Inherited primary arrhythmia disorders: cardiac channelopathies and sports activity

Abstract

Sudden cardiac death (SCD) in an apparently healthy individual is a tragedy. It is important to identify the cause of death and to prevent SCD in potentially at-risk family members. Inherited primary arrhythmia disorders are associated with exercise-related SCD. Despite the well-known benefits of exercise, exercise restriction has been a historical mainstay of therapy for these conditions. However, since familiarity with inherited arrhythmia conditions has increased and patients are often children and young adults, it is necessary to reassess the treatment guidelines regarding exercise constraints. The aim of this review is to analyze the risk of exercise-induced SCD in patients with inherited cardiac conditions and explore the challenges faced when advising patients about exercise limitations. We searched for publications on cardiac channelopathies in PubMed with the following medical subject headings (MeSH): "long QT syndrome"; "short QT syndrome"; "Brugada syndrome"; and "catecholaminergic polymorphic ventricular tachycardia". The abstracts of these articles were scanned, and articles of relevance, along with pertinent references, were read in full. The analysis was restricted to reports published in English. The findings of this analysis suggest that exercise with low-to-moderate cardiovascular demand may be possible under regular clinical follow-up in inherited primary arrhythmia disorders. Recent data show that patients with inherited primary arrhythmia disorders are at low risk for events once a comprehensive treatment program has been established. Recreational activity is likely safe for these individuals, with personalized management based on individual patient preferences and priorities.

Muerte súbita por fibrilación ventricular en deportista. Una presentación inusual del Síndrome de Brugada. Caso Clínico

“…Si no se dispone de bloqueadores del canal de sodio, y hay sospecha electrocardiográfica de SBr, la realización de un test de esfuerzo (TE) permite evidenciar un pBr I, transitoriamente en el peak del ejercicio 15 , pero de preferencia en los primeros tres minutos de etapa de recuperación, por desbalance autonómico con predominio parasimpático vagal, hallazgo que constituiría un factor independiente de riesgo de FV, principalmente en paciente que se presenta asintomático o con síncope 9,[16][17][18] .…”

Reporte de muerte súbita en Mexico (1998-2014)

“…Officially, 22.8% of all SD cases occurred in individuals between 15 and 45 years of age, and this is a worrisome situation. Preventive measures must be established, especially in high-performance athletes or in those children and young people in whom "innocent" clinical data (dyspnea, palpitations, and/or syncope) are not taken into consideration until it is done retrospectively after the SD of these subjects 19 .…”

Arrhythmogenesis of Sports: Myth or Reality?

“…[ 8 ] Exercise-induced QT prolongation may confer an increased risk in individuals with underlying long QT syndrome (LQTS) because adrenergic surges and emotional stress may trigger arrhythmias in LQT1 and LQT2, respectively. [ 50 – 53 ] Moreover, exercise-induced prolongation of the QT interval may pose considerable challenges in differentiating physiological adaptation from congenital LQTS, and potentially offering false reassurance to athletes at risk. A recent study demonstrated an exercise-induced QT prolongation phenotype, mimicking congenital LQTS, which reverts back to normal after a period of detraining.…”