What does ST depression mean on an ECG?

ST depression means the J point and ST segment sit below the baseline, measured from the onset of the QRS. New horizontal or downsloping depression of at least 0.5 mm in two contiguous leads suggests myocardial ischemia, usually subendocardial ischemia from unstable angina or NSTEMI. It can also be a reciprocal change to ST elevation, a posterior MI when it appears in V1–V3, or a non-ischemic effect of digoxin, hypokalemia, LVH or bundle branch block.

Is upsloping ST depression a sign of ischemia?

The Universal Definition of Myocardial Infarction counts new horizontal or downsloping ST depression of at least 0.5 mm in two contiguous leads, so upsloping depression does not meet the criterion by itself. The exception is the de Winter pattern, upsloping ST depression with tall, symmetric precordial T waves, which the 2026 fifth edition lists among ischemic findings. Otherwise, symptoms, troponin and serial ECGs decide how much weight it deserves.

What are the causes of T-wave inversion?

New, symmetric inversions in contiguous leads suggest ischemia, and deep or biphasic T waves in V2–V3 after chest pain suggest Wellens syndrome. Other causes include LVH (lateral leads), bundle branch block, pulmonary embolism (V1–V4), cerebral T waves after stroke or intracranial hemorrhage, hypertrophic cardiomyopathy, hypokalemia, digoxin and cardiac memory. T waves are normally inverted in aVR, may vary in V1–V2, and can be inverted anteriorly in children.

What is Wellens syndrome, and why is stress testing avoided?

Wellens syndrome is deep, symmetric (about 75% of cases) or biphasic (about 25%) T waves in V2–V3 in a patient with recent angina who is now pain-free, with little or no ST elevation, no Q waves and normal or slightly raised markers. It signals a critical proximal LAD stenosis. Stress testing can precipitate an anterior MI, so the patient needs catheterization and PCI.

What does ST elevation in aVR with widespread ST depression mean?

According to the 2018 Fourth Universal Definition of Myocardial Infarction, ST depression of 1 mm or more in six leads, which may come with ST elevation in aVR or V1 and hemodynamic compromise, suggests multivessel or left main coronary disease. It points to widespread ischemia from a left main or multivessel lesion rather than a single small territory, which makes it a high-risk finding.

ST Depression & T-Wave Inversion: Causes, Wellens, aVR

ST depression is a J point that sits below the baseline. It counts as ischemic when it is new, horizontal or downsloping, and at least 0.5 mm in two contiguous leads (Universal Definition of Myocardial Infarction, unchanged in the 2026 fifth edition), and it usually means subendocardial ischemia (unstable angina or NSTEMI), a reciprocal change to ST elevation elsewhere, or, in V1–V3, a posterior MI. T-wave inversion counts when it is new or dynamic and at least 1 mm deep in two contiguous leads; deep or biphasic T waves in V2–V3 after chest pain has settled is Wellens syndrome, a critical proximal LAD stenosis that needs angiography, not a stress test. Digoxin, hypokalemia, LVH, bundle branch block, pulmonary embolism and brain injury cause look-alike changes.

Draw it out in four strokes

Baseline. Draw the PR segment and mark where the QRS begins. That point is the reference level: the 2018 Fourth Universal Definition measures ST shift from the onset of the QRS, and ACC/AHA recommendations use the PQ junction (the end of the PR segment) rather than the TP segment.
J point. Draw the QRS and mark where it ends. The vertical distance from the baseline to the J point is the ST deviation.
Slope. Extend the ST segment from the J point: flat (horizontal), still falling (downsloping) or climbing back toward the baseline (upsloping).
T wave. Finish it upright or inverted, and note whether an inversion is shallow and asymmetric or deep and symmetric.

Two micro-mnemonics: ST depression goes down; T-wave inversion goes upside-down. And Wellens warns of the widow-maker, the proximal LAD.

Read your drawing

What you drew	Name	What it means
J point at least 0.5 mm below baseline, ST flat	Horizontal ST depression	Meets the ischemia criterion when new and in two contiguous leads
J point below baseline, ST still falling	Downsloping ST depression	Meets the ischemia criterion when new and in two contiguous leads
J point below baseline, ST climbing back up	Upsloping ST depression	Not part of the criterion; with tall, symmetric precordial T waves it is the de Winter pattern, an ischemic finding
T wave at least 1 mm below baseline in two contiguous leads	T-wave inversion	Ischemic when new or dynamic
T wave up, then down, in V2–V3 in a pain-free patient	Biphasic Wellens pattern (about 25%)	Critical proximal LAD stenosis
Deep, symmetric T inversion in V2–V3 in a pain-free patient	Deep Wellens pattern (about 75%)	Critical proximal LAD stenosis

The cutoffs support the clinical picture rather than replace it: smaller ST shifts or T inversions can also be ischemic.

Causes of ST depression

Cause	ECG pattern	Clue
Subendocardial ischemia (unstable angina, NSTEMI)	Horizontal or downsloping ST depression, often with T inversion	Chest pain; NSTEMI if serial troponin rises and/or falls with at least one value above the sex-specific 99th percentile, unstable angina if it does not
Reciprocal change	ST depression in leads opposite an ST-elevation territory	Find the ST elevation; reciprocal changes help separate STEMI from pericarditis and early repolarization
Posterior (inferobasal) MI	ST depression in V1–V3, especially with a dominant R wave (R > S) in V1–V2 or a positive terminal T wave	An ST-elevation equivalent: record V7–V9 (0.5 mm of ST elevation there counts; 1 mm is more specific)
Left main or multivessel disease	ST depression of 1 mm or more in six leads, sometimes with ST elevation in aVR or V1	May come with hemodynamic compromise; a high-risk pattern
Supply–demand mismatch (secondary MI; type 2 in the 2018 definition)	ST depression	Tachyarrhythmia, severe anemia, hypotension or shock, respiratory failure, severe hypertension
Digoxin	ST depression	Patient taking digoxin
Hypokalemia	ST depression with U waves	Low potassium
LVH or bundle branch block	LVH: ST-T changes with tall QRS voltage; LBBB: ST depression in V5–V6	Both confound the ischemia criteria
Pulmonary embolism	Nonspecific ST-T changes	Tachycardia, dyspnea

The ST-elevation side of the same leads is covered in the STEMI patterns 5-second rule.

T-wave inversion: normal, ischemic or something else

Pattern	Think	Clue
Inverted T in aVR; variable T in V1–V2	Normal	Nothing else abnormal
Anterior inversions in a child under 14	Juvenile T-wave pattern	Benign, from right ventricular dominance
New, symmetric, deep inversions in contiguous leads	Ischemia	Chest pain; a coronary territory
Deep or biphasic T waves in V2–V3 after pain has resolved	Wellens syndrome	Critical proximal LAD stenosis
Lateral inversions with tall QRS voltage	LVH	Meets voltage criteria
Inversion opposite the main QRS deflection	Bundle branch block (secondary change)	Wide QRS
Inversions in V1–V4	Pulmonary embolism (right heart strain)	Tachycardia; S1Q3T3 in only about 5%
Diffuse, deep, symmetric inversions	Cerebral T waves	Stroke or intracranial hemorrhage; the QT may be prolonged
Other causes	Hypertrophic cardiomyopathy, hypokalemia (biphasic T waves), cardiac memory after a period of abnormal ventricular activation, digoxin, acute upper abdominal disease	Context decides

Potassium's full ECG signature is reviewed in the hypokalemia and hyperkalemia Q-bank breakdown.

Wellens syndrome: the pattern you must not stress-test

Criteria:

Deep, symmetric T-wave inversion (about 75% of cases) or biphasic T waves that go up then down (about 25%) in V2–V3, sometimes extending to V1 and V4–V6
Isoelectric or minimally elevated ST segment (less than 1 mm)
No precordial Q waves, with preserved R-wave progression
Recent anginal chest pain, with the pattern present when the patient is pain-free
Normal or slightly elevated cardiac markers

The pattern marks a critical proximal LAD stenosis. Historically, 75% of patients managed medically went on to an anterior MI within weeks, and the pattern appears in 14–18% of patients admitted with unstable angina. Treat as ACS and proceed to cardiac catheterization with PCI; avoid stress testing, which can precipitate the infarct. Mimics include LVH, cocaine-induced vasospasm, pulmonary embolism, bundle branch block, cerebral T waves and myocardial bridging. Sources disagree on which pattern is labeled type A and which type B, so learn the two shapes rather than the letters.

Chest pain with ST depression: the Step 2 CK moves

Treat it as NSTE-ACS until proven otherwise, and use troponin to separate unstable angina from NSTEMI.
Start therapy: aspirin plus a P2Y12 inhibitor (the 2025 ACC/AHA ACS guideline makes dual antiplatelet therapy the default for at least 12 months in patients not at high bleeding risk), an anticoagulant and a high-intensity statin, with nitrates for pain.
ST depression in V1–V3: record V7–V9 to look for a posterior MI.
Time the angiogram by risk. Early stress testing is contraindicated when the working diagnosis is unstable angina, except in certain low-risk patients.
Wellens pattern: admit for angiography even though the patient is pain-free.

The STEMI and NSTEMI treatment pathways are compared in the STEMI vs NSTEMI management overview.

Exam traps

Wrong baseline: measure the ST shift from QRS onset (the end of the PR segment).
Upsloping ST depression does not meet the ischemia criterion on its own, but with tall, symmetric precordial T waves (de Winter T waves) it is listed as a sign of ischemia.
ST depression in V1–V3 may be a posterior MI; get posterior leads before calling it anterior ischemia.
Wellens patients are pain-free with normal or slightly raised markers, and the stress test is the wrong answer.
ST elevation in aVR with ST depression in six leads suggests left main or multivessel disease.
LBBB, LVH and pre-excitation confound the ischemia criteria; bundle branch blocks produce secondary ST-T changes opposite the QRS (see the bundle branch block comparison table).
An inverted T wave in aVR is normal, and V1–V2 can go either way.
S1Q3T3 is insensitive, seen in only about 5% of patients with pulmonary embolism.

Worked example

Vignette. A 57-year-old man with hypertension who smokes had two episodes of substernal chest pressure yesterday, each lasting about 20 minutes. He is pain-free in the emergency department, and his vital signs are normal. The ECG shows deep, symmetric T-wave inversions in V2–V4 with isoelectric ST segments, no Q waves and normal R-wave progression. High-sensitivity troponin is slightly above the 99th percentile. What is the most appropriate next step?

Answer: Admit him, treat as NSTE-ACS and arrange coronary angiography. This is Wellens syndrome (the deep, symmetric pattern), marking a critical proximal LAD stenosis.

Why the distractors are wrong:

Exercise stress test: it can precipitate an anterior MI in Wellens syndrome, and early stress testing is contraindicated when unstable angina is suspected, apart from certain low-risk patients.
Discharge because he is pain-free: historically, 75% of medically managed patients with this pattern had an anterior MI within weeks.
CT pulmonary angiography: pulmonary embolism can invert T waves in V1–V4, but he has no tachycardia or dyspnea.
Head CT: cerebral T waves are diffuse and follow a stroke or intracranial hemorrhage; he has no neurologic symptoms.
Reassurance for an LVH repolarization pattern: LVH inverts the lateral T waves with tall voltage, not the V2–V4 T waves after angina.

Key takeaways

Measure at the J point against QRS onset. New horizontal or downsloping ST depression of at least 0.5 mm in two contiguous leads is the ischemic pattern.
ST depression causes: subendocardial ischemia, reciprocal change, posterior MI (V1–V3, then V7–V9), left main or multivessel disease (six leads, sometimes with aVR elevation), supply–demand mismatch, digoxin, hypokalemia, LVH and bundle branch block.
T-wave inversion of at least 1 mm in two contiguous leads is ischemic when new or dynamic; T waves are normally inverted in aVR and variable in V1–V2.
Wellens: deep (75%) or biphasic (25%) T waves in V2–V3 in a pain-free patient mean a critical proximal LAD stenosis; get an angiogram, not a stress test.
Non-ischemic T inversions: LVH, bundle branch block, pulmonary embolism (V1–V4), cerebral T waves, cardiomyopathies, hypokalemia and digoxin.