2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death

Authors, Journal, Affiliations, Type, DOI

• Chair: Sana M. Al-Khatib, MD, MHS; Vice Chair: William G. Stevenson, MD
• Writing committee: 19 members including Michael J. Ackerman, David J. Callans, Anne B. Curtis, Gregg C. Fonarow, Christopher B. Granger, Robert J. Myerburg
• Journal: Journal of the American College of Cardiology, 2018;72(14):e91–e220 (co-published in Circulation and HeartRhythm)
• Sponsoring organisations: American College of Cardiology (ACC), American Heart Association (AHA), Heart Rhythm Society (HRS); endorsed by Heart Failure Society of America (HFSA)
• Type: Clinical Practice Guideline (supersedes 2006 ACC/AHA/ESC VA/SCD guideline and 2008 ACCF/AHA/HRS device-based therapy guideline ICD indications)
• DOI: https://doi.org/10.1016/j.jacc.2017.10.054

Overview

The 2017 AHA/ACC/HRS Guideline for Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death is the definitive American guideline superseding the 2006 ACC/AHA/ESC document. It covers the full spectrum from PVCs through VF across all structural and electrical heart diseases. Core evidence from MADIT-I/II, SCD-HeFT, AVID, CIDS, DEFINITE, and COMPANION underpins ICD indications. The DANISH trial (2016) raised questions about NICM primary prevention ICD benefit but the guideline maintained Class I A based on pooled RCT data. An explicit economic value framework is introduced, classifying primary prevention ICD in ischemic HD as "high value" (<$50,000/QALY) versus secondary prevention as "intermediate value" ($64,000-100,000/QALY). Disease-specific algorithms cover ischemic HD, NICM, ARVC, HCM, cardiac sarcoidosis, channelopathies, neuromuscular disorders, athletes, pregnancy, valvular HD, and adult congenital HD.

Keywords

Ventricular tachycardia · Ventricular fibrillation · Sudden cardiac death · Implantable cardioverter-defibrillator · Catheter ablation · Premature ventricular complex · Beta-blockers · Amiodarone · Subcutaneous ICD · Wearable defibrillator · Hypertrophic cardiomyopathy · Arrhythmogenic right ventricular cardiomyopathy · Long QT syndrome · Brugada syndrome · CPVT

Key Takeaways

Definitions

• Ventricular tachycardia (VT): ≥3 consecutive complexes originating in the ventricles at rate >100 bpm (CL <600 ms). Sustained = >30 s or requiring termination due to hemodynamic compromise in <30 s. Nonsustained = ≥3 beats, terminates spontaneously.
• VT/VF storm (electrical storm): ≥3 episodes of sustained VT, VF, or appropriate ICD shocks within 24 hours.
• Sudden cardiac arrest (SCA): Sudden cessation of cardiac activity → unresponsive + absent/gasping respirations + no perceptible pulse. Reversible with CPR/defibrillation.
• Sudden cardiac death (SCD): Unexpected death within 1 hour of symptom onset, or found dead within 24 h, presumed arrhythmic/hemodynamic.
• Primary prevention ICD: ICD in patient without prior sustained VT or SCA who is at increased risk.
• Secondary prevention ICD: ICD after prior SCA, sustained VT, or syncope from VA.
• Structural heart disease: encompasses ischemic HD, all cardiomyopathies, valvular HD, and adult congenital HD.

Epidemiology of SCD (US Data)

• SCD accounts for approximately 50% of all cardiovascular deaths in the United States.
• Estimated 230,000–350,000 SCD per year in the US (range <170,000 to >450,000 depending on methodology). The 2017 AHA cardiovascular statistics estimated 356,500 out-of-hospital cardiac arrests annually.
• Survival from out-of-hospital cardiac arrest: ~10% overall (6% when arrest occurs at home; 24% in-hospital arrest).
• At least 25% of SCDs are the first clinical manifestation of cardiac disease.
• Ischemic HD remains the most common substrate, but its SCD incidence is declining; cardiomyopathies with fibrosis and LV hypertrophy are increasing proportionally.
• Age-stratified SCD risk: ~1/100,000/year in children/adolescents; age-associated transition zone mid-20s to 35–40 years; ~1/1,000/year in general population from age 35 onward. SCD is uniformly more common in men at all ages.
• SCD decreases in incidence after age 75 (Framingham data), suggesting less ICD benefit in the very elderly.
• Younger populations: inherited structural disorders (HCM, ARVC), channelopathies, myocarditis, and coronary anomalies predominate. By mid-20s–mid-30s, ischemic HD >40% of SCA causes.

Mechanisms of Ventricular Arrhythmia

• Automaticity: Spontaneous phase 4 depolarization; accounts for idiopathic VT from outflow tracts and accelerated idioventricular rhythm in AMI.
• Triggered activity:
  • Early afterdepolarizations (EADs): Occur during repolarization; trigger torsades de pointes in long-QT conditions (congenital or acquired). Worsened by bradycardia, hypokalemia, QT-prolonging drugs.
  • Delayed afterdepolarizations (DADs): Occur after complete repolarization under calcium overload (tachycardia, catecholamines, hypokalemia, digoxin toxicity, HF, HCM). Mechanism for CPVT, digoxin toxicity VT, and idiopathic outflow tract VA.
• Reentry: Dominant mechanism for sustained VT in structural heart disease. Scar-based (anatomical obstacle from MI or surgical repair); functional reentry (spiral wave/rotor). Rationale for VT ablation targeting slow conduction channels in scar.
• Phase 2 reentry: Heterogeneous repolarization → endocardial-epicardial current flow → reexcitation; relevant in Brugada syndrome and ischemia.

Evaluation of Patients with VA

• Syncope with suspected VA → hospitalize for evaluation, monitoring, management (Class I B-NR).
• 12-lead ECG during wide complex tachycardia, in sinus rhythm, and exercise testing (Class I B-NR).
• Ambulatory ECG (Holter), implanted cardiac monitors for suspected intermittent VA (Class I).
• Cardiac imaging (echo, CMR) for structural heart disease assessment.
• EP study: Useful (Class IIa) in ischemic cardiomyopathy, NICM, or adult congenital HD with syncope not meeting ICD criteria. NOT indicated solely for risk stratification in patients who already meet ICD criteria (Class III No Benefit). NOT recommended for channelopathies (LQTS, CPVT, Short QT, ERS) (Class III No Benefit).
• Coronary angiography after SCA: exclusion of obstructive/thrombotic coronary lesions; coronary anomalies (causes 10–17% of SCD in young patients at autopsy).

Pharmacological Therapies for VA

Antiarrhythmic Drugs

• Class I sodium channel blockers (flecainide, encainide, quinidine): Limited role in prevention; CAST demonstrated increased mortality in post-MI patients treated with class I agents despite VA suppression. Specific uses: IV lidocaine for refractory VF/cardiac arrest; oral mexiletine for congenital LQT3; quinidine for Brugada syndrome; flecainide for CPVT.
• Beta-blockers: First-line antiarrhythmic therapy; reduce all-cause mortality and SCD in HFrEF (bisoprolol, carvedilol, sustained-release metoprolol succinate). Also first-line for LQTS and CPVT (nadolol, propranolol preferred). Safe in structural heart disease; avoid high-dose IV beta-blocker when shock risk (age >70, HR >110, SBP <120, symptoms <12h in STEMI).
• Amiodarone: Multichannel blocker (Na+, K+, Ca²⁺, beta). Effective for VA suppression; no clear survival benefit over placebo in primary prevention (SCD-HeFT showed no benefit vs placebo; secondary analysis of SCD-HeFT showed increased mortality in NYHA class III). IV amiodarone superior to lidocaine for incessant VT (24-hour survival). Adverse effects: pulmonary fibrosis/pneumonitis, thyroid dysfunction (hyper/hypo), corneal microdeposits, hepatitis, peripheral neuropathy, photosensitivity.
• Sotalol: Do NOT use in LVEF <20% (negative inotropic effects). Effective for VA suppression; OPTIC trial: amiodarone + BB > sotalol > BB alone for reducing ICD shocks (38.5% vs 24.3% vs 10.3%).
• Procainamide IV: Superior to amiodarone for termination of hemodynamically stable VT (single RCT n=62; procainamide terminated more, but both had hypotension adverse events). Also superior to lidocaine for stable VT.
• Ranolazine: Late Na+ channel blocker; no significant reduction in primary endpoint (VT/VF or death) in high-risk ICD patients; reduced ATP-treated events in prespecified analysis.
• Non-antiarrhythmic medications: Statins reduce SCD in ischemic HD (mechanism: plaque stabilization + cardioprotection); benefit not confirmed in non-ischemic HF. n-3 PUFAs (fish oil): early data promising but subsequent RCTs showed no benefit.

GDMT for SCD Prevention in HFrEF

• Class I A: In patients with HFrEF (LVEF ≤40%), treatment with beta-blocker + MRA + (ACEi or ARB or ARNI) is recommended to reduce SCD and all-cause mortality. Beta-blockers (bisoprolol, carvedilol, metoprolol succinate) proven to reduce all-cause mortality, VA, and SCD. Sacubitril/valsartan (ARNI): reduced SCD and cardiac mortality vs ACEi in PARADIGM-HF.

ICD — Secondary Prevention

Ischemic Heart Disease:

• Class I (B-R for hemodynamically unstable VT; B-NR for stable VT): ICD in patients with ischemic HD who survive SCA due to VT/VF, or have hemodynamically unstable VT or stable sustained VT, not due to reversible causes, if meaningful survival >1 year expected. (Evidence: AVID — 2-year relative risk reduction in mortality 27%, absolute risk reduction 7%; CIDS; meta-analysis of 3 RCTs showing statistically significant all-cause and arrhythmic mortality reduction)
• Class I B-NR: Unexplained syncope + inducible sustained monomorphic VT on EPS → ICD if meaningful survival >1 year expected.
• Value: Intermediate ($64,000–$100,000/QALY) — ICD for secondary prevention is intermediate value; benefit most pronounced when arrhythmic death risk is high and nonarrhythmic competing mortality is low.
• ICD NOT implanted if life-threatening VA attributable to reversible causes (acute MI, proarrhythmic drugs, electrolyte disturbances).

Coronary Artery Spasm:

• Class I: Calcium channel blocker + smoking cessation for VA due to vasospasm.
• Class IIa: ICD if medical therapy ineffective/not tolerated in SCA survivor due to spasm.
• Class IIb: ICD in addition to medical therapy in SCA survivor due to spasm.

ICD — Primary Prevention

Ischemic Heart Disease:

• Class I A: LVEF ≤35% due to IHD + NYHA class II or III HF + ≥40 days post-MI + ≥90 days post-revascularization + GDMT → ICD if meaningful survival >1 year expected. (Evidence: SCD-HeFT [LVEF ≤35% threshold], MADIT-II)
• Class I A: LVEF ≤30% due to IHD + NYHA class I HF + ≥40 days post-MI + ≥90 days post-revascularization + GDMT → ICD. (Evidence: MADIT-II subgroup analysis)
• Class I B-R: NSVT due to prior MI + LVEF ≤40% + inducible sustained VT or VF at EPS → ICD. (Evidence: MUSTT)
• Class IIa B-NR: Non-hospitalized NYHA class IV candidates for cardiac transplantation or LVAD → ICD reasonable.
• Class III C-EO: NYHA class IV medication-refractory HF, not a candidate for transplantation/LVAD/CRT-D → ICD NOT indicated.
• Value: High value (<$50,000/QALY) — primary prevention ICD in ischemic HD provides high value when arrhythmic death risk is high and competing nonarrhythmic mortality is low; consistent across MADIT-I, MADIT-II, SCD-HeFT analyses. ICD not beneficial in CABG-Patch (early post-CABG prophylactic ICD without LVEF criterion).
• Waiting periods: 40-day post-MI waiting period is mandatory (IRIS, DINAMIT showed no benefit from early post-MI ICD); 90-day post-revascularization waiting period to allow for LVEF recovery.

Nonischemic Cardiomyopathy (NICM):

• Class I A: NICM + NYHA class II-III symptoms + LVEF ≤35% + despite ≥3 months GDMT → ICD if meaningful survival >1 year expected. (Evidence: SCD-HeFT, DEFINITE, pooled analysis showing 31% relative risk reduction in all-cause mortality; DANISH [2016] showed no significant all-cause mortality benefit but did halve SCD — guideline retained Class I A based on pre-DANISH evidence pool)
• Class IIa B-NR: Lamin A/C (LMNA) mutation + ≥2 of the following risk factors: NSVT, LVEF <45%, nonmissense mutation, male sex → ICD beneficial if meaningful survival >1 year expected.
• Class IIb B-R: NICM + NYHA class I + LVEF ≤35% + despite GDMT → ICD may be considered.
• Class III C-EO: Medication-refractory NYHA class IV HF, not a candidate for transplantation/LVAD/CRT-D → ICD should NOT be implanted.
• All NICM patients must complete ≥3 months GDMT before primary prevention ICD assessment (LVEF may improve).

Catheter Ablation for VA

General principles:

• Catheter ablation is an important option when AADs are ineffective, not tolerated, or not desired.
• Monomorphic VA has an identifiable origin/substrate; polymorphic VT/VF only if an initiating PVC focus can be identified.
• Requires advanced operator and laboratory expertise; surgical backup and specialized mapping equipment needed for scar-related VT.

Idiopathic VA (no structural heart disease):

• Focal mechanisms (triggered activity or abnormal automaticity), most often from outflow tracts or fascicular tissue.
• Ablation for symptomatic patients when AADs fail/not tolerated/not desired; usually endocardial approach, occasionally epicardial.

Scar-related VT (structural heart disease):

• Post-MI scar: subendocardial left ventricular substrate; electroanatomical mapping identifies slow conduction channels within scar.
• NICM scar: more variable location; often subepicardial or intramyocardial; epicardial approach required in ~30% of NICM versus ~1% of ischemic VT.
• Ablation success (VT-free survival at 1 year): ischemic 57% > NICM 40.5%.
• For recurrent VT after AADs in ICD patients: amiodarone or sotalol (Class IIa), catheter ablation (Class IIa in NICM).

Acute Management of VA

• VF or pulseless VT: CPR + defibrillation (Class I).
• Hemodynamically unstable VT: Synchronized cardioversion (Class I).
• Hemodynamically stable VT: IV procainamide preferred over amiodarone for VT termination. Amiodarone preferred over lidocaine for incessant VT (improved 24-hour survival). Verapamil/calcium channel blockers should NOT be given for wide QRS tachycardia (presumed VT) — risk of hemodynamic collapse; exception: verapamil-sensitive fascicular VT in structurally normal heart.
• Epinephrine (standard dose 1 mg q3-5 min): Improved return of spontaneous circulation and survival to admission in cardiac arrest, but no survival to discharge benefit. High-dose epinephrine offers no additional advantage over standard dose.
• IV magnesium: Effective for VA in acquired long QT; no benefit for refractory VF (2 RCTs).
• Amiodarone vs lidocaine for VF/pulseless VT: No difference in survival to hospital discharge (NEJM trials); amiodarone improved short-term survival to admission in some studies.
• Prophylactic lidocaine/procainamide in AMI: associated with increased mortality — do NOT use routinely.

Disease-Specific Management

Ischemic Heart Disease

• Revascularization (PCI or CABG) in sustained VA + ischemic HD: reduces myocardial ischemia as VA substrate; CABG associated with better long-term survival in patients with complex ischemic HD and low LVEF vs medical therapy. Revascularization alone usually insufficient to prevent recurrent sustained monomorphic VT when scar is present.
• Anomalous coronary origin (10–17% of SCD in young patients at autopsy): repair/revascularization recommended (Class I C-EO).
• Early post-CABG VT/VF: polymorphic → ischemia/electrolytes; monomorphic → usually old scar (not acute ischemia). Reassess LVEF 3 months after revascularization before ICD decision.
• VT/VF storm in ischemic HD: amiodarone + BB; consider EP ablation.

Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)

• Class I: Clinical screening of first-degree relatives + genetic counseling and testing if proband has disease-causing mutation.
• Class I: Cardiac MRI useful for diagnosis and risk stratification in suspected ARVC with VA or ECG abnormalities.
• Class I B-NR: ICD if additional marker of increased SCD risk: resuscitated SCA, sustained VT, significant ventricular dysfunction (RVEF or LVEF ≤35%).
• Class IIa: ICD in selected younger patients with syncope presumed due to VA and ARVC features.
• EP study: EPS-inducible sustained VT present in ~60% of ARVC patients; in asymptomatic patients without VA on monitoring, negative EPS has limited value in ICD decision-making.
• Exercise restriction from competitive sports: recommended for patients with ARVC (Class I).

Hypertrophic Cardiomyopathy (HCM)

• HCM is the most common cause of SCD in individuals <40 years; ~1% annual SCD risk.
• SCD risk stratification should be performed at initial evaluation and periodically thereafter (every 1–3 years) (Class I B-NR).
• Class I B-NR: ICD in patients with HCM who survived SCA due to VT/VF or have spontaneous sustained VT causing syncope or hemodynamic compromise, if meaningful survival >1 year expected.
• Class IIa: ICD in patients with HCM + ≥1 of the following risk factors: (a) maximum LV wall thickness ≥30 mm; (b) SCD in ≥1 first-degree relatives presumably caused by HCM; (c) ≥1 episode of unexplained syncope within preceding 6 months.
• Class IIa: ICD in HCM + spontaneous NSVT or abnormal BP response with exercise + additional SCD risk modifiers or high-risk features.
• Class IIb: ICD in HCM + NSVT or abnormal BP exercise response without any other SCD risk modifiers (uncertain benefit).
• Class III No Benefit: Invasive EP study with programmed ventricular stimulation for HCM risk stratification.
• Class III No Benefit: ICD in patients with HCM genotype alone (in absence of SCD risk factors and no phenotypic expression).
• Potential risk modifiers: Age <30, LGE on CMR (associated with higher SCD risk), LVOTO, syncope >5 years ago.
• High-risk subsets: LV aneurysm (associated with sustained monomorphic VT), LVEF <50%.
• First-degree relatives: ECG + echo (Class I); genetic counseling + testing if known causative mutation (Class I).
• AHA/ACC approach uses individual risk factors rather than a quantitative risk calculator (contrasts with ESC HCM Risk-SCD calculator approach).

Cardiac Channelopathies

• Class I B-NR: Genetic counseling + mutation-specific testing in first-degree relatives of patients with LQTS, CPVT, Short QT syndrome, or Brugada syndrome.
• Class I B-NR: ICD in patients with cardiac channelopathy and SCA if meaningful survival >1 year expected.
• Asymptomatic low-risk channelopathy patients: ICD implantation generally not appropriate (individual disease sections detail specific criteria).
• EP study does NOT have prognostic value for risk stratification in LQTS, CPVT, Short QT, or early repolarization syndrome (Class III No Benefit).
• Brugada syndrome (BrS): Quinidine for quinidine-sensitive VT/VF; EPS for asymptomatic BrS remains controversial (systematic review commissioned).
• LQTS: Beta-blockers first-line (nadolol, propranolol); mexiletine for LQT3; left cardiac sympathetic denervation for LQTS when beta-blocker therapy fails.
• CPVT: Flecainide as add-on to beta-blockers; LCSD for refractory cases.

Neuromuscular Disorders

• Class I: Primary and secondary prevention ICDs in neuromuscular disorders (same indications as for NICM patients) if meaningful survival >1 year expected.
• Class IIa: ICD in Emery-Dreifuss and limb-girdle type 1B muscular dystrophies (Lamin A/C) with progressive cardiac involvement.
• Class IIb: ICD in myotonic dystrophy type 1 with pacemaker indication, to also protect against VT-related SCA.
• SCD accounts for ~1/3 of deaths in Lamin A/C muscular dystrophy patients; ~1/3 of deaths in myotonic dystrophy type 1.

Heart Failure (HFpEF)

• No specific ICD data for HFpEF; no recommendations beyond standard structural heart disease criteria.

LVAD Recipients

• ICD + LVAD: associated with 19% relative risk reduction in mortality (UNOS registry, n=9,478 LVAD patients).

Heart Transplantation

• Secondary prevention ICD indications are identical to other patients; ICD beneficial in selected transplant recipients (allograft vasculopathy, unexplained syncope, SCA history, severe LV dysfunction).

Athletes

• PVCs common in trained athletes; generally not associated with increased death risk in athletes without other cardiovascular abnormalities (limited data). Complex PVCs in endurance athletes may not be benign; EPS may be needed.
• Competitive sports participation restriction varies by underlying disease.

Pregnancy

• Dedicated section on VA management in pregnancy; Beta-blockers generally safe (sotalol, mexiletine also used); ICD can be implanted with radiation shielding.

Older Patients with Comorbidities

• ERC systematic review commissioned specifically for this question: "What is the impact of ICD for primary prevention in older patients and patients with significant comorbidities?"
• ICD benefit is attenuated by competing nonarrhythmic mortality; individualized shared decision-making essential; patients with SCD risk that is low relative to total comorbid burden may not benefit.

Alternative Defibrillators

Subcutaneous ICD (S-ICD)

• Implanted in left chest (over sixth rib, between left midaxillary and left anterior axillary lines); no intracardiac leads.
• Preferred when pacing is not needed; avoids lead-related complications.
• Higher risk of T-wave oversensing (inappropriate shocks); screening ECG required to assess eligibility.
• Relevant for HCM, channelopathies, younger patients avoiding transvenous lead complications.

Wearable Cardioverter-Defibrillator (WCD)

• Role in early phase post-revascularization when ICD benefit uncertain pending LVEF reassessment; bridge to definitive ICD decision.
• No survival benefit demonstrated in unselected post-MI low LVEF patients (VEST trial data discussed).

Automated External Defibrillator (AED)

• Prompt CPR + AED access associated with improved OHCA survival.
• Public access defibrillation programs endorsed.

Catheter Ablation Special Considerations

• Patient selection for VT ablation: requires LVEF assessment, prior medication trials, careful operator selection given complexity.
• Epicardial access (subxiphoid pericardial puncture) required for some NICM, Chagas, and ARVC substrates.
• Ablation failure most often due to inability to provoke arrhythmia for mapping or inaccessible substrate.

Postmortem Evaluation of SCD

• Comprehensive autopsy recommended for all SCD victims <50 years; should include cardiac pathology, toxicology, and genetic specimen (blood/tissue storage for molecular autopsy).
• Genetic testing of decedent's tissue and clinical screening of first-degree relatives recommended when specific diagnosis suspected.

Shared Decision-Making and Terminal Care

• Shared decision-making discussion of ICD risks (infection, lead complications, inappropriate shocks, emotional burden) and benefits is essential.
• Patients have the right to deactivate an ICD; ICD deactivation discussion is part of end-of-life care.
• Terminal care section emphasizes that ICD deactivation is ethically appropriate in patients receiving hospice care.

Quality of Life

• ICD shocks (appropriate and inappropriate) are associated with significant psychological morbidity and reduced QoL.
• ATP therapy terminates most VT episodes without need for shocks; optimal programming to minimize shocks is essential.

Limitations of the Document

• Literature search through March 2017; some evidence (e.g., longer DANISH follow-up, SGLT2i trials, WCD efficacy data) not available.
• DANISH trial results (2016) introduced uncertainty for NICM primary prevention ICD — guideline maintained Class I A but acknowledged the tension; subsequent real-world data suggest benefit may be attenuated in contemporary GDMT-treated patients.
• HCM risk stratification based on expert consensus risk factors rather than validated quantitative score (ESC approach uses HCM Risk-SCD calculator) — difference may affect practical ICD recommendation rates.
• Guideline applies to adults ≥18 years; some pediatric data reviewed but no specific pediatric recommendations.
• Value statements based on pre-SGLT2i/ARNI era cost-effectiveness analyses; modern GDMT may shift the value equation.
• Many recommendations carry LOE B-NR or C-EO due to absence of RCT data in specific disease subgroups.

Key Concepts Mentioned

• concepts/Sudden-Cardiac-Death — epidemiology, risk stratification, SCA survival statistics
• entities/ICD — comprehensive primary and secondary prevention indications; value framework
• concepts/Electrical-Storm — definition: ≥3 VT/VF episodes or ICD shocks within 24h
• concepts/Antiarrhythmic-Drugs — Vaughan Williams classification, CAST findings, AAD comparison table
• concepts/PVC-Induced-Cardiomyopathy — threshold >10,000–20,000 PVCs/day; reversible with PVC control
• concepts/VT-Ablation-Ischemic-Cardiomyopathy — scar-based substrate ablation; success rates
• concepts/HCM-Risk-SCD — AHA/ACC risk factor-based approach (contrasts with ESC calculator)
• concepts/Left-Cardiac-Sympathetic-Denervation — autonomic modulation for refractory VA
• concepts/Torsades-de-Pointes — long-short initiating sequence; EAD mechanism
• concepts/Wide-Complex-Tachycardia — verapamil contraindication in VT; procainamide preferred
• concepts/VA-Risk-Stratification-DCM — Lamin A/C risk factors; NICM ICD criteria

Key Entities Mentioned

• entities/ARVC — Class I ICD indications; MRI role; exercise restriction
• entities/HCM — SCD risk factors table; ICD recommendations; genetics
• entities/Brugada-Syndrome — quinidine; EPS controversy; pharmacological unmasking
• entities/Long-QT-Syndrome — beta-blockers; mexiletine; LCSD
• entities/CPVT — flecainide + beta-blockers; LCSD
• entities/Short-QT-Syndrome — ICD for SCA; quinidine
• entities/S-ICD — subcutaneous ICD role and limitations
• entities/LMNA — specific ICD criteria: ≥2 of 4 risk factors (NSVT, LVEF <45%, nonmissense mutation, male sex)
• entities/Amiodarone — pharmacological profile; toxicity spectrum; OPTIC trial findings

Wiki Pages Updated

• wiki/sources/va-scd-aha-2017.md (created)
• wiki/sourceindex.md (updated)
• wiki/wikiindex.md (updated)
• wiki/entities/ICD.md (updated — AHA 2017 guideline recommendation section added)
• wiki/concepts/Sudden-Cardiac-Death.md (updated — AHA 2017 US epidemiology and SCA survival data)
• wiki/concepts/Electrical-Storm.md (updated — AHA 2017 definition cross-referenced)
• wiki/concepts/HCM-Risk-SCD.md (updated — AHA/ACC risk factor approach vs ESC calculator comparison)