Multifactorial Brugada Phenocopy

Abstract

Multifactorial Brugada PhenocopyTo the Editor We read with interest the article by Heckle et al 1 recently published in the Challenges in Clinical Electrocardiography section of JAMA Internal Medicine. The authors addressed the case of a woman in her 50s who presented with altered mental status and respiratory distress requiring intubation in the field. An electrocardiogram (ECG) was recorded on presentation, which was interpreted by the authors as a normal sinus rhythm with a right bundle branch pattern and loss of P-wave amplitude in the precordial leads. It was pointed out that the most profound ECG abnormality was the greater than 5-mm coved-type ST-segment elevation in leads V 1 to V 2 with the presence of Q waves. After decreasing the potassium level, the ECG no longer presented segment elevation in leads V 1 to V 2 .The authors attributed the ST-segment changes to hyperkalemia in the setting of rhabdomyolysis, acute renal failure, acidosis, and angiotensin-converting enzyme inhibitor use. In our opinion, the ECG showed in leads V 1 to V 2 a typical Brugada type-1 pattern with 2 mm or more coved ST-segment elevation followed by a negative T-wave. Considering this, it would have been desirable to perform, once hyperkalemia resolved, a provocative challenge with a sodium channel blocker. If negative, the diagnosis to consider is Brugada phenocopy. 2 Brugada phenocopies are clinical entities with identical electrocardiographic patterns as true congenital Brugada syndrome, but caused by various clinical circumstances. There are several factors that we would like to discuss and that could have played an important role in the development of this pattern.Hyperkalemia, among others, has been identified as a metabolic condition that can reproduce the BS pattern by decreasing the resting membrane potential, which determines an inactivation of the sodium channels. This produces an imbalance between the entrance of sodium to the cell and the exit of potassium with predominance of the latter which is more pronounced in the right ventricle and more active in the epicardial cells than in the endocardium and in the M cells. 3 Another factor that was not taken into account by the authors was the intake of amitriptyline. This tricyclic antidepressant can reproduce the Brugada ECG pattern both in clinical practice and in experimental models. 4 On the other hand, it is well known that cocaine blocks the sodium channels and therefore could have some role in unmasking true Brugada syndrome.

An unusual ECG change after a car crash

“…The presentation and transient dynamic changes of ECGs in our case were compatible with the type 1 Brugada phenocopy (BrP), which are clinical entities that refer to ECG patterns identical to ECG presentations observed in Brugada syndrome ( de Oliveira Neto et al, 2019 ) . However, they may have different etiologies, such as metabolic conditions, mechanical compression, myocardial ischemia, pulmonary embolism, myocardial or pericardial disease, antiarrhythmic drug application, and others ( Baranchuk et al, 2012 ; Zhang et al., 2017 ; Sreenivasan et al, 2018 ; Gottschalk et al., 2016 ) . The potential reason for the BrP in our case may be associated with chest blunt trauma.…”

Brugada Phenocopy Type 1 Secondary to Synthetic Cannabinoids

“…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].…”