| Literature DB >> 33801474 |
Nicolò Martini1, Martina Testolina2, Gian Luca Toffanin2, Rocco Arancio3, Luca De Mattia4, Sergio Cannas2, Giovanni Morani2, Bortolo Martini2.
Abstract
The so-called Brugada syndrome (BS), first called precordial early repolarization syndrome (PERS), is characterized by the association of a fascinating electrocardiographic pattern, namely an aspect resembling right bundle branch block with a coved and sometime upsloping ST segment elevation in the precordial leads, and major ventricular arrhythmic events that could rarely lead to sudden death. Its electrogenesis has been related to a conduction delay mostly, but not only, located on the right ventricular outflow tract (RVOT), probably due to a progressive fibrosis of the conduction system. Many tests have been proposed to identify people at risk of sudden death and, among all, ajmaline challenge, thanks to its ability to enhance latent conduction defects, became so popular, even if its role is still controversial as it is neither specific nor sensitive enough to guide further invasive investigations and managements. Interestingly, a type 1 pattern has also been induced in many other cardiac diseases or systemic diseases with a cardiac involvement, such as long QT syndrome (LQTS), arrhythmogenic right ventricular cardiomyopathy (ARVC), hypertrophic cardiomyopathy (HCM) and myotonic dystrophy, without any clear arrhythmic risk profile. Evidence-based studies clearly showed that a positive ajmaline test does not provide any additional information on the risk stratification for major ventricular arrhythmic events on asymptomatic individuals with a non-diagnostic Brugada ECG pattern.Entities:
Keywords: Brugada syndrome; ajmaline challenge; arrhythmogenic right ventricular cardiomyopathy; early repolarization syndrome; hypertrophic cardiomyopathy; long QT syndrome
Year: 2021 PMID: 33801474 PMCID: PMC7958847 DOI: 10.3390/jcm10051025
Source DB: PubMed Journal: J Clin Med ISSN: 2077-0383 Impact factor: 4.241