ECG criteria
- Leads V1–V2 (sometimes involving V3); when searching for a concealed pattern, high positions in the 2nd–4th intercostal spaces with mandatory labeling of electrode placement
- As part of the complete saddleback morphology, the initial high r' wave (pseudo-RBBB) and/or J-point elevation must be ≥2 mm; a single high r' or a single J-point elevation is insufficient
- Saddleback ST shape with a minimum ST-segment level of at least 1 mm above the isoelectric line (values less than 1 mm do not meet type 2 criteria)
- Subsequent ST elevation transitioning into a positive or biphasic T wave
- The overall shape of the complex resembles the letter "M" or a saddle, unlike the coved convex elevation in type 1
- The QRS may have an RBBB-like morphology; QRS widening and true RBBB are evaluated separately and are not mandatory criteria for type 2
- The pattern can be unstable—disappearing and reappearing on repeat recordings with changes in body temperature, heart rate, or autonomic tone
What it looks like on ECG
In leads V1–V2 (less commonly V3), the QRS complex has the appearance of a incomplete right bundle branch block: a high r' and/or J-point elevation ≥2 mm, after which the ST segment does not descend monotonically, but forms a saddleback trough. The minimum level of the ST segment remains at least 1 mm above the isoelectric line, after which the ST segment rises again to a positive or biphasic T wave.
This fundamentally distinguishes type 2 from type 1, where a high J-point elevation is immediately followed by a smoothly descending, coved ST segment with a negative T wave and no intermediate elevation. If ST <1 mm, type 2 criteria are not met; such a shape may be described as historical type 3 (both coved and saddleback morphologies are possible), but by itself it does not diagnose Brugada syndrome and is not considered a separate standalone variant.
| Sign | Type 1 (coved) | Type 2 (saddleback) |
|---|---|---|
| ST shape | convex, monotonically decreasing | saddleback, M-shaped |
| J-point / r' elevation | ≥2 mm | ≥2 mm |
| ST minimum | not applicable — ST decreases without a trough | ≥1 mm above the isoelectric line |
| T wave | negative | positive / biphasic |
| Diagnostic utility | diagnostic ECG pattern when recorded correctly and phenocopies are excluded | suspicious, non-diagnostic, requires confirmation with type 1 |
The pattern is better detected when recording V1–V2 one to two intercostal spaces higher than the standard position (usually the 2nd and 3rd intercostal spaces), which increases the sensitivity for detecting concealed forms.
Mechanism
Depolarization and/or repolarization abnormalities in the right ventricular outflow tract are postulated due to sodium channel dysfunction (SCN5A gene and others) or other ion currents; the specific mechanism remains debated. One model explains the pattern by a transmural voltage gradient due to shortening of the epicardial action potential relative to the endocardium, while another attributes it to conduction slowing and abnormal activation in the right ventricular outflow tract. In type 2, the changes are less pronounced or transient, so the ST shape does not reach the marked convex elevation seen in type 1, but rather fluctuates, forming a saddleback configuration. The pattern is sensitive to modulators such as increased vagal tone, fever, sodium channel blockers, and electrolyte shifts.
Causes
- The syndrome has a genetic basis in a subset of patients; the SCN5A gene is the best known, but a pathogenic variant is not identified in everyone. A negative genetic test does not exclude the syndrome; inheritance in familial forms is usually autosomal dominant with incomplete penetrance
- Fever is a unmasking/triggering factor that can reveal a concealed pattern
- Administration of sodium channel-blocking drugs (certain class IA/IC antiarrhythmics, some tricyclic antidepressants, occasionally psychotropic agents) is an unmasking/triggering factor, not a phenocopy; standardized provocation testing is based on this principle and is performed only in specialized settings
- Severe electrolyte disturbances (hyperkalemia, hypercalcemia)
- Autonomic imbalance with parasympathetic predominance
- Structural abnormalities of the right ventricle and outflow tract, mechanical compression, and other reversible causes (phenocopies of the Brugada pattern without primary channelopathy)
- In some patients, a clear cause or mutation is not found, which does not rule out the syndrome
Differential diagnosis
- Brugada type 1 pattern — coved ST elevation ≥2 mm with a negative T wave, diagnostically significant when recorded correctly and phenocopies are excluded
- Incomplete right bundle branch block — a similar r' in V1, but without saddleback ST elevation with a minimum ≥1 mm; the T wave is usually positive without provocation
- Early repolarization syndrome — J-point elevation is more common in the inferior and lateral leads, rather than isolated to V1–V2
- Athlete's ECG with a high r' variant in the right precordial leads — lacks the characteristic saddleback shape with a J-point/r' elevation ≥2 mm and an ST minimum ≥1 mm
- Normal variant of ST-segment morphology in healthy individuals, especially young men — repeated recording and pharmacological provocation testing help differentiate this
Clinical significance and management
The type 2 pattern is a suspicious, non-diagnostic finding. Type 1, spontaneous or induced by a sodium channel blocker, is a diagnostically significant ECG sign; the diagnosis of Brugada syndrome is established taking into account clinical data, family history, and the exclusion of phenocopies, without automatically labeling an asymptomatic patient with an isolated drug-induced type 1 as sick. Type 2 alone does not establish a diagnosis of Brugada syndrome.
The physician should:
- Repeat the ECG, including with electrodes in high positions (2nd–4th intercostal spaces)
- Take a history: unexplained syncope, cases of sudden cardiac death at a young age in relatives, association of symptoms with fever or specific medications
- Exclude phenocopies and reversible causes (e.g., severe electrolyte disturbances, ischemia, mechanical compression, etc.); separately evaluate fever and sodium channel-blocking drugs as potential unmasking/triggering factors rather than phenocopies
- If suspicion persists, especially in the presence of symptoms or a family history, consider a pharmacological provocation test with a sodium channel blocker, performed only in a specialized unit according to protocol, taking into account contraindications, with continuous monitoring and resuscitation readiness — a positive test reveals an induced type 1, and its diagnostic significance is evaluated along with clinical presentation, family history, and exclusion of phenocopies
- Use the Shanghai Brugada score as an auxiliary tool combining ECG data, clinical presentation, family history, and genetics for a structured assessment of the probability of diagnosis after excluding phenocopies
- In the absence of symptoms and family history, a type 2 pattern without type 1 confirmation is treated as an isolated ECG finding requiring monitoring rather than immediate invasive measures
Common interpretation errors
- Confusing type 2 with type 1 and diagnosing Brugada syndrome based solely on ST morphology without type 1 confirmation
- Failing to record the ECG in high precordial electrode positions, causing the pattern to be missed
- Mistaking incomplete right bundle branch block for the Brugada pattern and vice versa
- Automatically considering fever or drug intake as a phenocopy without distinguishing between an unmasking factor and a true phenocopy
- Drawing conclusions from a single recording without dynamic follow-up and without evaluating family history
1. Which feature distinguishes the Brugada type 2 pattern from type 1?
A saddleback shape with an ST minimum ≥1 mm and a positive or biphasic T wave is the key difference between type 2 and the convex coved type 1.
2. In which leads is the type 2 Brugada pattern sought?
The pattern is localized to the right precordial leads; sensitivity is increased by recording in the 2nd–4th intercostal spaces.
3. Can Brugada syndrome be diagnosed based solely on the type 2 pattern without additional data?
The type 2 pattern by itself is non-diagnostic — confirmation by spontaneous or induced type 1, exclusion of phenocopies, and a comprehensive clinical assessment are required.
Frequently asked questions
Is the Brugada type 2 pattern dangerous?
By itself, it does not equal a diagnosis of Brugada syndrome and does not prove a high risk of sudden cardiac death. The danger is determined by the clinical context — syncope, a family history of sudden death, and the result of a provocative test.
How to distinguish Brugada type 1 pattern from type 2?
Type 1 is a coved, monotonically descending ST elevation with a negative T wave in V1–V2, with a J-point/ST elevation of ≥2 mm. Type 2 has a saddleback configuration with an r'/J-point elevation of ≥2 mm, an ST-segment trough of at least 1 mm, and positive or biphasic T waves.
Is a provocative test necessary for a type 2 pattern?
The decision is made following a clinical evaluation: tracing quality, potential unmasking factors and phenocopies, symptoms, and family history. If suspicion persists, particularly in cases of syncope or a positive family history, a sodium channel blocker challenge may be indicated, which is performed exclusively in a specialized unit with monitoring and resuscitation readiness available.
Can the type 2 pattern disappear on repeat ECGs?
Yes, this is typical for a channelopathy — the ST-segment morphology is variable and depends on body temperature, autonomic tone, certain medications, and electrode placement.
Can Brugada syndrome be diagnosed based solely on the type 2 pattern?
No, the type 2 pattern is not diagnostic on its own. Specialized evaluation is required: searching for spontaneous or induced type 1, ruling out phenocopies, and taking clinical and family history into account. The Shanghai score is an auxiliary tool to structure this assessment, not an alternative to type 1.
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Related terms
More in the «Channelopathies and Cardiomyopathies» section
Sources
- Surawicz B., Knilans T. Chou's Electrocardiography in Clinical Practice
- Hampton J. The ECG in Practice
- AHA/ACCF/HRS Recommendations for the Standardization and Interpretation of the Electrocardiogram, 2009
- Orlov V.N. Guide to Electrocardiography
Educational material for medical students and physicians. Does not replace clinical guidelines and physical examination; the ECG must always be interpreted in conjunction with the clinical picture.