ECG criteria
- J-point elevation ≥ 2 mm (0.2 mV) in at least one of leads V1 or V2
- ST-segment shape is coved: a descending convex curve resembling a dome
- Smooth transition of the ST elevation directly into a negative T wave without returning to the isoelectric line
- The sign is evaluated in V1 and/or V2 in the standard position (4th intercostal space); if a concealed pattern is suspected, electrodes are additionally placed in the 2nd and 3rd intercostal spaces
- The pattern may be spontaneous or induced by a provocative test with a sodium channel blocker
- Type 1, spontaneous or drug-induced, after excluding phenocopies, is diagnostic for Brugada syndrome; clinical criteria (history of VT/VF, arrhythmogenic syncope, family history, nocturnal agonal respiration) are used for risk stratification and management selection, rather than as mandatory prerequisites for the diagnosis itself
What it looks like on ECG
The primary sign is elevation of the J point and ST segment in leads V1 and/or V2 (in standard or high positions) with a characteristic coved shape: the ST segment rises, peaks immediately after the QRS complex, then smoothly descends and transitions into a negative T wave without returning to the isoelectric line between ST and T. Changes limited exclusively to V3 are not part of the current major diagnostic criteria.
| Element | Type 1 pattern |
|---|---|
| J point | elevation ≥ 2 mm |
| ST shape | coved, convex upward |
| ST→T transition | continuous, without isoelectric line |
| T wave | negative in one or both leads V1–V2 |
| QRS | may be somewhat wider in V1 (pseudo-rSR') |
The negative T wave immediately follows the coved ST elevation in the same lead — it does not have to be negative simultaneously in both V1 and V2. Lead V1 often shows a pseudo-r' before the descending limb of ST, which can mimic incomplete right bundle branch block; pseudo-rSR′ and ST-T changes may resemble RBBB, but differentiation is not based on a single sign — QRS morphology in Brugada is variable, and both conditions can coexist. The pattern may be intermittent: disappearing and reappearing on different recordings in the same patient, and worsening with fever, vagal stimulation, or certain medications. For verification in doubtful cases, leads V1–V2 are additionally placed one intercostal space higher (3rd and even 2nd), which increases the sensitivity for detecting coved elevation.
Mechanism
The underlying mechanism is cardiomyocyte sodium channel dysfunction (most commonly SCN5A gene mutations), leading to a reduction in inward sodium current. The pathophysiology is heterogeneous and debated within two main models. The repolarization model focuses on phase 2: reduced sodium current shortens the action potential of the right ventricular outflow tract epicardium, creating a transmural voltage gradient between the epicardium and endocardium that appears on the surface ECG as ST elevation; the potential difference between myocardial layers provides the substrate for phase 2 reentry — a mechanism capable of triggering polymorphic ventricular tachycardia and ventricular fibrillation. The depolarization model links the pattern to slowed and heterogeneous conduction in the right ventricular outflow tract and structural micro-inhomogeneity of this zone. Reduced sodium current is one of the mechanisms, but neither model alone fully explains the entire pattern.
Causes
- Genetically determined Brugada syndrome (mutations in SCN5A and other ion channel genes) is the basis of the disease
- Fever is a frequent factor unmasking a concealed pattern in a substrate carrier
- Administration of sodium channel blockers (class IA and IC antiarrhythmics), tricyclic antidepressants, and certain psychotropic drugs can unmask the true pattern in a syndrome carrier
- Excessive vagal tone, sleep periods (nocturnal episodes)
- Alcohol and cocaine abuse
- Phenocopies of Brugada syndrome: hyperkalemia, certain intoxications (e.g., tricyclic antidepressants), and structural right ventricular pathology (outflow tract compression) can mimic the pattern without a true genetic syndrome; when identified, the cause must be corrected and the ECG re-evaluated
Differential diagnosis
- Incomplete right bundle branch block — usually has S-wave slurring in leads I and V6, lacks true coved ST elevation, T wave is usually positive; the sign is not absolute, and QRS morphology in Brugada is variable
- Early repolarization syndrome — J-point elevation with a notch or slur at the end of QRS, ST segment is usually concave, T wave is positive, more commonly in lateral and inferior leads
- Brugada type 2 pattern — saddleback shape with J-point elevation ≥ 2 mm, ST elevation ≥ 1 mm, and positive or biphasic T wave; not diagnostic by itself and requires evaluation of type 1 inducibility
- Saddleback pattern with J-point elevation ≥ 2 mm and ST < 1 mm — is not diagnostic; historically termed type 3, no longer used as an independent type in modern criteria
- Acute anterior STEMI — ST elevation is usually convex, but accompanied by reciprocal changes, dynamic troponin changes, typical clinical presentation, and often involves V3–V6
- Phenocopies of Brugada syndrome — a similar pattern in hyperkalemia, tricyclic antidepressant overdose, right ventricular outflow tract compression (mediastinal tumor, pectus excavatum) — differ by their reversibility after correction of the cause
Clinical significance and management
Type 1 in leads V1–V2, spontaneous or induced by a sodium channel blocker, after excluding a phenocopy, establishes the diagnosis of Brugada syndrome; clinical data (documented VT/VF, arrhythmogenic syncope, family history of sudden death at a young age or Brugada syndrome, typical nocturnal agonal respiration) are used for risk assessment and management choice, rather than as mandatory diagnostic criteria. In asymptomatic spontaneous type 1 pattern, expert clinical risk assessment is performed, phenocopies are excluded, first-degree relatives are screened, and genetic testing is discussed; the decision for ICD implantation should not be made based on the Shanghai score alone — it is used as a diagnostic system, not a validated tool for sudden death risk stratification. In case of fever in a patient with known Brugada syndrome, active temperature normalization is required, as fever is a frequent trigger of life-threatening arrhythmias. ICD is recommended for secondary prevention after cardiac arrest due to VF or hemodynamically unstable sustained polymorphic VT, if a reversible cause is excluded; other cases of sustained ventricular arrhythmias require individual assessment considering hemodynamic tolerance and context. In spontaneous type 1 and syncope likely related to ventricular arrhythmia, ICD implantation is a recognized option to consider after evaluation by an arrhythmologist, as this is a recognized high-risk factor. Isolated asymptomatic spontaneous type 1 pattern without other risk factors is generally not an indication for ICD by itself. In all cases, drugs that enhance sodium channel blockade must be avoided (a list of contraindicated and conditionally contraindicated drugs is known and must be checked before prescribing any new agent).
Common interpretation errors
- Mistaking the saddleback type 2 pattern for diagnostic type 1 — confusing ST morphology
- Failing to account for pattern intermittency: a single normal ECG does not rule out Brugada syndrome
- Forgetting to record high V1–V2 positions when a concealed pattern is suspected
- Confusing pseudo-r' in V1 with complete right bundle branch block
- Failing to exclude phenocopies (hyperkalemia, intoxications, structural right ventricular pathology) before final interpretation, confusing them with triggers (fever, drugs) that unmask the true syndrome
"Coved" — ST looks like a dome (cove), dropping immediately into a negative T without an isoelectric pause.
1. Which feature is mandatory for the Brugada type 1 pattern?
This ECG corresponds to type 1; after excluding a phenocopy, it is a diagnostic sign of Brugada syndrome. Clinical data are primarily needed for risk assessment and management.
2. In which leads is the Brugada type 1 pattern sought?
The pattern reflects dysfunction of the right ventricular outflow tract, which is projected onto leads V1–V2.
3. Which of the following can unmask a concealed type 1 Brugada pattern?
Fever exacerbates sodium channel dysfunction and is a classic trigger for the appearance or enhancement of the type 1 pattern.
Frequently asked questions
How does the type 1 pattern differ from type 2?
In type 1, the ST segment is coved (convex), without returning to the baseline before the negative T wave. In type 2, the shape is saddleback with a J-point elevation of ≥2 mm, ST elevation of ≥1 mm, and a positive or biphasic T wave. Only type 1 is diagnostically significant without a provocative test; type 2 by itself is insufficient for diagnosis.
Is a single ECG sufficient to diagnose Brugada syndrome?
A spontaneous or drug-induced type 1 pattern, after exclusion of phenocopies, is diagnostic for Brugada syndrome on its own. Clinical data—VT/VF, syncope, family history—are needed to assess risk and guide management. The pattern can be transient, so a normal ECG on another day does not rule out the syndrome.
Is the type 1 Brugada pattern dangerous?
Yes, it is associated with the risk of polymorphic ventricular tachycardia and ventricular fibrillation, which can lead to sudden cardiac death, especially in the presence of fever or provoking drugs.
How does fever affect the Brugada pattern?
Fever is one of the most frequent factors unmasking or enhancing the type 1 pattern in a mutation carrier, and it acts as a trigger for life-threatening arrhythmias. Therefore, any fever in such a patient requires active management.
Is a provocative test necessary in the presence of a type 1 pattern?
No, when a spontaneous type 1 pattern is present, a provocative test with a sodium channel blocker is not required for diagnosis—it is used to unmask the pattern in patients with a type 2 pattern or suspicious clinical features without a spontaneous type 1 pattern.
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Related terms
More in the «Channelopathies and Cardiomyopathies» section
Sources
- Surawicz B., Knilans T. Chou's Electrocardiography in Clinical Practice, 6th ed.
- AHA/ACCF/HRS Recommendations for the Standardization and Interpretation of the Electrocardiogram, 2009
- Orlov V.N. Guide to Electrocardiography
- HRS/EHRA/APHRS Expert Consensus Statement on the Diagnosis and Management of Patients with Inherited Primary Arrhythmia Syndromes, 2013
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.