BrS is an autosomal dominant genetic channelopathy that is associated with sudden cardiac death (SCD) secondary to ventricular tachyarrhythmia in the setting of a structurally normal heart [1–3]. It is inherited in an autosomal dominant pattern with variable penetrance with male predominance [4, 5]. The gene most associated with BrS is SCN5A which encodes for a cardiac sodium channel [5]. Mutations in this channel lead to unopposed potassium current in the RV epicardium through the I_to potassium channel. BrS is characterized by characteristic appearance on the ST segment and T wave in the anterior precordial leads [5, 6]. BrS is subclassified into three types depending on phenotypic appearance on the EKG (Table 1). Type 1 is referred to as the coved pattern, Type 2 is referred to as the saddle-back pattern, while Type 3 is a combination of both Types 1 and 2 without satisfying the criteria for either Type 1 or 2 [2–4, 7].

BrS ECG alterations can be dynamic, i.e., characteristic ECG patterns are absent at baseline but are “unmasked” due to derangements in homeostasis such as pyrexia and electrolyte abnormalities. Similar to BrS, BrP is also considered multifactorial [8, 9]. Patients with BrS are usually asymptomatic until they present with syncope or SCD [5]. Ventricular arrhythmia associated with BrS tends to occur nocturnally, in the setting of pyrexia particularly with children, or at rest especially after a large meal [3]. Adults usually succumb to either polymorphic VT or VF while the predominant arrhythmia in children is monomorphic VT. There is no medication that is indicated for management of BrS; rather individuals that receive a diagnosis of BrS require implantation ICD to prevent SCD.

BrP on the other hand is described as a selection of clinical disorders that demonstrate classic BrS ECG phenotypical appearance but lack the propensity to cause ventricular tachyarrhythmia and sudden death [2, 4, 10]. These disorders are classified by their etiological category which include metabolic imbalance, mechanical compression, ECG modulation, myocardial or pericardial disease, ischemia or pulmonary embolism, and miscellaneous causes.

It is important to properly identify unmasked BrS vs. BrP in patient who develops characteristic Brugada ECG pattern. The International Registry of Brugada Phenocopies have proposed an algorithm which allows for appropriate diagnosis of BrP (Figure 3) [11]. Of most importance in the algorithm is the provocation/challenge test with sodium channel blockers [1, 5]. These medications act by blocking predominantly sodium currents thus increasing the already-present ionic imbalance. This test should only be performed in a setting where continuous ECG monitoring is available and in the presence of health care providers who can provide management in the setting of an emergency. A positive result is connoted by the depiction of Brugada pattern [3]. The inability to demonstrate Brugada pattern constitutes a negative result and a diagnosis of BrP. The appearance of QRS widening, occurrence of frequent PVCs, or complex ventricular arrhythmias should lead to the cessation of the challenge. Isoprenaline infusion may be utilized to counteract the development of ventricular arrhythmias [3].

Once diagnosed, BrP is classified in the same vein as BrS, i.e., depending on the phenotypic appearance on ECG. A further subclassification is designated to BrP depending on the criteria met in the aforementioned algorithm. Class A represents cases in which all criteria were met, class B includes cases in which not all criteria are met but BrP is highly suspected, and class C are cases with unjustified provocative testing [1, 12]. The utilization of the algorithm is most important as it has been demonstrated that an experienced cardiologist cannot discern between BrP and BrS by ECG alone [1, 12, 13].

Our patient presented to the ED after drug overdose. It is unclear what he may have consumed as he was not forthcoming with details surrounding the events before his loss of consciousness. His toxicology screen demonstrated the presence of synthetic cannabinoids despite the fact he reported use of heroin multiple times in the past.

Drugs of abuse such as cannabinoids, heroin, and cocaine have been associated with BrP [14]. Changes in the ECG secondary to heroin such as QTc prolongation, torsades de pointes, and bradyarrhythmia are also well documented [15]. Ramsaroop et al. described a patient who required Naloxone to be resuscitated with positive toxicology screen for alcohol and opiates [15]. Ghovanloo et al. demonstrated that cannabinoids have a potential inhibitory effect on sodium channels under certain circumstances [16]. However, synthetic cannabinoids effect on sodium channels is not described in literature; also, our review of literature failed to demonstrate any reports or cases of synthetic cannabinoids leading to unmasked BrS or BrP.

The patient's EKG demonstrated Type 1 Brugada pattern which spontaneously resolved after several hours. Our patient also reported several episodes of loss of consciousness in the past. He was unclear what the etiology of his syncope was, but he believed it to be secondary to drug abuse although he was uncertain. As a result, we had to entertain the idea of a diagnosis of unmasked BrS vs. BrP. We proceeded with sodium channel provocation/challenge test. Procainamide was chosen as the challenge drug due to availability. Once it was ensured that all affairs were in order, we proceeded with the test. There was no QT prolongation, ventricular arrhythmia, PVC, or development of Type 1 Brugada pattern. The patient remained asymptomatic throughout the entirety of the examination.