Correction of residual hemodynamic/structural abnormalities contributing to VT may improve ventricular function and reduce symptoms, but Recommendations for Adult Congenital Heart Disease (Continued) COR LOE Recommendations CLINICAL STATEMENTS AND GUIDELINES it may inadequately prevent the risk of subse- quent VT or SCA. The use of ICDs in adult con- genital heart disease patients for secondary prevention accounts for approximately 50% of implantations presently, at a mean age of 36 to Patientswithadultcongenital heart disease experience appropriate shock rates of 3% to 6% per year, with equivalent or slightly increased frequency of appropriate shocks for sec- ondary prevention indications.S10.8-14,S10.8-15,S10.8-17 Table 11. Congenital Heart Disease: Risk Factors for VA/SCD Congenital Heart Disease Incidence of VA Incidence of SCD Higher Risk Characteristics Simple complexity RV dilatation Pulmonary hypertension Moderate complexity Tetralogy of FallotS10.8-1,S10.8-2,S10.8-5,S10.8-6,S10.8 28,S10.8 34,S10.8 36,S10.8 Frequent or complex VA Sustained VT QRS duration 180 ms Inducible sustained VT Atrial tachycardia Decreased LVEF Dilated right ventricle Severe PR Severe PS Aortic stenosis S10.8 27,S10.8 44,S10.8 56 Severe LV hypertrophy Aortic stenosis mean pressure gradient >40 mmHg Ventricular dysfunction Coarctation of aortaS10.8 28,S10.8 29, 2% 2% Aneurysm at repair site Aortic stenosis Systemic hypertension Premature coronary artery disease Atrial fibrillation Wide complex tachycardia Mitral regurgitation Dilated RVOT Severe complexity Transposition of the great arteriesS10.8 27,S10.8 44 S10.8 48,S10.8 Atrial switch Atrial switch 2% 3% 9.5% Mustard repair Arterial switch 2% 1% Prior VSD closure cc-TGA 10% 17% 25% Unexplained syncope Atrial tachycardia Coronary orifice stenosis Systemic ventricular dysfunction Severe tricuspid regurgitation 10% 4% Multiple surgical repairs Coronary anomalies Ventricular dysfunction and/or hypertrophy Fontan repair for univentricular physiology*S10.8 27,S10.8 37, Longer duration of follow-up Ascites Protein-losing enteropathy *Univentricular physiology includes: Tricuspid atresia, Double inlet left ventricle, Mitral atresia, Hypoplastic left heart, Unbalanced AV septal defect. 