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Ventricular tachycardia and sudden cardiac death

Ventricular arrhythmias and sudden cardiac death in adults, from mechanisms and wide-complex tachycardia diagnosis through acute treatment, electrical storm, catheter ablation, defibrillator therapy, inherited arrhythmia syndromes, and the evaluation of arrest survivors.

Definitions and classification of ventricular arrhythmias

Ventricular arrhythmias are classified by duration, QRS morphology, hemodynamic effect, and substrate. The 2017 American Heart Association/American College of Cardiology/Heart Rhythm Society (AHA/ACC/HRS) guideline on ventricular arrhythmias and the prevention of sudden cardiac death (SCD) is the governing US document; the 2022 European Society of Cardiology (ESC) guideline is its European counterpart.

Definitions from the 2017 AHA/ACC/HRS guideline and the 2024 European Heart Rhythm Association (EHRA) consensus on electrical storm, which adds that the episodes are separated by at least 5 minutes.

Sudden cardiac arrest (SCA) is the abrupt cessation of cardiac activity with hemodynamic collapse, typically from sustained VT or VF; SCD is SCA that is not reversed. By convention, SCD is unexpected death from a cardiac cause within 1 hour of symptom onset when witnessed, or within 24 hours of last being seen well when unwitnessed.

Epidemiology of sudden cardiac arrest and sudden cardiac death

SCA and SCD account for approximately half of all cardiovascular deaths, and at least a quarter of SCD victims have no prior cardiac symptoms. US estimates range from 230,000 to 350,000 SCDs per year, depending on the method of case ascertainment. Emergency medical services respond to roughly 357,000 out-of-hospital cardiac arrests annually, 97% in adults, and about 209,000 in-hospital arrests occur each year. Overall survival after out-of-hospital arrest is about 10%, falling to about 6% for the 70% of arrests that occur at home. Survival is highest with a witnessed public arrest, bystander resuscitation, an automated external defibrillator (AED), and a shockable rhythm.

Risk rises steeply with age. After age 35, the annual incidence is about 1 per 1,000; in adolescents and young adults it is about 1 per 100,000. Between the mid-20s and 35 to 40 years, the dominant causes shift from inherited disease toward ischemic heart disease, and SCD is more common in men at every age. The proportion of arrests presenting with VF or pulseless VT has fallen as pulseless electrical activity and asystole have risen.

The prevention paradox. The highest individual risk lies in small subgroups, such as arrest survivors and patients with a severely reduced ejection fraction, but most deaths occur in the far larger low-risk population, often as the first manifestation of coronary disease. ICD therapy reaches only the high-risk minority; risk-factor control, public-access defibrillation, and bystander resuscitation address the larger denominator.

About half of patients resuscitated from out-of-hospital VF who survive to admission have acute myocardial infarction (MI). Among patients hospitalized with acute MI, 5% to 10% have VF or sustained VT before arrival and about 5% after arrival, most within 48 hours.

Mechanisms of ventricular arrhythmia: scar re-entry, triggered activity, and automaticity

Scar-related re-entry. Healed infarcts and the patchy fibrosis of nonischemic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy (ARVC), sarcoidosis, and Chagas disease contain surviving myocyte bundles separated by collagen. A wavefront that conducts slowly through such a protected channel and exits after the surrounding myocardium has recovered re-excites the ventricle and sustains a circuit. Because the circuit is anatomically fixed, the QRS is monomorphic, and its morphology reflects the exit site at the border of the scar. Bipolar voltage mapping defines the substrate: normal endocardium has an amplitude above 1.5 mV and dense scar below 0.5 mV, and the border zone between contains most critical channels.

Triggered activity. Early afterdepolarizations occur during phase 2 or 3 of a prolonged action potential, when L-type calcium channels reactivate; they initiate torsades de pointes in congenital and acquired long QT syndrome, and dispersion of repolarization across the wall sustains the arrhythmia. Delayed afterdepolarizations follow full repolarization and result from calcium overload with spontaneous release from the sarcoplasmic reticulum; they underlie catecholaminergic polymorphic VT (CPVT), digoxin toxicity, and most idiopathic outflow-tract arrhythmias. Outflow-tract triggered activity is mediated by cyclic AMP, which explains its termination by adenosine.

Abnormal automaticity. Partially depolarized myocytes or Purkinje fibers fire spontaneously in acute ischemia, after reperfusion, and with electrolyte disturbance. Accelerated idioventricular rhythm is the clinical example.

Mechanisms of ventricular arrhythmia and their clinical correlates.

Presentation of ventricular tachycardia and differential diagnosis of wide-complex tachycardia

The consequences of VT depend on rate, ventricular function, and loss of atrioventricular (AV) synchrony. Patients with preserved ventricular function can tolerate VT at 150 to 200/min for hours, whereas the same rhythm with an ejection fraction of 20% causes shock. Presentations range from palpitations and presyncope to syncope, heart failure, ICD shock, and arrest.

Hemodynamic stability does not exclude VT. An alert, normotensive patient with a wide-complex tachycardia is often assumed to have supraventricular tachycardia (SVT) with aberrant conduction, an inference that leads to verapamil and collapse. Signs of AV dissociation in VT are intermittent cannon a waves and beat-to-beat variation in the first heart sound and systolic pressure.

Incessant VT or frequent nonsustained VT can produce a tachycardia-mediated cardiomyopathy.

Differential diagnosis. A wide-complex tachycardia has a QRS duration of 120 ms or more at a rate above 100/min. The differential diagnosis is limited, but the consequences of error are asymmetric: misclassifying VT as SVT can be fatal, whereas misclassifying SVT as VT rarely is. The 2017 AHA/ACC/HRS guideline therefore states that a wide-complex tachycardia is presumed to be VT if the diagnosis is unclear (Class 1). A 12-lead electrocardiogram (ECG) is recorded during every sustained, hemodynamically stable wide-complex tachycardia (Class 1); a single monitor lead cannot apply any of the diagnostic criteria.

Differential diagnosis of a wide-complex tachycardia in adults.

In the Brugada derivation series, 384 of 554 wide-complex tachycardias (69%) were VT, and prior infarction raises the probability further.

ECG criteria that distinguish ventricular tachycardia from aberrant conduction

Aberrant conduction begins in the His-Purkinje system and activates the ventricles rapidly at first; VT begins in working myocardium and activates them slowly. The initial QRS is therefore slurred in VT and sharp in aberrancy.

AV dissociation. Independent P waves at a slower rate than the QRS are diagnostic of VT but are visible in a minority of tracings. Retrograde 1:1 conduction occurs in some VT, so a P wave after every QRS does not exclude it.

Fusion and capture beats. A capture beat is a narrow, early QRS from a sinus impulse conducted during VT; a fusion beat is intermediate between sinus and VT complexes. Both are specific for VT.

QRS width and axis. In the absence of antiarrhythmic drugs and pre-excitation, a QRS duration longer than 140 ms with right bundle branch block morphology or longer than 160 ms with left bundle branch block morphology favors VT. A frontal axis between −90° and ±180° (northwest axis, negative in leads I and aVF) is rare in aberrancy and favors VT.

Precordial concordance. Negative concordance (all precordial QRS complexes predominantly negative) is highly specific for VT arising near the apex. Positive concordance occurs in VT from the base of the left ventricle and in antidromic tachycardia over a left posterior accessory pathway.

Comparison with a prior ECG. A QRS during tachycardia identical to a baseline bundle branch block favors SVT. A bundle branch block pattern contralateral to the baseline block favors VT. Bundle branch re-entrant VT can mimic typical bundle branch block.

Morphology criteria for VT used in step 4 of the Brugada algorithm. Criteria favoring VT must be present in both V1–V2 and V6 for step 4 to classify the rhythm as VT.

Brugada and Vereckei algorithms, R-wave peak time, and the VT score

Brugada algorithm (1991). Four sequential questions are applied to a regular wide-complex tachycardia; an affirmative answer at any step classifies it as VT, and four negative answers as SVT with aberrancy. (1) Is an RS complex absent from all precordial leads? (2) Is the longest RS interval, from the onset of R to the nadir of S, longer than 100 ms in any precordial lead? (3) Is AV dissociation present? (4) Are morphology criteria for VT present in both V1–V2 and V6? In the prospective derivation set of 554 tachycardias, sensitivity was 98.7% and specificity 96.5%. Independent validations, including the VT score study, found an accuracy near 80%, reflecting interobserver variation in the morphology step.

Vereckei aVR algorithm (2008). In aberrancy, activation proceeds away from aVR, and the QRS begins negative and steep. VT from the apex or inferior wall produces an initial R wave in aVR, and VT from any site produces slow initial activation. The algorithm asks, in order: (1) Is there an initial R wave in aVR? (2) Is an initial r or q wave wider than 40 ms? (3) Is there a notch on the initial downstroke of a predominantly negative QRS? (4) Is the ventricular activation-velocity ratio (vi/vt) 1 or less? The vi and vt are the vertical excursions, in millivolts, during the initial and terminal 40 ms of the same QRS complex; a ratio of 1 or less indicates slow initial activation and VT. An affirmative answer at any of the first three steps, or a vi/vt of 1 or less, classifies the rhythm as VT. In 483 wide-complex tachycardias from 313 patients, the aVR algorithm had higher accuracy than the Brugada algorithm, with greater sensitivity for VT.

R-wave peak time in lead II. The interval from the onset of the QRS to the first change in polarity in lead II (R-wave peak time) was 76.7 ± 21.7 ms in 163 VTs and 26.8 ± 9.5 ms in 55 SVTs. An R-wave peak time of 50 ms or more identified VT with an area under the curve of 0.97 and a positive likelihood ratio of 34.8. Later series reported lower sensitivity.

VT score (2016). Seven features are scored: an initial dominant R wave in V1 (R, Rs with R at least as tall as S, or Rsr′), an initial r wider than 40 ms in V1 or V2, a notched S wave in V1, an initial R wave in aVR, an R-wave peak time of 50 ms or more in lead II, absence of an RS complex in V1 to V6 (1 point each), and AV dissociation (2 points). In 786 wide-complex tachycardias from 587 patients, a score of 1 or more had an accuracy of 83%, compared with 81% for the Brugada algorithm and 72% for the aVR algorithm in the same cohort. A score of 3 or more was present in 66% of VTs and was 99.6% specific; a score of 4 or more was present in 33% and was 100% specific.

No algorithm reliably separates VT from antidromic tachycardia, and none is validated during antiarrhythmic therapy, hyperkalemia, or pacing.

Applying the Brugada, Vereckei aVR, and VT score criteria to a tracing

The three methods share ECG features. The tool applies all three to one set of entries and shows the step that decides each classification.

Brugada algorithm after Brugada et al. 1991; aVR algorithm after Vereckei et al. 2008; VT score after Jastrzebski et al. 2016, in which AV dissociation scores 2 points and each other feature 1 point (maximum 8). The criteria classify a tracing; they do not replace the rule that an undifferentiated wide-complex tachycardia is treated as VT.

Adenosine and drugs that cause harm in wide-complex tachycardia

Intravenous adenosine may be considered in a stable patient with a regular, monomorphic wide-complex tachycardia, to treat and to aid diagnosis when the cause cannot be determined (2025 AHA, Class 2b); it is potentially harmful in unstable, irregular, or polymorphic wide-complex tachycardia (Class 3: Harm). Idiopathic outflow-tract VT also terminates with adenosine, so termination does not prove a supraventricular origin, whereas transient AV block that unmasks flutter waves establishes it. Adenosine is avoided in irregular or polymorphic wide-complex tachycardia.

Intravenous verapamil and diltiazem in a wide-complex tachycardia of unknown origin are potentially harmful (2017 AHA/ACC/HRS, Class 3: Harm). They precipitate hypotension and VF in VT. The exception is verapamil for known or classic idiopathic left fascicular VT.

Pre-excited atrial fibrillation. AV-nodal blockade favors conduction over the accessory pathway and can accelerate the ventricular rate into VF. The 2015 ACC/AHA/HRS SVT guideline classifies intravenous digoxin, intravenous amiodarone, intravenous or oral beta-blockers, diltiazem, and verapamil as potentially harmful for acute treatment of pre-excited atrial fibrillation (Class 3: Harm). Unstable patients are cardioverted; stable patients receive intravenous procainamide or ibutilide, followed by pathway ablation.

Mimics with specific treatment. Hyperkalemia is treated with intravenous calcium, insulin with glucose, and potassium removal; sodium-channel-blocker toxicity with hypertonic sodium bicarbonate; and sustained ventricular arrhythmia from digoxin toxicity with digoxin-specific antibody fragments (Class 1).

Acute management of sustained ventricular tachycardia

1. Pulseless VT or VF: cardiopulmonary resuscitation and defibrillation according to advanced cardiovascular life support (ACLS) algorithms (Class 1). Epinephrine is recommended (2025 AHA, Class 1), at 1 mg every 3 to 5 minutes (Class 2a) and, with a shockable rhythm, after initial defibrillation attempts have failed (Class 2a); the 2017 AHA/ACC/HRS guideline graded the same dosing Class 2b. High-dose epinephrine provides no benefit (Class 3: No Benefit).
2. VT or VF that persists or recurs after a maximal-energy shock: intravenous amiodarone to facilitate a stable rhythm after further defibrillation (2017 AHA/ACC/HRS, Class 1), and lidocaine in witnessed arrest due to VF or polymorphic VT unresponsive to CPR, defibrillation, and vasopressors (2017, Class 2a). The 2025 AHA advanced life support guideline grades amiodarone or lidocaine for VF or pulseless VT unresponsive to defibrillation as Class 2b.
3. VT with a pulse and hemodynamic instability (hypotension, altered consciousness, ischemic chest pain, acute heart failure): synchronized direct-current cardioversion (Class 1).
4. Stable monomorphic VT: 12-lead ECG, then intravenous procainamide (Class 2a), or amiodarone or sotalol (Class 2b). Synchronized cardioversion under sedation is appropriate at any point and is preferred when drugs fail.
5. Polymorphic VT or VF with ST-elevation MI: emergency angiography and revascularization (Class 1). Polymorphic VT due to ischemia: intravenous beta-blockers (Class 2a).

Amiodarone and lidocaine in cardiac arrest. In the Amiodarone, Lidocaine, or Placebo Study (ALPS), survival to hospital discharge in shock-refractory out-of-hospital VF or pulseless VT was 24.4% with amiodarone, 23.7% with lidocaine, and 21.0% with placebo, differences that were not significant. Survival was higher with either drug in the prespecified witnessed-arrest subgroup. The 2025 AHA guideline retains amiodarone (300 mg, then 150 mg) and lidocaine (1 to 1.5 mg/kg, then 0.5 to 0.75 mg/kg) for VF or pulseless VT that persists after shocks (Class 2b). For VF or pulseless VT persisting after three or more consecutive shocks, the usefulness of vector change and of double sequential defibrillation has not been established (Class 2b).

Procainamide versus amiodarone for stable VT. In the randomized PROCAMIO trial, intravenous procainamide (10 mg/kg over 20 minutes) and amiodarone (5 mg/kg over 20 minutes) were compared for tolerated wide-QRS tachycardia. Major cardiac adverse events within 40 minutes occurred in 9% of patients given procainamide and 41% of those given amiodarone, and the tachycardia terminated within 40 minutes in 67% and 38%, respectively. The trial was small (62 patients analyzed) and open-label. Procainamide is avoided in hypotension, severe heart failure, and prolonged QT; amiodarone terminates VT slowly and serves mainly to suppress recurrence.

Acute intravenous drugs for ventricular arrhythmias. Doses and classes from the 2017 AHA/ACC/HRS guideline (Table 5 and Section 5) and the 2025 AHA advanced life support guideline. Prophylactic lidocaine or high-dose amiodarone to prevent VT in suspected acute MI is potentially harmful (Class 3: Harm).

The 2025 AHA advanced life support guideline states that intravenous amiodarone, procainamide, or sotalol may be considered for stable wide-complex tachycardia (Class 2b), and that synchronized cardioversion is recommended when vagal maneuvers and drug therapy are ineffective or contraindicated (Class 1); its tachycardia algorithm gives infusion doses for procainamide and amiodarone. Combining several QT-prolonging or conduction-slowing drugs compounds proarrhythmic risk.

Polymorphic ventricular tachycardia and ventricular fibrillation

The QT interval of the conducted beats separates two treatment pathways.

Polymorphic VT with a normal QT interval is acute ischemia until proved otherwise. It responds to revascularization, beta-blockers, and amiodarone or lidocaine, and not to magnesium. Without ischemia, the differential diagnosis comprises CPVT, Brugada syndrome, short-coupled idiopathic VF, early repolarization and short QT syndromes, and structural disease.

Torsades de pointes occurs with a prolonged QT interval, often after a short-long-short sequence, when QT-prolonging drugs combine with hypokalemia, hypomagnesemia, bradycardia, female sex, or structural disease. Treatment comprises drug withdrawal, intravenous magnesium (Class 1), potassium repletion to 4.0 mmol/L or more with magnesium repletion to normal (Class 1), and, for bradycardia-dependent recurrence despite magnesium, temporary pacing or isoproterenol (Class 1). QT-prolonging drugs are potentially harmful in congenital or acquired long QT syndrome (Class 3: Harm).

Ventricular fibrillation produces no cardiac output, and survival falls with each minute of delay to defibrillation. VF in the first 48 hours of acute MI is treated as a complication of the infarct, and the decision about a defibrillator then rests on ventricular function reassessed after the waiting period. VT or VF at any time during MI is nonetheless associated with higher 90-day mortality, and VT or VF that occurs after 48 hours carries a higher risk of death than early events.

Electrical storm: definition, triggers, and stepwise management

Electrical storm is 3 or more episodes of sustained VT or VF within 24 hours requiring termination by antitachycardia pacing or shock; the 2024 EHRA consensus adds a separation of at least 5 minutes. Each shock raises sympathetic tone and lowers the threshold for the next episode, and breaking this cycle is the central objective of treatment.

1. Device interrogation: separates appropriate therapy from inappropriate shocks for atrial fibrillation, sinus tachycardia, oversensing, or lead noise; therapy is reprogrammed to favor antitachycardia pacing.
2. Correction of triggers: ischemia, decompensated heart failure, hypokalemia, hypomagnesemia, thyroid excess, proarrhythmic drugs, and inotropes.
3. Sympathetic suppression: analgesia and anxiolysis, then deeper sedation and mechanical ventilation when storm persists. Beta-blockers are given unless contraindicated. In a randomized trial of 60 ICD recipients with storm treated with intravenous amiodarone, oral propranolol (160 mg/day) resulted in fewer arrhythmic events and shocks than metoprolol (200 mg/day), with 90% versus 53% free of events at 24 hours.
4. Antiarrhythmic drugs chosen by substrate: amiodarone, with lidocaine added for ischemic or recurrent VT.
5. Catheter ablation for recurrent monomorphic VT in scar, performed early once the patient is stabilized (Class 1 after failure or intolerance of amiodarone or other antiarrhythmic drugs in prior MI).
6. Autonomic modulation for refractory storm: percutaneous stellate ganglion block as a bridge, and cardiac sympathetic denervation when beta-blockers, antiarrhythmic drugs, and ablation are ineffective, not tolerated, or not possible (Class 2b).
7. Temporary mechanical circulatory support (venoarterial extracorporeal membrane oxygenation or a percutaneous ventricular assist device) for hemodynamic collapse, or to permit ablation in unstable patients; referral for transplant or durable ventricular assist device in end-stage disease.

In an international registry of 121 patients with structural heart disease, 1-year freedom from sustained VT or ICD shock after cardiac sympathetic denervation was 58%, and bilateral procedures outperformed left-sided ones.

Electrical storm management by substrate, from the 2017 AHA/ACC/HRS guideline and the 2024 EHRA consensus. CPVT, catecholaminergic polymorphic ventricular tachycardia.

Antiarrhythmic drugs for long-term suppression

Antiarrhythmic drugs reduce recurrence and ICD therapies, but none has reduced mortality in patients with structural heart disease, and several have increased it. The Cardiac Arrhythmia Suppression Trial (CAST) randomized 1,498 patients after MI with asymptomatic ventricular ectopy to encainide, flecainide, or placebo. After a mean of 10 months, arrhythmic death occurred in 43 patients receiving active drug and 16 receiving placebo, despite effective PVC suppression. Class IC drugs are therefore contraindicated after MI (2017 AHA/ACC/HRS, Class 3: Harm), and suppression of asymptomatic ectopy is not a therapeutic goal.

Oral antiarrhythmic drugs for ventricular arrhythmias, adapted from the 2017 AHA/ACC/HRS guideline (Table 5). Dofetilide and ranolazine are alternatives in selected patients.

In patients with ischemic heart disease and recurrent ventricular arrhythmias causing symptoms or ICD shocks despite optimal device programming and a beta-blocker, amiodarone or sotalol is useful to suppress recurrence (Class 1). In nonischemic cardiomyopathy the same strategy can be beneficial (Class 2a). Amiodarone may be considered to prevent SCD in patients with nonischemic cardiomyopathy who are ineligible for an ICD (Class 2b). Amiodarone was neutral against placebo for mortality in the Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT).

Monomorphic VT in ischemic cardiomyopathy

Healed infarction is the most common substrate for sustained monomorphic VT, which can appear months to decades after the infarct. Recurrence is the rule: an ICD terminates VT but does not prevent it. Coronary revascularization alone does not prevent recurrent sustained monomorphic VT (Class 3: No Benefit), because the circuit lies in fixed scar. Revascularization is indicated when ischemia is present and for polymorphic VT or VF from active ischemia.

Ablation versus drugs. Four randomized trials define the role of catheter ablation.

Randomized trials of catheter ablation for ischemic VT. HR, hazard ratio.

The 2017 AHA/ACC/HRS guideline recommends catheter ablation for prior MI with recurrent symptomatic sustained VT, or with VT or VF storm, after failure or intolerance of amiodarone (Class 1, Level B-R) or other antiarrhythmic drugs (Class 1, Level B-NR). Ablation as first-line therapy for recurrent or hemodynamically tolerated monomorphic VT may be considered (Class 2b). VANISH2 postdates the guideline. An initial ablation strategy reduced the composite outcome compared with drugs, driven mainly by fewer episodes of sustained VT below the detection rate, without a significant difference in mortality. The 2022 ESC guideline states that ablation should be considered as an alternative to an ICD in selected patients with well-tolerated monomorphic VT and an LVEF of 40% or more when procedural end points are achieved (Class IIa). US guidance retains the ICD.

VT in nonischemic cardiomyopathy, sarcoidosis, myocarditis, and genetic cardiomyopathies

Nonischemic dilated cardiomyopathy. Scar in nonischemic cardiomyopathy is patchy, intramural or epicardial, in the basal septum or inferolateral wall. Late gadolinium enhancement on cardiac magnetic resonance (CMR) adds risk information to the ejection fraction (Class 2a), and epicardial ablation is often required. In nonischemic cardiomyopathy with recurrent monomorphic VT despite or with intolerance of antiarrhythmic drugs, ablation can be useful (Class 2a). Genetic counseling and testing are reasonable when conduction disease or ventricular dysfunction develops before age 40, or with a first-degree relative with cardiomyopathy or SCD before age 50 (Class 2a).

Lamin A/C and other arrhythmogenic genotypes. LMNA cardiomyopathy presents with AV conduction disease, atrial arrhythmias, and ventricular arrhythmias that often precede severe ventricular dysfunction. An ICD can be beneficial in LMNA carriers with 2 or more of nonsustained VT, LVEF below 45%, a nonmissense variant, and male sex (2017 AHA/ACC/HRS, Class 2a). The 2022 ESC guideline uses a validated LMNA risk calculator for the same decision. Filamin C, desmoplakin, and phospholamban variants carry similar risk. In neuromuscular disease, Emery-Dreifuss and limb-girdle type 1B dystrophy with progressive cardiac involvement are reasonable ICD indications (Class 2a).

Cardiac sarcoidosis. Granulomas and scar cause AV block and VT out of proportion to ventricular dysfunction. An ICD is recommended for sustained VT, survival of arrest, or LVEF 35% or less (Class 1). With an LVEF above 35%, an ICD is reasonable for syncope, myocardial scar on CMR or positron emission tomography (PET), or a pacing indication (Class 2a). An electrophysiologic study with ICD implantation for inducible sustained VT is also reasonable (Class 2a). Immunosuppression combined with antiarrhythmic drugs can reduce arrhythmia burden when fluorodeoxyglucose PET shows active inflammation (Class 2a). Young and middle-aged adults with unexplained AV block or monomorphic VT are evaluated for sarcoidosis.

Myocarditis. Life-threatening VT or VF with confirmed or suspected myocarditis is an indication for referral to a center with mechanical circulatory support and advanced arrhythmia management (Class 1). Giant cell myocarditis presents with heart failure, heart block, and VT; an ICD or an antiarrhythmic drug may be considered after VF or unstable VT (Class 2b). In other forms, the defibrillator decision is deferred until the acute phase has passed.

Chagas cardiomyopathy. Chronic Trypanosoma cruzi infection causes right bundle branch block with left anterior fascicular block, basal inferolateral aneurysms, and epicardial scar that supports monomorphic VT. Amiodarone, ICD therapy, and combined endocardial and epicardial ablation are used, and serology is tested in adults from endemic regions with this ECG pattern or an inferolateral aneurysm.

Primary prevention. Patients with nonischemic cardiomyopathy, an LVEF of 35% or less, and New York Heart Association (NYHA) class II to III symptoms despite guideline-directed therapy have a Class 1 ICD recommendation in US guidance, whereas the 2022 ESC guideline grades an ICD in dilated or hypokinetic nondilated cardiomyopathy with an LVEF of 35% or less after at least 3 months of optimal medical therapy as Class IIa and adds late gadolinium enhancement and high-risk genotypes to the decision; the DANISH trial, the role of age, and the waiting period are discussed on the heart failure with reduced ejection fraction page.

Arrhythmogenic right ventricular cardiomyopathy

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an inherited disease of the desmosome, most often from variants in PKP2, in which myocytes are replaced by fibrous and fatty tissue, predominantly in the right ventricular free wall, outflow tract, and inferior wall. Left ventricular involvement is common. The disease presents in adolescence to middle age with palpitations, syncope, VT of left bundle branch block morphology, or SCD, often during exercise, and endurance exercise accelerates it.

Diagnosis uses the 2010 Task Force criteria, which grade structural, tissue, repolarization, depolarization, arrhythmic, and family or genetic findings as major or minor. Characteristic features are T-wave inversion in V1 to V3 after adolescence without complete right bundle branch block, epsilon waves, VT with left bundle branch block morphology and a superior axis, regional right ventricular akinesia or aneurysm with dilation or dysfunction, and a pathogenic variant. The 2020 Padua criteria add late gadolinium enhancement to recognize left ventricular involvement.

ARVC recommendations from the 2017 AHA/ACC/HRS guideline. RVEF, right ventricular ejection fraction.

For primary prevention in patients without prior sustained arrhythmia, the ARVC risk calculator (age, sex, recent cardiac syncope, nonsustained VT, 24-hour PVC count, number of leads with T-wave inversion, and right ventricular ejection fraction) estimates the annual risk of sustained ventricular arrhythmia. In 528 patients with definite ARVC, it discriminated with an optimism-corrected C-index of 0.77 and reduced ICD placements by 20.6% for the same proportion of protected patients compared with a consensus algorithm. The 2019 HRS consensus on arrhythmogenic cardiomyopathy recommends shared decision-making for ICD placement.

Bundle branch re-entry, repaired tetralogy of Fallot, hypertrophic cardiomyopathy, and postoperative ventricular tachycardia

Bundle branch re-entrant VT. In dilated cardiomyopathy or after aortic valve surgery, slowed His-Purkinje conduction permits a circuit down the right bundle and up the left, producing fast VT with left bundle branch block morphology and an HV interval during VT equal to or longer than in sinus rhythm. Right bundle ablation is curative for the circuit (Class 1), but the myocardium often supports other VTs and an ICD is still indicated.

Repaired tetralogy of Fallot. VT uses anatomic isthmuses between the ventriculotomy or outflow patch, the pulmonary annulus, and the septal patch. Risk markers include syncope, QRS duration of 180 ms or more, inducible VT, ventricular dysfunction, and severe pulmonary regurgitation. An ICD is reasonable with inducible or spontaneous sustained VT (Class 2a), residual lesions are corrected first (Class 1), and isthmus ablation can be effective (Class 2a).

Hypertrophic cardiomyopathy (HCM). Sudden death risk stratification, the 2024 AHA/ACC major-risk-factor pathway, and the HCM Risk-SCD calculator are on the hypertrophic cardiomyopathy page.

After cardiac surgery. Polymorphic VT or VF early after surgery usually reflects ischemia, electrolyte shifts, or inotropes.

Idiopathic outflow-tract, fascicular, papillary muscle, and annular VT

Idiopathic VT is diagnosed only after structural, ischemic, and inherited disease have been excluded with a sinus ECG, echocardiography, and, when indicated, CMR and exercise testing. It carries a low risk of sudden death and is often curable by ablation.

Idiopathic ventricular arrhythmias in the structurally normal heart; classes from the 2017 AHA/ACC/HRS guideline (Sections 8.1 to 8.3).

Syncope, a family history of SCD, multiple or atypical morphologies, ventricular dysfunction, right precordial T-wave inversion or epsilon waves, and late gadolinium enhancement make an idiopathic diagnosis uncertain. Left bundle branch block VT with a superior axis is ARVC or another right ventricular cardiomyopathy until imaging excludes it.

In the 2022 ESC guideline, catheter ablation is recommended as first-line treatment for symptomatic idiopathic VT or PVCs from the right ventricular outflow tract or the left fascicles (Class I); US guidance places drugs and ablation as alternatives guided by patient preference.

Premature ventricular complexes and PVC-induced cardiomyopathy

PVCs appear on a 12-lead ECG in 0.6% of healthy people younger than 20 years and 2.7% of those older than 50, and in about half of all people on extended monitoring. Frequent PVCs (at least 1 on a 12-lead ECG, or more than 30 per hour) and multifocal PVCs are associated with higher cardiovascular risk, and PVCs during exercise testing, particularly in recovery, predict higher mortality. In trained athletes without other abnormalities, PVCs have not been associated with excess risk.

Evaluation. Frequent PVCs are assessed by burden on ambulatory monitoring of 24 hours or longer, 12-lead morphology, echocardiography (Class 1), CMR when structural disease is suspected (Class 2a), and exercise testing when ectopy is exertional (Class 1). Ectopy that suppresses with exercise favors a benign process; ectopy that increases with exercise raises concern for ischemia, CPVT, or cardiomyopathy.

PVC-induced cardiomyopathy. Very frequent PVCs, more than 10,000 to 20,000 per day, can cause left ventricular dysfunction that reverses when the PVCs are suppressed. In 174 patients referred for ablation of idiopathic PVCs, the 33% with reduced LVEF had a mean burden of 33% compared with 13% in those with normal function. A burden above 24% best separated the groups (sensitivity 79%, specificity 78%), and the lowest burden associated with reversible cardiomyopathy was 10%. No threshold proves causality. The diagnosis is established retrospectively when ventricular function improves after suppression. Cardiomyopathy with frequent PVCs is often a primary cardiomyopathy with secondary ectopy, which CMR scar and atypical morphologies suggest.

Management of premature ventricular complexes. Asymptomatic PVCs with normal ventricular function and no structural disease require reassurance and periodic reassessment of function when the burden is high.

Nonsustained VT and accelerated idioventricular rhythm

Nonsustained VT in a structurally normal heart carries a low risk. In structural heart disease its weight depends on the substrate: it is a modifier in HCM, part of the ARVC and LMNA risk models, and in ischemic cardiomyopathy a trigger for electrophysiologic testing. In the Multicenter Unsustained Tachycardia Trial (MUSTT), 704 patients with coronary disease, LVEF 40% or less, nonsustained VT, and inducible sustained VT were randomized. Electrophysiologically guided therapy reduced arrest or arrhythmic death at 5 years (25% versus 32%), a benefit confined to defibrillator recipients (relative risk 0.24). An ICD is therefore recommended for nonsustained VT after MI with LVEF 40% or less and inducible sustained VT or VF (Class 1).

An electrophysiologic study is useful in ischemic cardiomyopathy, nonischemic cardiomyopathy, or adult congenital heart disease with syncope or other arrhythmic symptoms in patients who do not meet a primary-prevention ICD indication (Class 2a). It is not indicated solely to induce ventricular arrhythmia in a patient who already meets ICD criteria (Class 3: No Benefit). It has no role in risk stratification of long QT syndrome, CPVT, short QT syndrome, or early repolarization syndrome (Class 3: No Benefit).

Accelerated idioventricular rhythm is a regular ventricular rhythm faster than the ventricular escape rate and close to the sinus rate, with fusion as the two pacemakers compete. It is common in acute MI and during primary percutaneous coronary intervention, is benign in most patients, and requires no antiarrhythmic treatment.

Brugada syndrome: diagnosis, risk stratification, and treatment

Brugada syndrome combines coved right precordial ST elevation with a risk of polymorphic VT and VF, typically at rest or during sleep, in a structurally normal heart. The worldwide pooled prevalence is about 0.5 per 1,000, highest in Southeast Asia. It is far more common in men, presents most often in the third and fourth decades, and accounts for a share of unexplained nocturnal death in young Southeast Asian men. Pathogenic SCN5A loss-of-function variants are found in 15% to 30% of clinically diagnosed patients; genetic testing may be useful to facilitate cascade screening (Class 2b).

ECG diagnosis. The type 1 pattern is coved ST elevation of 2 mm (0.2 mV) or more followed by a negative T wave in at least one right precordial lead (V1 or V2), recorded in the standard or in a higher (second or third) intercostal space. The type 2 (saddleback) pattern is not diagnostic. The pattern fluctuates and is unmasked by fever, sodium-channel blockers, vagal tone, and a large meal.

Sodium-channel-blocker challenge for suspected Brugada syndrome without a spontaneous type 1 pattern (2017 AHA/ACC/HRS, Class 2a). It is performed with continuous 12-lead monitoring, high right precordial leads, and resuscitation equipment, and stopped for a type 1 pattern, excess QRS widening, or arrhythmia.

Risk and treatment. Risk is highest after cardiac arrest or documented sustained ventricular arrhythmia, intermediate with arrhythmic syncope and a spontaneous type 1 pattern, and low in asymptomatic patients with only a drug-induced pattern, for whom observation without therapy is recommended (Class 1). An ICD is recommended in patients with a spontaneous type 1 pattern and cardiac arrest, sustained ventricular arrhythmia, or recent syncope presumed arrhythmic (Class 1). In asymptomatic patients with a spontaneous type 1 pattern, programmed ventricular stimulation with single and double extrastimuli may be considered (Class 2b). Recurrent ICD shocks for polymorphic VT, or symptomatic ventricular arrhythmia in patients who decline or are ineligible for an ICD, are treated with quinidine or catheter ablation (Class 1). Ablation targets the abnormal epicardial substrate of the right ventricular outflow tract; the 2022 ESC guideline upgraded it to Class IIa for recurrent appropriate shocks.

All patients avoid drugs that provoke the pattern (class I antiarrhythmic drugs, certain psychotropic and anesthetic agents, and cocaine), excessive alcohol, and large meals, and fever is treated promptly with antipyretics.

Catecholaminergic polymorphic ventricular tachycardia: diagnosis and treatment

CPVT is an inherited disorder of intracellular calcium handling in which adrenergic stimulation produces bidirectional or polymorphic VT in a structurally normal heart. Variants in RYR2 (autosomal dominant) or CASQ2 (usually recessive) are found in roughly 60% of patients. Most present in childhood or adolescence with exertional or emotional syncope, but adult diagnosis, often after a relative's death, is common. The resting ECG and imaging are normal, and exercise testing is the key test (Class 1): ectopy appears at a reproducible heart rate and escalates to bidirectional and polymorphic VT. Genetic counseling and testing are reasonable (Class 2a).

A beta-blocker is recommended (Class 1), preferably nonselective nadolol. Recurrent sustained VT or syncope despite maximal beta-blockade is treated with flecainide, left cardiac sympathetic denervation, and/or an ICD (Class 1). In a randomized crossover trial of 14 patients, flecainide completely suppressed exercise-induced arrhythmia in 11 of 13. An ICD alone is inadequate, because a shock is an adrenergic stimulus that can perpetuate the arrhythmia; devices are programmed with long detection times and high rate cutoffs.

Early repolarization syndrome, short QT syndrome, and idiopathic ventricular fibrillation

Early repolarization. The pattern is J-point elevation of 0.1 mV or more, with slurring or notching of the terminal QRS, in two or more contiguous inferior or lateral leads. It is common in young men and athletes and benign in nearly all. Among 206 survivors of idiopathic VF it was present in 31%, compared with 5% of controls, and predicted recurrent VF (hazard ratio 2.1). Asymptomatic patients with the pattern are observed (Class 1); an ICD is recommended after arrest or sustained ventricular arrhythmia (Class 1); genetic testing is not recommended (Class 3: No Benefit).

Short QT syndrome. Gain-of-function variants in potassium-channel genes shorten repolarization and predispose to atrial fibrillation, VF, and SCD. Asymptomatic patients with a short corrected QT interval (QTc) are observed (Class 1). An ICD is recommended after cardiac arrest or sustained ventricular arrhythmia (Class 1), quinidine can be useful for recurrent arrhythmia (Class 2a), and isoproterenol can terminate storm (Class 2a).

Idiopathic VF. Idiopathic VF is a diagnosis of exclusion in a survivor of VF in whom structural, ischemic, toxic, metabolic, and known channelopathic causes have been excluded after a complete evaluation. A subset has short-coupled PVCs originating in the Purkinje network or the outflow tract that trigger VF. An ICD is recommended after resuscitation from idiopathic polymorphic VT or VF (Class 1), and catheter ablation is useful for recurrent VF initiated by PVCs of a consistent morphology (Class 1). Young survivors (younger than 40 years) of unexplained arrest, unexplained near drowning, or recurrent exertional syncope without structural disease are evaluated for genetic arrhythmia syndromes (Class 1).

Long QT syndrome. Congenital and acquired long QT syndrome, QT measurement, genotype-specific triggers, beta-blocker therapy, and ICD indications are on the long QT syndrome and QT prolongation page.

Evaluating survivors of sudden cardiac arrest

Evaluation after resuscitation seeks a reversible trigger and the persistent substrate. Ischemia, an electrolyte disturbance, or a drug does not by itself establish complete reversibility, and survivors without a securely reversible cause generally receive a secondary-prevention ICD.

Sequence of testing after unexplained cardiac arrest, after the 2017 AHA/ACC/HRS guideline and the 2020 APHRS/HRS consensus.

Timing of angiography. Patients resuscitated from out-of-hospital arrest with ST elevation undergo emergency angiography. In those without ST elevation, two randomized trials found no benefit from immediate angiography. In COACT (552 patients with a shockable rhythm, no ST elevation, and no cardiogenic shock), survival at 90 days was 64.5% with immediate and 67.2% with delayed angiography. In TOMAHAWK (554 patients), 30-day mortality was 54.0% with immediate and 46.0% with delayed or selective angiography (hazard ratio 1.28, P=0.06). The 2025 ACC/AHA acute coronary syndrome guideline recommends against immediate angiography in comatose survivors without ST elevation who are electrically and hemodynamically stable.

Coronary spasm can cause VF. Maximally tolerated calcium-channel blockers and smoking cessation are indicated (Class 1); an ICD is reasonable when medical therapy is ineffective or not tolerated (Class 2a) and may be reasonable in addition to medical therapy (Class 2b). An anomalous coronary origin suspected of causing arrest is repaired or revascularized (Class 1).

Postmortem evaluation and screening of families after sudden death

A structurally normal autopsy in a young victim of sudden death points toward a primary electrical disorder or a cardiomyopathy too early to leave structural change. A standardized cardiac autopsy is recommended in victims of SCD without an obvious cause (Class 1), ideally reviewed by a cardiovascular pathologist with full toxicology. Blood or frozen tissue suitable for DNA analysis is retained. Postmortem genetic testing is reasonable when the autopsy suggests a heritable cardiomyopathy or finds no structural disease (Class 2a), and is useful when the decedent had a known phenotype that was never genotyped (Class 2a).

First-degree relatives of SCD victims aged 40 years or younger undergo cardiac evaluation, with genetic counseling and testing as indicated by the findings (Class 1). The evaluation comprises a three-generation family history, ECG with high right precordial leads, exercise testing, echocardiography, and, guided by the suspected phenotype, ambulatory monitoring, CMR, and sodium-channel-blocker challenge. A pathogenic variant identified in the decedent permits cascade testing; a variant of uncertain significance is not used to diagnose relatives.

ICD for secondary prevention of sudden cardiac death

Three trials compared the ICD with amiodarone in survivors of VF or hemodynamically significant VT: the Antiarrhythmics Versus Implantable Defibrillators trial (AVID), the Cardiac Arrest Study Hamburg (CASH), and the Canadian Implantable Defibrillator Study (CIDS). In the individual-patient meta-analysis, the ICD reduced all-cause mortality by 28% (hazard ratio 0.72) and arrhythmic death by 50% (hazard ratio 0.50), extending mean survival by 4.4 months over 6 years. Patients with an LVEF of 35% or less derived more benefit.

Secondary-prevention ICD indications from the 2017 AHA/ACC/HRS guideline. Every indication assumes meaningful survival greater than 1 year. In ischemic heart disease, sustained monomorphic VT is evaluated for ischemia and revascularized as appropriate (Class 1), but revascularization does not remove the ICD indication.

ICD for primary prevention, the wearable cardioverter-defibrillator, and advanced heart failure

Primary-prevention decisions rest on trial-tested ejection fraction thresholds, timing, guideline-directed therapy, functional class, and expected survival.

Primary-prevention ICD indications based on ventricular dysfunction, 2017 AHA/ACC/HRS guideline; all assume meaningful survival greater than 1 year.

The trials behind these thresholds (MADIT-II, SCD-HeFT, DANISH), the 40-day and 90-day waiting periods, and their interaction with modern drug therapy and CRT are covered on the heart failure with reduced ejection fraction page. In hypertrophic cardiomyopathy, the ICD decision follows the 2024 AHA/ACC major risk factors and the HCM Risk-SCD estimate on the hypertrophic cardiomyopathy page. In congenital long QT syndrome, ICD indications after beta-blocker failure or with high-risk features are on the long QT syndrome page.

Wearable cardioverter-defibrillator. The wearable device detects VT or VF and shocks after an alert that a conscious patient can abort. It is reasonable after explantation of an ICD for infection in a patient with prior SCA or sustained ventricular arrhythmia (Class 2a). It may be reasonable when risk is increased but an ICD is not yet appropriate: within 40 days of MI with LVEF 35% or less, newly diagnosed nonischemic cardiomyopathy, within 90 days of revascularization, myocarditis or secondary cardiomyopathy, systemic infection, or awaiting transplantation (Class 2b). In VEST (2,302 patients after MI with LVEF 35% or less), arrhythmic death at 90 days was 1.6% with the wearable device and 2.4% without (P=0.18). Only 12 of 48 deaths in the device group occurred while it was worn.

Advanced heart failure, ventricular assist devices, and transplantation. In patients awaiting transplant who would not otherwise qualify (NYHA class IV or inotrope-dependent) and will be discharged home, an ICD is reasonable (Class 2a). An ICD can also be beneficial with a left ventricular assist device (LVAD) and sustained ventricular arrhythmia (Class 2a). Patients with an LVAD can tolerate VT or VF for hours because the pump maintains flow, but right ventricular failure follows. After transplantation, an ICD may be reasonable with severe allograft vasculopathy and left ventricular dysfunction (Class 2b). Refractory ventricular arrhythmia is an indication for transplant evaluation.

Transvenous, subcutaneous, and extravascular ICD systems

Transvenous ICD. A right ventricular lead with one or two shocking coils provides defibrillation, bradycardia pacing, antitachycardia pacing, and, with added leads, atrial sensing and CRT. Its long-term liabilities are lead failure, venous occlusion, tricuspid regurgitation, and endovascular infection.

Subcutaneous ICD. A parasternal lead avoids the vascular space but cannot provide bradycardia pacing, antitachycardia pacing, or CRT, and surface-ECG screening confirms adequate QRS-to-T-wave ratios. It is recommended with inadequate vascular access or high infection risk when pacing is neither needed nor anticipated (Class 1) and is reasonable in any ICD candidate without a pacing need (Class 2a). It is not implanted when pacing, CRT, or antitachycardia pacing is required (Class 3: Harm). In PRAETORIAN (849 patients), the composite of device complications and inappropriate shocks at 48 months was 15.1% with the subcutaneous and 15.7% with the transvenous ICD (noninferior). The subcutaneous group had fewer complications and more inappropriate shocks.

Extravascular ICD. A single lead in the substernal space provides defibrillation, antitachycardia pacing, and pause-prevention pacing without entering the vasculature. In the pivotal study, defibrillation at implantation succeeded in 98.7% of 302 tested patients, freedom from major complications at 6 months was 92.6%, antitachycardia pacing terminated 50.8% of treated episodes, and 29 patients received 118 inappropriate shocks.

Young patients, prior device infection, dialysis, and limited venous access favor a nonvascular system; monomorphic VT amenable to antitachycardia pacing and any need for pacing or CRT favor a transvenous system.

ICD programming, shocks, complications, MRI, driving, and deactivation

Programming. Antitachycardia pacing terminates much monomorphic VT painlessly, and many episodes of nonsustained VT end spontaneously if detection is delayed. MADIT-RIT randomized 1,500 primary-prevention patients to conventional programming, high-rate therapy (2.5-second delay, therapy only at 200/min or more), or delayed therapy (60 seconds at 170 to 199/min, 12 seconds at 200 to 249/min, 2.5 seconds at 250/min or more). High-rate and delayed programming reduced first inappropriate therapy (hazard ratios 0.21 and 0.24) and all-cause mortality (hazard ratios 0.45 and 0.56; the latter not significant). Contemporary primary-prevention programming therefore uses high rate cutoffs, long detection durations, antitachycardia pacing before shocks, and supraventricular discriminators, as set out in the 2015 HRS/EHRA/APHRS/SOLAECE consensus on ICD programming.

Shocks and prognosis. In SCD-HeFT, 33% of patients with an ICD received at least one shock over a median 45.5 months. An appropriate shock was associated with a 5.7-fold higher subsequent risk of death and an inappropriate shock with a 2.0-fold higher risk. The most common mode of death after any shock was progressive heart failure. A shock is therefore a prompt to reassess heart failure therapy, ischemia, and antiarrhythmic and ablative options. Shocks also cause anxiety, depression, and post-traumatic stress.

Inappropriate shocks. The causes are supraventricular tachycardia (atrial fibrillation with a rapid ventricular response, sinus tachycardia, atrial flutter) exceeding the detection rate; oversensing of T waves, myopotentials, or electromagnetic interference; and nonphysiologic noise from lead fracture or loose connection, which appears as very short, irregular intervals on stored electrograms. Recalled leads (Sprint Fidelis conductor fracture, Riata externalized conductors) illustrate how abrupt impedance changes and runs of very short intervals identify failure before a shock.

Complications. Pocket hematoma, pneumothorax, lead dislodgement, perforation, and infection occur after implantation; device infection requires complete system extraction.

Magnetic resonance imaging. MR-conditional systems are scanned under the manufacturer's conditions with tachyarrhythmia therapies programmed off, monitoring, and an external defibrillator available.

Driving. The AHA/HRS statement on driving restricts private driving for 6 months after an ICD implanted for secondary prevention, and for 6 months after an appropriate shock in any patient. After a primary-prevention ICD, driving is avoided for 1 week while the incision heals, and asymptomatic patients then have no restriction. US federal rules preclude certification for commercial driving with any ICD.

Deactivation and shared decision-making. Shared decision-making is recommended for every patient with ventricular arrhythmias or increased risk of SCD (Class 1). Patients considering a new ICD or generator replacement are informed of their risk of sudden and nonsudden death and of the device's effectiveness and complications (Class 1). At implantation, replacement, and advance care planning, patients are told that shocks can be deactivated at any time consistent with their goals (Class 1). Clinicians discuss deactivation with patients who have refractory heart failure or refractory ventricular arrhythmia, or who are approaching death from another illness (Class 1). Pacing can remain active, and a magnet over most ICDs suspends shocks while it remains in place.

Catheter ablation of VT: mapping, outcomes, and alternatives

Activation mapping during tolerated VT locates the diastolic pathway. Entrainment identifies isthmus sites by concealed fusion, a post-pacing interval within 30 ms of the tachycardia cycle length, and a stimulus-to-QRS interval equal to the electrogram-to-QRS interval. Most VTs are not tolerated long enough to map, so substrate ablation in sinus rhythm targets late potentials, fractionated electrograms, and pace-map matches within scar and border zone. Noninducibility after ablation is associated with fewer recurrences.

Epicardial access is required more often in nonischemic cardiomyopathy, ARVC, Chagas disease, and Brugada syndrome, and epicardial ablation can be useful after failed endocardial ablation (Class 2a). The 2019 HRS/EHRA/APHRS/LAHRS expert consensus defines indications, end points, and facility standards.

Surgical ablation may be reasonable for monomorphic VT refractory to drugs and catheter ablation (Class 2b), usually combined with aneurysm resection or other cardiac surgery.

Stereotactic body radiotherapy. A single 25-Gy fraction is delivered to scar defined by imaging and noninvasive electrocardiographic mapping. In the phase I/II ENCORE-VT trial of 19 patients, VT episodes fell by 94% in the first 6 months; later follow-up reported pericardial effusion and a gastropericardial fistula more than 2 years after treatment. Radioablation remains investigational, reserved for patients in whom catheter ablation has failed or is not possible.

Sports participation, commotio cordis, and sudden death in athletes

In a 20-year study of National Collegiate Athletic Association (NCAA) athletes, 143 SCDs were identified (overall incidence 1 in 63,682 athlete-years), and the incidence declined by 29% for each 5-year period (incidence rate ratio 0.71). Incidence was 1 in 43,348 athlete-years in men and 1 in 164,504 in women, and was highest in male Division I basketball players and in Black athletes. Half of the events were exertional. The principal causes in young athletes are cardiomyopathies, autopsy-negative sudden unexplained death, anomalous coronary origin, myocarditis, and aortic disease; after age 35, coronary disease predominates.

The 2025 AHA/ACC scientific statement on competitive sports replaces disqualification-based recommendations with shared decision-making among athlete, clinician, and institution, and no longer treats CPVT as a uniform disqualification. An ICD solely to permit sports is not an indication. Every athletic venue requires an emergency action plan and an AED reachable within minutes.

Commotio cordis is VF triggered by a blunt blow to the precordium (a baseball, hockey puck, or fist) in a structurally normal heart. Experimentally, VF results when the impact falls on the upslope of the T wave, about 30 to 15 ms before its peak. In the US Commotio Cordis Registry, 95% of 216 victims were male (mean age 15 years). Survival rose from 10% before 1994 to 58% in 2006 to 2012, in association with resuscitation within 3 minutes and on-site AED use.

Ventricular arrhythmias in pregnancy

Pregnancy increases ectopy and occasionally unmasks outflow-tract VT, and the postpartum period carries increased risk in long QT syndrome, particularly LQT2. Sustained VT prompts evaluation for peripartum cardiomyopathy, congenital heart disease, and inherited syndromes.

Management of ventricular arrhythmias in pregnancy. Peripartum cardiomyopathy and the wearable defibrillator are covered on the heart failure with reduced ejection fraction page.

Sources of error in wide-complex tachycardia and ventricular arrhythmia care

• Stable blood pressure taken as evidence of SVT: hemodynamic tolerance does not distinguish VT from aberrancy, and verapamil given on that basis can cause collapse.
• Adenosine termination taken as proof of SVT: idiopathic outflow-tract VT also terminates with adenosine.
• AV-nodal blockers in an irregular, very fast wide-complex rhythm: pre-excited atrial fibrillation accelerates and can degenerate to VF.
• Algorithms applied during antiarrhythmic therapy, hyperkalemia, or pacing: drug and metabolic QRS widening and paced complexes defeat the width, axis, and slurred-onset criteria.
• Isoproterenol given for polymorphic VT without a known mechanism: it suppresses Brugada and short QT storms and bradycardia-dependent acquired torsades, but provokes CPVT, congenital LQTS events, and ischemic VT.
• Repeated shocks in electrical storm without interrogation: inappropriate therapy from atrial fibrillation, oversensing, or lead fracture is missed, and sympathetic drive is not addressed.
• An electrolyte abnormality or troponin rise accepted as a fully reversible cause of arrest: survivors without a securely reversible cause remain candidates for a secondary-prevention ICD.
• A normal echocardiogram and coronary angiogram treated as a complete evaluation after unexplained arrest: CMR, serial ECGs, provocative testing, and family screening identify cardiomyopathies and channelopathies.

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