Recognition of catechol- aminergic polymorphic ventricular tachycardia as the cause for exertional symptoms should prompt aggressive therapy to prevent the sig- nificant risk of SCD. Therapy for catechol- aminergic polymorphic ventricular tachycardia is not guided by genotype status, but screen- ing of first-degree relatives may be facilitated with genetic testing.S7.9.1.2-20 Ryanodine recep- tor mutations have been reported in 47% of probands, which were de novo mutations Ryanodine genotype status has not correlated with disease severity or response to medications.S7.9.1.2-7 In very young patients presenting with idiopathic VF, muta- tions in calmodulin have been identified and are associated with high lethality.S7.9.1.2-21 S7.9.1.2-24 Studies of proposed pathogenic mutations in catecholaminergic polymorphic ventricular tachycardia genes report up to 15% of variants were present in exome databases of the general population, raising questions as to the mono- genic cause of catecholaminergic polymorphic CLINICAL STATEMENTS AND GUIDELINES 7.9.1.3. Brugada Syndrome Recommendations for Brugada Syndrome References that support the recommendations are summarized in Online Data Supplement 42 and Systematic Review Report. 