T inversion in v1 to v3
T wave inversion V1 V2 V3 ECG leads

This diagnostic image is a 12-lead electrocardiogram (ECG) demonstrating several clinically significant abnormalities. Key findings include deep, symmetrical, and biphasic T-wave inversions primarily across the precordial leads V2 to V5, with the most pronounced inversion occurring in V3. Similar, though less severe, T-wave inversions are also noted in the inferior limb leads (II, III, and aVF). The tracing exhibits poor R-wave progression across the precordial leads, characterized by the failure of the R-wave amplitude to increase appropriately from V1 through V6. Additionally, there is evidence of right axis deviation. These visual features are often associated with right ventricular strain, as seen in clinical contexts such as acute pulmonary embolism or the Zurkurnai ECG pattern. The ECG is recorded at a standard paper speed of 25.0 mm/s and a voltage gain of 10.0 mm/mV, showing a sinus rhythm. This educational resource illustrates key ECG markers used in the identification of pulmonary hypertension and acute right heart strain.

A 12-lead electrocardiogram (ECG) demonstrating the classic 'Type A' Wellens' Syndrome pattern. The recording shows a regular rhythm with normal QRS complexes; however, there is a pathognomonic T-wave morphology in the precordial leads, specifically V2 and V3. These leads exhibit biphasic T-waves characterized by an initial shallow positive deflection followed by a deep, terminal negative deflection. The terminal inversion is more prominent in amplitude than the initial upward phase. Such findings in the context of clinical stability are highly specific for critical stenosis of the proximal left anterior descending (LAD) coronary artery. The ECG also includes standard limb leads (I, II, III), augmented limb leads (aVR, aVL, aVF), and the full precordial series (V1-V6), with rhythm strips for V1, II, and V5 at the bottom. The paper speed is noted at 25mm/s with a sensitivity of 10mm/mV, providing a standard diagnostic reference for ischemic heart disease and acute coronary syndrome (ACS) evaluation.

This diagnostic image displays a focused 12-lead electrocardiogram (ECG) tracing specifically highlighting the precordial leads V1 through V6. The visual focuses on the right precordial leads (V1, V2, and V3), which are marked with red circles and arrows to indicate diagnostic abnormalities. Key morphological features include prominent T-wave inversions in leads V1-V3, while the lateral leads V4-V6 show upright T-waves. A critical finding is the presence of an 'epsilon wave,' identified as a small positive deflection or notch at the terminal end of the QRS complex, occurring between the end of the S-wave and the start of the T-wave. These electrocardiographic signs—T-wave inversion in right precordial leads beyond V1 and the presence of epsilon waves—are highly characteristic of Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC). This image serves as a clinical teaching tool for identifying subtle depolarization and repolarization abnormalities associated with fibrofatty replacement of the right ventricular myocardium.

A 12-lead electrocardiogram (ECG) demonstrating a classic presentation of arrhythmogenic cardiomyopathy (AC) in a young athlete. The most significant finding is the presence of deep, symmetric T-wave inversions (TWI) in the right precordial leads, extending from V1 through V4. These inversions are most prominent in V2 and V3. The limb leads (I, II, III, aVL, and aVF) show generally upright QRS complexes and T-waves, while lead aVR shows expected global inversion. There is no evidence of complete right bundle branch block (QRS < 120 ms). The primary clinical significance of this ECG pattern is its recognition as a major diagnostic criterion for arrhythmogenic cardiomyopathy, especially when identified during pre-participation screenings for athletes. This visual serves as an educational reference for distinguishing pathologic anterior T-wave inversions from benign athletic adaptations, which typically lack this degree of precordial extension and depth.
"T wave inversion" precordial leads ECG differential diagnosis
| Cause | Key Feature |
|---|---|
| Normal variant (V1 only) | T inversion in V1 alone is normal in all ages |
| Persistent juvenile pattern | TWI in V1-V3 that persists into adulthood; more common in women; asymptomatic |
| Post-tachycardia / post-pacemaker | TWI that normalizes over time after rate returns to normal |



| Condition | Notes |
|---|---|
| Brugada syndrome | RBBB pattern with ST elevation V1-V3; TWI may accompany |
| Hypertrophic cardiomyopathy | May have deep TWI across precordials |
| Myocarditis | Diffuse TWI; often with ST changes and elevated troponins |
| Intracranial hemorrhage / CNS events | Classically deep, wide "cerebral T waves" across precordials; associated with Stokes-Adams |
| Spontaneous pneumothorax | Axis deviation with TWI in right precordials |
| Cardiac sarcoidosis | Can mimic ARVC; PR prolongation helps differentiate |
V1-V3 TWI
│
├── V1 only → likely normal
│
├── Pain-free + biphasic/deep TWI V2-V3 + no Q waves → WELLENS (urgent cath)
│
├── Chest pain + dyspnea + S1Q3T3 + tachycardia → PE (CT-PA)
│
├── Young patient + epsilon waves + LBBB VT → ARVC (echo, cardiac MRI)
│
├── Wide QRS + slurred S in V6 → RBBB (secondary change, not ischemic)
│
├── Neuro event + deep wide T waves → Cerebral T waves (CT head)
│
└── Troponin rise + symptoms → NSTEMI / ACS (risk stratify, cath)
| Cause | Symmetry | Depth | Associated findings |
|---|---|---|---|
| Wellens A | Deep, symmetric | >2 mm | No Q waves, minimal ST change |
| Wellens B | Biphasic | Variable | No Q waves |
| PE/RV strain | Variable | Variable | S1Q3T3, tachycardia, RBBB |
| ARVC | Symmetric | Variable | Epsilon waves, LBBB VT |
| RBBB | Asymmetric (secondary) | Shallow | Wide QRS, slurred S in V6 |
| Cerebral T waves | Deep, wide | Very deep | Neurological symptoms, QT prolongation |
| Juvenile pattern | Symmetric | Shallow | Asymptomatic, young female |