Brugada syndrome (BrS) is a genetic disorder in which the electrical activity of the heart is abnormal due to channelopathy.

[2] It was first described by Andrea Nava and Bortolo Martini, in Padova, in 1989;[11] it is named after Pedro and Josep Brugada, two Spanish cardiologists, who described the condition in 1992.

However, blackouts can occur in those with Brugada syndrome despite a normal heart rhythm, because of a sudden drop in blood pressure, known as vasovagal syncope.

Sodium-channel-blocking medications, commonly used to treat cardiac arrhythmia, may also worsen the tendency to abnormal heart rhythms in patients with Brugada syndrome and should be avoided.

[5] Over 290 mutations in the SCN5A gene have been discovered to date, each altering sodium channel function in subtly different ways.

[32] Some argue that the main reason these arrhythmias arise is due to abnormally slow electrical conduction in areas of the heart, specifically the right ventricle.

The sodium current is a major contributor to the characteristic flow of electrical charge across the membrane of heart muscle cells that occurs with each heartbeat known as the action potential.

INa causes the initial rapid upstroke of the action potential (phase 0), and decreasing the early peak current, as occurs in BrS-associated genetic variants, leads to slowing of the electrical conduction through the heart muscle.

Given the right circumstances, this wavebreak can allow the waves of electricity to perform a U-turn within the muscle, travelling in the reverse direction before beginning to rapidly circle around a point, referred to as re-entry, and causing an abnormal heart rhythm.

[8] Those who support this view (known as the depolarisation hypothesis) argue that conduction slowing may explain why arrhythmias in those with Brugada syndrome tend to occur in middle age, when other factors such as scarring or fibrosis that accompany old age have exacerbated the tendency to conduction slowing caused by the genetic mutation.

[32] Others suggest that the main cause of arrhythmias is a difference in the electrical properties between the inside (endocardium) and outside (epicardium) of the heart (known as the repolarisation hypothesis).

The action potential in cells from the epicardium shows a prominent notch after the initial spike due to a transient outward current.

Once again, this wavebreak can allow the waves of electricity which usually travel in only one direction to instead begin circling around a point as a re-entrant circuit, causing an arrhythmia.

[14] The pattern seen on the ECG includes ST elevation in leads V1-V3 with a right bundle branch block (RBBB) appearance.

These patterns may be present all the time, but may appear only in response to particular drugs (see below), when the person has a fever, during exercise, or as a result of other triggers.

[9] Some medications, particularly antiarrhythmic drugs that block the cardiac sodium current INa, can reveal a Type 1 Brugada pattern in susceptible people.

[5] This means that carrying a genetic mutation associated with Brugada syndrome does not necessarily imply that a person is truly affected by the condition.

[5] Ambulatory ECG monitoring, including implantation of a loop recorder, is sometimes used to assess whether dizziness or faints in a person with Brugada syndrome are due to abnormal heart rhythms or other causes such as vasovagal syncope.

[41][42] In people felt to be at higher risk of sudden cardiac death, an implantable cardioverter-defibrillator (ICD) may be recommended.

[43] An ICD can also function as a pacemaker, preventing abnormally slow heart rates that can also occur in people with Brugada syndrome.

Implanting an ICD is a relatively low-risk procedure and is frequently performed as a day case under local anaesthetic.

[9] Quinidine is an antiarrhythmic drug that may reduce the chance of serious abnormal heart rhythms occurring in some people with Brugada syndrome.

[9] Isoprenaline, a drug that has similarities with adrenaline, can be used in an emergency for people with Brugada syndrome who are having frequent repeated life-threatening arrhythmias, known as an "electrical storm".

The tip of one of these wires is used to make a series of tiny burns, intentionally damaging the area of abnormal heart muscle that has been causing the problem.

Local names vary – in the Philippines the condition has been known as Bangungut meaning "a scream followed by sudden death during sleep",[48] while in Thailand it was known as Lai Tai, and in Japan Pokkuri.

[52] Research into Brugada syndrome is ongoing, identifying new genetic variants, exploring mechanisms of arrhythmias, and searching for better treatments.