brugada syndrome ( bs ) was first described in 1992 as a new autosomal dominantly inherited channelopathy caused by a defective gene located on chromosome 3 in a structurally normal heart .
it is characterized by st - segment elevation in the right precordial leads and increases susceptibility to ventricular tachyarrhythmias .
importantly , fluctuations in ecg patterns seem to be common among bs patients . for instance , vagotonic agents , -adrenergic agonists , fever and bradycardia are some of the conditions that may reveal the abnormality on a surface ecg .
subarachonoid hemorrhage results in repolarisation abnormalities and changes in autonomic nervous system activity . in this report , we present the case of a patient with subarachonoid hemorrhage who was admitted to the emergency department after suffering an out - of - hospital cardiac arrest with typical st - segment elevation and an ecg pattern characteristic of bs .
a 48-year - old man with no past medical history was presented to our emergency department after collapsing suddenly while shopping .
a store employee trained in basic life support was the first to assist the patient and started to cardiopulmonary resuscitation ( cpr ) .
upon arrival to the local emergency medical service , the paramedics commenced ventricular fibrillation ( vf ) and an automated external defibrillator was used to defibrillate the patient .
after two separate defibrillations and 5  min of cpr the patient regained spontaneous circulation , but remained unconscious .
he was flaccid , non - febrile and comatose ( glasgow coma scale of 4 ) , with a heart rate of 75  bpm and blood pressure of 110/75  mmhg .
meanwhile , vf was performed several times and the patient was defibrillated successfully to a normal sinus rhythm .
electrocardiography revealed bizarre coved - type st - segment elevation in leads v1 through v3 , with t wave inversion consistent with the type 1 brugada pattern ( fig .  1 ) and reciprocal st depression in inferior and lateral leads .
emergent cardiac catheterization was performed , which revealed no stenosis or flow abnormalities in his coronary arteries .
after contrast injection into those coronary arteries , st - segment elevation was resolved and did not recur ( fig .  2 ) .
laboratory tests , including cardiac biomarkers and coagulation studies , produced results that were within normal reference limits . since the patient was not responding , a non - contrasted brain computed tomography scan was performed and revealed a diffuse subarachnoid hemorrhage .
he was admitted to the intensive care unit and determined to be brain dead after further neurological testing .
brugada syndrome is characterized by st - segment elevation in the right precordial ecg leads , specifically v1-v3 , and a high incidence of sudden death due to ventricular tachyarrhythmias in patients with structurally normal hearts .
the syndrome is generally thought to be responsible for 412% of all sudden deaths and at least 20% of deaths in patients with structurally normal hearts ; the most common presentation is syncope .
the syndrome is inherited and auotosomally dominant , and in 25% of the cases the responsible mutation is found on the cardiac sodium transport gene ( scn5a ) , located on chromosome 3 . because the ecgs of patients with brugada syndrome are complex and often conceal the condition , it is difficult to estimate the true incidence of the disease in the general population .
however , three types of repolarisation patterns in the right precordial leads are currently recognized .
type 1 is diagnostic of bs and is characterized by a coved st - segment elevation 2 mm ( 0.2mv ) , followed by a negative t wave .
type 2 has a saddleback appearance with a high take - off st - segment elevation of 2 mm , followed by a trough displaying 1 mm st - segment elevation and either a positive or biphasic t wave .
type 3 has either a saddleback or coved appearance with an st - segment elevation of < 1 mm .
sodium - channel blockers , vagotonic agents , -adrenergic agonists , -adrenergic blockers , tricyclic antidepressants , glucose - induced insulin secretion , fever , bradycardia , ischemia , hypothermia , hyperkalemia , hypokalemia , hypercalcemia , alcohol and cocaine can expose or induce these ecg patterns .
additionally , st - segment elevation in the brugada patients is significantly influenced by heart rate and autonomic tone .
the ventricular myocardium is composed of at least three electrophysiologically distinct cell types : epicardial , endocardial and m cells .
the st - segment elevation and t wave inversions seen in the right precordial leads of those with bs are thought to be due to an alteration in the action potential of the epicardial and possibly the m cells , but not the endocardial cells .
the resulting dispersion of repolarisation across the ventricular wall , which is most pronounced in the right ventricle , results in a transmural voltage gradient that is manifested in the electrocardiogram as st - segment elevation .
this dispersion of repolarisation facilitates the development of phase 2 reentry , which generates a phase 2 reentrant extrasystole that takes advantage of the window of opportunity to precipitate the ventricular tachycardia and/or fibrillation that often results in sudden cardiac death .
a bs diagnosis is confirmed when a type 1 st - segment elevation is observed in more than one right precordial lead ( v1-v3 ) , in the presence or absence of a sodium channel block , and in conjunction with one of the following : documented ventricular fibrillation , self - terminating polymorphic ventricular tachycardia , a family history of scd ( < 45years ) , coved type ecgs in family members , inducibility of vt with programmed electrical stimulation , syncope or nocturnal agonal respiration .
cardiac arrhythmias or repolarisation abnormalities occur after a stroke in approximately 6070% of patients and may have important prognostic implications . in one report ,
investigated the circulatory collapse mechanisms in patients who experienced out - of - hospital cardiac arrest ( ohca ) due to subarachnoid hemorrhage .
pulseless electrical activity and asystole were common among study patients , but no ventricular fibrillation was observed .
found that the return of spontaneous circulation rate was higher than other etiologies of ohca , but long - term survival was poor .
a rate of vf similar to the initial cardiac rhythm was observed in a study by inamasu et  al .
researchers concluded that the prognosis was more favourable if the initial rhythm causing circulatory collapse was vf , but not brainstem damage . in another study ,
brouwers et  al . demonstrated that ecg changes were most prominent 2472 hours after subarachnoid hemorrhage .
specifically , this event leads to repolarisation and several electrocardiographic abnormalities , including qt segment prolongation , aberrant q waves , non - specific st - segment changes , t wave abnormalities and the appearance of u waves .
evidence of subendocardial infarction or anterolateral ischemia is common after a stroke , especially after subarachnoid hemorrhage .
myocardial injury during a stroke is most likely the result of a centrally mediated release of catecholamines , due to hypoperfusion of the posterior hypothalamus .
transient coronary vasospasm secondary to increased sympathetic tone during a stroke has also been described .
the depression of ica and activation of ik - atp during ischemia associated with vasospasm involving right ventricular outflow tract results in st - segment elevation similar to that observed in cases of bs . in our patient , subarachnoid hemorrhage created a transmural voltage gradient due to its effect on repolarisation or increased -adrenergic activity and resulted in a bs - like ecg pattern .
subarachnoid hemorrhage may be one of the factors predisposing the patient to the electrocardiographic and arrhythmic manifestations of bs . to conclude ,
when a patient without known structural heart disease presents with ventricular tachyarrhythmia and bs - like st - segment elevation , subarachnoid hemorrhage should be kept in mind , since its prompt and accurate treatment could be life saving .
 brugada syndrome is an autosomal dominantly inherited channelopathy estimated to be responsible for 412% of all sudden deaths , particularly among middle - aged men . 
 it is characterized by st - segment elevation in the right precordial leads , in the absence of acute coronary syndrome . 
 this report discuses a patient with subarachonoid hemorrhage who developed the characteristic electrocardiographic features of brugada syndrome . 
Introduction
Case report
Discussion
Conflict of interest