V2‑V3 for men < 40 years, ≥2 mm for men ≥ 40 years, ≥1.5 mm for women in V2‑V3, and ≥1 mm in any other lead, present in at least two contiguous leads. 9

ST‑Segment Elevation (STEMI)

• The American College of Cardiology (ACC) states that new ST elevation at the J point in two or more contiguous leads is the hallmark finding of STEMI. 10
• ESC‑2012 criteria specify the same voltage thresholds listed above for V2‑V3 and a universal ≥1 mm (0.1 mV) requirement for all other leads. 11
• Prolonged ST elevation lasting >20 minutes together with reciprocal ST depression strongly suggests an acute coronary occlusion and evolving myocardial necrosis. 12

ST‑Segment Depression

• New horizontal or down‑sloping ST depression ≥0.5 mm (0.05 mV) in two contiguous leads indicates sub‑endocardial ischemia. 12
• ST depression in leads V1‑V3 with a positive terminal T wave constitutes an “ST‑elevation equivalent” for posterior (inferobasal) MI; posterior leads V7‑V9 should be recorded for confirmation. 11

T‑Wave Changes

• Hyperacute, tall, symmetric T waves may appear in the earliest phase of acute MI, often preceding ST elevation. 10
• Symmetric T‑wave inversion ≥1 mm (0.1 mV) in two contiguous leads, accompanied by a prominent R wave or R/S > 1, signifies ischemia and should be documented on two consecutive ECGs obtained several hours apart. 10

QRS Complex Changes (Pathological Q Waves)

• Pathological Q waves defined as ≥0.03 s duration and ≥0.1 mV depth in at least two contiguous non‑precordial leads (or QS complexes) indicate a prior myocardial infarction. 10
• The presence of such Q‑wave criteria on a single ECG is sufficient to label the event as a prior MI. 10
• Loss of precordial R‑wave amplitude may accompany acute ischemia. 12

Special Lead Assessment

• When circumflex artery occlusion is suspected, record posterior leads V7‑V9 at the fifth intercostal space; ST elevation ≥0.05 mV confirms posterior ischemia, and a threshold of ≥0.1 mV improves specificity in men ≥ 40 years. 9 & 12
• Right‑precordial leads V3R and V4R should be obtained in all inferior MIs; ST elevation >0.05 mV (or >0.1 mV in men < 30 years) in these leads indicates right‑ventricular infarction. 11 & 12

Timing and Serial ECG Strategy

• The ESC recommends acquiring and interpreting the first 12‑lead ECG within 10 minutes of first medical contact. 9
• If the initial tracing is nondiagnostic but clinical suspicion remains high, repeat ECGs at 15‑30‑minute intervals to capture dynamic ST‑T changes. 12
• A pre‑discharge ECG should be obtained to serve as a baseline for future comparison. 12

Confounders and Pitfalls

• In the presence of a new or presumed new left bundle‑branch block (LBBB), concordant ST elevation (elevation in leads with positive QRS deflection) is the most reliable indicator of acute MI. 11
• Patients with new LBBB and ongoing ischemic symptoms should be taken directly to emergency angiography. 11
• Right bundle‑branch block does not materially interfere with ST‑segment interpretation. 11
• Ventricular pacing obscures ST‑segment analysis; urgent angiography may be required, and reprogramming should be considered in patients not pacing‑dependent. 9
• Left ventricular hypertrophy and Wolff‑Parkinson‑White syndrome are additional ECG confounders. 10 & 12
• Non‑ischemic conditions that can mimic STEMI include acute pericarditis, LVH, Brugada syndrome, stress cardiomyopathy, and early repolarization; comparison with prior ECGs is essential to differentiate. 12

Management Implications

• A normal ECG does not exclude myocardial infarction; sensitive cardiac biomarkers are required to detect necrosis that does not produce QRS changes. 10
• Occlusion of the circumflex artery may present without ST elevation; nevertheless, suspicion of ongoing ischemia warrants a primary PCI strategy even in the absence of diagnostic ST changes. 9

Prognostic Implications

• Greater magnitude of ST‑segment shift or more extensive T‑wave inversion across multiple territories correlates with a larger ischemic burden and predicts a worse prognosis. 12