Sudden cardiac death post arrest care and prevention

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sara Zand, M.D.[2] Edzel Lorraine Co, DMD, MD[3] Nehal Eid, M.D.[4]

See also Post cardiac arrest syndrome care pathway

Post-Cardiac Arrest Care and Prevention of Sudden Cardiac Death

Post-cardiac arrest care (PCAC) is a critical component of the chain of survival and demands a comprehensive, structured, multidisciplinary system of care. The following sections are organized according to the 2025 American Heart Association (AHA) Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care (Part 11: Post-Cardiac Arrest Care),[1] the 2025 AHA Executive Summary,[2] the 2023 AHA Focused Update on Adult Advanced Cardiovascular Life Support,[3] the 2024 AHA/Neurocritical Care Society Scientific Statement on Critical Care Management of Patients After Cardiac Arrest,[4] the 2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death,[5] the 2022 ESC Guidelines for the Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death,[6] the 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes,[7] and the 2025 ACC/AHA/ASE/HFSA/HRS/SCAI/SCCT/SCMR Appropriate Use Criteria for Implantable Cardioverter-Defibrillators, Cardiac Resynchronization Therapy, and Pacing.[8]

Initial Management

Hemodynamic Stabilization

Hypotension and shock occur in at least two thirds of patients after cardiac arrest.Closing </ref> missing for <ref> tag

Recommendations for temperature control after cardiac arrest (2025 AHA)
Class 1 (Level of Evidence: B-R)

All adults who do not follow commands after ROSC, regardless of arrest location or presenting rhythm, should receive treatment that includes a deliberate strategy for temperature control.[9][2]

Class 1 (Level of Evidence: B-R)

A constant temperature between 32°C and 37.5°C should be selected and maintained during post-arrest temperature control.[9][2]

Class 2a (Level of Evidence: B-R)

A minimum of 36 hours of total temperature control is the shortest recommended duration.[9][2]

Class 2a (Level of Evidence: C-LD)

Cooling through surface or intravascular methods are reasonable alternatives.[9]

Class 2a (Level of Evidence: C-LD)

Patients with spontaneous hypothermia after ROSC who do not follow commands should not be routinely actively or passively rewarmed faster than 0.5°C per hour.[9][3]

Key trial data regarding temperature control:

TTM2 trial (2021): Randomized 1900 patients to 33°C or to normothermia with early treatment of fever (37.8°C) for 28 hours after randomization. There was no difference in the primary outcome of Cerebral Performance Category 1 or 2 at 6 months.[3][10]

CAPITAL CHILL trial: Randomized 389 patients to moderate (31°C) versus mild (34°C) therapeutic hypothermia for 24 hours. The primary outcome of mortality or poor neurological outcome (Disability Rating Scale score >5) at 6 months did not differ across arms.[3]

HYPERION trial (2019): Randomized 584 patients with both in- and out-of-hospital cardiac arrest with an initial nonshockable rhythm. Found a higher percentage of participants surviving with a favorable neurologic outcome compared with targeted normothermia, but there was no significant difference in mortality.[11]

A 2023 updated ILCOR systematic review incorporating 6 additional randomized trials found no difference in survival when applying temperature control at 32°C to 34°C versus 36°C or normothermia; however, the confidence intervals did not exclude a potential beneficial effect of temperature control at colder temperatures. None of the included trials found worse outcomes with lower temperature goals.[9]

An individual patient data meta-analysis of the TTM2 and HYPERION trials found no difference between hypothermic and normothermic temperature control in patients with nonshockable rhythms.[11][9]

Seizure and Myoclonus Management

Seizures and status epilepticus are common acute neurologic complications in the post-cardiac arrest period, occurring in 10% to 35% of patients who do not follow commands after ROSC.Closing </ref> missing for <ref> tag

No MCS device has demonstrated positive results specifically in cardiac arrest patients in randomized trials. MCS use after cardiac arrest should not be routine; in selected patients with cardiogenic shock based on advanced hemodynamic phenotyping, MCS can be considered, balancing the risk of post-arrest severe hypoxic brain injury.[12]

Long-Term Management

Neuroprognostication

Hypoxic-ischemic brain injury is the leading cause of morbidity and mortality in patients who achieve ROSC after OHCA.Closing </ref> missing for <ref> tag

Recommendations for ICD therapy for secondary prevention of SCD
2017 AHA/ACC/HRS Guideline[5]
Class 1 (Level of Evidence: B-R / B-NR)

In patients with ischemic heart disease who either survive sudden cardiac arrest due to VT/VF or experience hemodynamically unstable VT (LOE: B-R) or stable sustained VT (LOE: B-NR) not due to reversible causes, an ICD is recommended if meaningful survival greater than 1 year is expected.[5]

Class 1 (Level of Evidence: B-NR)

In patients with ischemic heart disease and unexplained syncope who have inducible sustained monomorphic ventricular tachycardia on electrophysiological study, an ICD is recommended if meaningful survival of greater than 1 year is expected.[5]

2022 ESC Guideline[6]
Class I (Level of Evidence: A)

ICD therapy for secondary prevention of SCD is recommended in patients with documented VF or hemodynamically poorly tolerated VT in the absence of reversible causes or within 48 hours after myocardial infarction, who are receiving chronic optimal medical therapy and have a reasonable expectation of survival with a good functional status >1 year.[6][8]

Class IIa (Level of Evidence: B)

In patients with coronary artery disease, LVEF ≥40%, and hemodynamically well-tolerated VT, catheter ablation may be considered as an alternative to ICD therapy.[6]

Key evidence for secondary prevention ICD:

A meta-analysis using individual patient data from the AVID, CASH, and CIDS trials comparing ICD therapy versus amiodarone demonstrated a significant reduction in death from any cause with the ICD (hazard ratio 0.72; 95% CI: 0.60–0.87; P = 0.006). This 28% reduction in relative risk of death was almost entirely due to a 50% reduction in risk of arrhythmic death. Patients with an LVEF ≤35% derived significantly more benefit from ICD therapy than those with more preserved LV function.[8]

Although the evidence supporting ICD therapy for secondary prevention is based on randomized trials performed more than 20 years ago, more contemporary registries and observational studies in clinical practice support these findings.[8]

In patients who present with sustained ventricular arrhythmias and a transient or reversible cause (such as acute myocardial infarction, electrolyte abnormalities, or proarrhythmia due to medication), initial treatment should be directed at the underlying disorder and a thorough evaluation is warranted. However, it is often difficult to exclude primary arrhythmic etiologies. In the AVID trial, patients identified as having "potentially transient or potentially correctable" causes of VT/VF remained at high mortality risk.[8]

Among persons presenting with VF due to acute myocardial infarction with coronary plaque rupture and/or thrombus (typically <48 hours), risk of a recurrent event is reduced after early revascularization; ICD is generally not indicated for secondary prevention in this setting.[13]

An alternative to conventional ICD with transvenous leads is a subcutaneous ICD, in which the lead is tunneled subcutaneously instead of passing through the blood vessels. Subcutaneous ICDs have fewer long-term lead-related complications than conventional ICDs and may be reasonable for younger patients with primary arrhythmia syndromes. However, conventional transvenous ICDs are recommended for patients who require pacing for bradyarrhythmias, cardiac resynchronization therapy with coronary sinus lead, or antitachycardia pacing for VT (ESC Class IIa, LOE B).[13][6]

Catheter Ablation for Ventricular Tachycardia

Catheter ablation is an important therapeutic option for the management of recurrent ventricular tachycardia in cardiac arrest survivors, particularly those with ischemic cardiomyopathy.[6][5]

Recommendations for catheter ablation of VT in structural heart disease
2022 ESC Guideline[6]
Class I (Level of Evidence: B)

Catheter ablation is recommended in patients with ischemic heart disease and recurrent VT despite chronic amiodarone therapy, or in patients who are intolerant of or unwilling to take amiodarone.[6]

Class I (Level of Evidence: B)

Catheter ablation is recommended in patients with ischemic heart disease and incessant VT or electrical storm.[6]

2017 AHA/ACC/HRS Guideline[5]
Class 1 (Level of Evidence: B-NR)

Catheter ablation is recommended in patients with ischemic heart disease and recurrent sustained monomorphic VT despite antiarrhythmic drug therapy, including those with VT storm.[5]

Key trial data regarding catheter ablation versus antiarrhythmic drugs:

VANISH2 trial (2025): An international randomized trial of 416 patients with prior myocardial infarction and clinically significant ventricular tachycardia, all with an ICD, compared first-line catheter ablation versus antiarrhythmic drug therapy (sotalol or amiodarone based on prespecified clinical criteria). The primary endpoint was a composite of death from any cause, VT storm, appropriate ICD shock, or sustained VT treated by medical intervention (all >14 days after randomization). Over a median follow-up of 4.3 years, a primary endpoint event occurred in 50.7% of patients assigned to catheter ablation versus 60.6% assigned to drug therapy (hazard ratio 0.75; 95% CI: 0.58–0.97; P = 0.03). Adverse events within 30 days after the procedure included death in 1.0% and nonfatal adverse events in 11.3% of the ablation group, compared with death attributed to drug therapy in 0.5% and nonfatal adverse events in 21.6% of the drug therapy group.[14]

VANISH2 substudy (2026): A prespecified substudy stratified outcomes by drug eligibility. In the sotalol-eligible stratum (199 patients), catheter ablation resulted in a lower risk of the primary composite endpoint compared with sotalol (46% vs. 59%; HR 0.64; 95% CI: 0.43–0.94; P = 0.02). In the amiodarone-eligible stratum (217 patients with more severe heart disease or VT storm), catheter ablation and amiodarone had comparable efficacy for the primary endpoint (55% vs. 61%; HR 0.86; 95% CI: 0.61–1.22; P = NS). However, patients allocated to amiodarone had approximately 3-fold higher noncardiac death (5.6% vs. 16.5%), 2-fold higher respiratory failure (4.6% vs. 11.0%), and a 4.6% incidence of pulmonary fibrosis/infiltrate (vs. 0%) compared with ablation.[15]

Despite ICD implantation, cardiac arrest survivors remain at risk of spontaneous VT or VF, with a reported recurrence rate of 37% during a 2-year follow-up. Adjunctive pharmacotherapy (especially amiodarone) or catheter ablation may be used in combination with ICD.[13]

Recovery and Survivorship

Survivors of cardiac arrest experience emotional, social, physical, neurological, and cognitive sequelae, which can manifest during or after hospitalization. Survivorship is the journey from stabilization through rehabilitation, recovery, and societal reintegration.Closing </ref> missing for <ref> tag

Recommendations for recovery and survivorship after cardiac arrest (2025 AHA)
Class 1 (Level of Evidence: B-NR)

Structured assessment for anxiety, depression, posttraumatic stress, and fatigue is recommended for cardiac arrest survivors and their caregivers.[9][2]

Class 1 (Level of Evidence: C-LD)

Cardiac arrest survivors should have multimodal rehabilitation assessment and treatment for physical, neurological, cardiopulmonary, and cognitive impairments before discharge from the hospital.[9][2]

Class 1 (Level of Evidence: C-LD)

Cardiac arrest survivors and their caregivers should receive comprehensive, multidisciplinary discharge planning, to include medical and rehabilitative treatment recommendations and return to activity/work expectations.[9][2]

Class 2a (Level of Evidence: B-R)

Psychosocial interventions for cardiac arrest survivors and their caregivers are reasonable to reduce emotional distress.[9]

Class 2a (Level of Evidence: C-LD)

Well-being interventions or referrals for follow-up mental health services for health care professionals who care for cardiac arrest patients are reasonable to mitigate distress and burnout.[9]

Key points regarding recovery and survivorship:

Approximately one fourth of cardiac arrest survivors and their caregivers experience emotional distress, including anxiety, depression, and posttraumatic stress. Fatigue is also common and may be related to distress and physical and cognitive symptoms. These symptoms often begin during hospitalization and can persist from months to years.[9]

Cognitive impairments, particularly in memory, attention, and executive function, are common in cardiac arrest survivors. Physical, neurological, and cardiopulmonary impairments are also prevalent.[9]

Community reintegration and return to work or other daily activities may be slow and depend on availability of social support and degree of post-arrest sequelae. Survivors and caregivers need direction on managing their post-arrest challenges and returning to daily activities.[9]

An RCT of semistructured cognitive, medical, and psychosocial support offered to adult OHCA and IHCA survivors for 6 months after discharge demonstrated significant improvement in multiple domains of quality of life at 12 months compared with no intervention, and was found to be potentially cost-effective.[16]

Clinically significant depression has been reported in 8% to 45%, anxiety in 13% to 42%, and posttraumatic stress disorder (PTSD) in 19% to 27% of cardiac arrest survivors. In the longest follow-up reported (up to 8 years), PTSD was noted in 27% of survivors, with these individuals also reporting lower quality of life, more limited self-care, and more pain and depressed mood.[17]

Organ Donation

Patients with cardiac arrest make up an important pool of potential organ donors because cardiac arrest is common and a substantial proportion of those who cannot recover are still able to donate.Closing </ref> missing for <ref> tag

Extracorporeal perfusion can be initiated after failed CPR specifically to facilitate uncontrolled DCD in patients deemed to have no possibility of recovery. In the United States, the default position is an opt-in approach in which patients are presumed not to be organ donors unless they have specified a wish to do so. Ethical considerations include maintaining public trust, ensuring that decisions for end-of-life care are made independently of organ donation considerations, and equitable distribution of resources.[18]

Special Populations

Primary Prevention of SCD in Heart Failure with Reduced Ejection Fraction

Sudden cardiac death is a leading cause of death in patients with heart failure with reduced ejection fraction (HFrEF). ICD therapy for primary prevention is recommended in select patients with reduced LVEF despite guideline-directed medical therapy (GDMT).[5][6][1]

Recommendations for primary prevention ICD in HFrEF
2022 AHA/ACC/HFSA Heart Failure GuidelineClosing </ref> missing for <ref> tag

Identification of specific arrhythmogenic genetic variants such as LMNA/C, desmosomal proteins, phospholamban, and Filamin-C carry implications for implantation of ICDs for primary prevention of sudden death even in patients who have LVEF >35% or <3 months of GDMT.[19]

Nearly 80% of the >300,000 ICDs inserted annually in the United States are for primary prevention. Although NYHA functional class, heart failure etiology, recent coronary revascularization, medical therapy, and likelihood of meaningful survival >1 year are considered when determining eligibility for an ICD, LVEF is the first major branch point in decision making.[20]

Cardiac Resynchronization Therapy

Cardiac resynchronization therapy (CRT) is recommended in select patients with heart failure, reduced LVEF, and QRS prolongation to reduce mortality, reduce hospitalizations, and improve symptoms and quality of life.Closing </ref> missing for <ref> tag

Secondary prevention:

  • Myocardial Infarcation: The optimal approach to prevention of SCD following ST-elevation MI (STEMI) has been evaluated in multiple randomized trials. In general, post-STEMI patients should be treated with evidence-based therapies that have been associated with a reduction in SCD including beta-blockers, ACE-inhibitors (or ARBs in patients who are ACEI intolerant) and statins.
  • VF due to acute MI with coronary plaque rupture and/or thrombus (typically <48 hours), risk of a recurrent event is reduced after early revascularization such as percutaneous coronary intervention. Implantable cardioverter-defibrillator (ICD) is not indicated for secondary prevention.[6],[21]
  • Heart failure: In patients who have symptomatic congestive heart failure (CHF), an aldosterone antagonist may be a reasonable additional therapy. Despite the intuitive benefits of antiarrhythmic, amiodarone and sotalol have not been shown to reduce all-cause mortality following STEMI, although amiodarone may be useful in reducing the frequency of shocks in patients with ICDs who have unacceptably high rates of shock.
  • In general terms, ICD placement is indicated in those patients with a reduced left ventricular ejection fraction at 40 days post-MI and/or 3 months following revascularization (PCI or CABG) for STEMI given the survival benefits in this population.
  • Coronary anomalies: Surgical intervention is recommended to survivors with coronary anomalies such as congenital left main artery atresia and anomalous aortic origin of a coronary artery to prevent recurrence.[6][22][23]
  • Toxins: .If the cardiac arrest involved stimulants or supplements, avoidance of these substances can prevent recurrence. For patients with an event caused by an opioid overdose, counseling, education, and medications to treat opioid use disorder (eg, buprenorphine, methadone, and naltrexone) are recommended to decrease the risk of recurrence.[24]
  • Epilepsy: Survivors with a previously undiagnosed seizure disorder should be treated and closely followed up given a more than 20-fold higher risk of sudden unexplained death in persons with epilepsy compared with the general population.[25]
  • After exclusion of non-cardiac or reversible causes are excluded, sudden cardiac arrest survivors who remain at high risk of recurrent ventricular arrhythmias.[26] ICD implants as secondary prevention is indicated,[27][28][29] particularly for those diagnosed with structural heart disease, such as dilated cardiomyopathy, or arrhythmia syndromes, such as LQTS, Brugada syndrome, and CPVT.
  • Subcutaneous ICD is an alternative to conventional ICD with transvenous leads.Subcutaneous ICDs have fewer long-term lead-related complications,so they may be reasonable for younger patients with primary arrhythmia syndromes. However, according to recent ESC guidelines (classIIa,levelB), conventional transvenous ICDs are recommended for patients who require pacing for bradyarrhythmias or LQTS, cardiac resynchronization therapy with coronary sinus lead, or antitachycardia pacing for VT.[30],[31]

Other methods for secondary prevention:

Adjunctive pharmacotherapy, especially amiodarone,[32],[33] or catheter ablation[32],[34],[35] may be used in com bination with ICD.This based on the fact that survivors with ICD placement remain at risk of spontaneous VT or VF, with a reported recurrence rate of 37% during a 2-year follow-up among Australian adults.[36]

Prevention in primary arrythmia syndromes:

  • Certain medications and lifestyle habits such as exercise should be avoided in patients with specific primary arrhythmia syndromes:
  • LQTS patients should avoid QT-prolonging medications (eg, ciprofloxacin and odansetron) and genotype-specific triggers that increase ventricular arrhythmia risk (strenuous exercise in LQT type 1 [LQT1]; emotions such as extreme stress or fear, and sudden loud noise in LQT2) should be avoided.
  • Brugada syndrome patients should avoid excessive alcohol use and certain drugs (eg,tricyclic antidepressants,class 1A or class 1C antiarrhythmics such as procainamide or flecainide, cocaine, and other drugs; see https://www.brugadadrugs.org/drug-lists/). Fever (temperature >38.0°C) increases VF in Brugada syndrome. It should be promptly reduced with antipyretics.[6],[37]
  • CPVT patients should avoid strenuous exercise and high psychological stress due to increased adrenergic activity.
Secondary Prevention in Young Adult Survivors of Sudden Cardiac Arrest[6]
Strength of recommendationa General SCA Idiopathic VF Long QT syndrome Brugada syndrome Catechol aminergic General polymorphic VT Coronary anomalies Vasospastic angina Chronic CAD Dilated or hypokinetic nondilated cardio myopathy Arrhythmo genic right ventricular cardio myopathy Hypertrophic cardio myopathy Myocarditis Cardiac sarcoidosis
I ICD ICD ICD with β-blockerb; LCSDc; Avoid QT-prolonging drugs, genotype specific triggers for arrhythmias; Electrolytes correction ICD; avoid cocaine, excessive alcohol intake, or drugs that may induce ST elevation in right precordial leads; fever control ICD with β-blocker and flecainide; avoid precipitants such as competitive sports, strenuous exercise, and stressful environments Surgery ICDd ICD ICD with β-blocker ICD ICD in chronic phase ICD
IIa ICD or LCSDe LCSD ICD
IIb Amiodarone; ablation (otherwise see specific etiologies)c Ablation with ICD Antiar rhythmics in acute phaseg
III Invasive EPSh Antiarrhthmics High-intensity exercisei

aClass I indicates strong evidence or consensus that a procedure or treatmentis beneficial (“recommended” or “indicated”); class IIa, weight of evidence in favor of its efficacy (“should be considered”); class IIb, the efficacy is less well established by evidence or consensus (“may beconsidered”); and class III, evidence or consensus shows the procedure or treatment is ineffective or potentially harmful (“not recommended”).

bMexiletine for long QT type 3 instead of β-blocker.

cWhen ICD therapy is unavailable, contraindicated, or declined treat with amiodarone or ablation.

dMorethan48hoursaftermyocardialinfarction.

eWhen β-blocker or genotype-specific therapies are not tolerated or contraindicated at the therapeutic dose.

fWhen β-blocker and flecainide are either not effective, not tolerated, or contraindicated.

gAmiodarone and β-blocker.

hTo evaluate for ventricular arrhythmias and arrhythmia syndromes such as Wolff-Parkinson-White syndrome or Brugada syndrome that can precipitate sudden cardiac arrest.

iIn cases of LMNA variants.

2022 ESC Guidelines for the management of patients with ventricular arrythymias and the prevention of sudden cardiac death [6]

Recommendations for risk stratification and primary prevention of sudden cardiac death
Class I (Level of Evidence: C)
Class I (Level of Evidence: A)
Class IIa (Level of Evidence: B)
Class IIa (Level of Evidence: B)
Class III (Level of Evidence: A)
Recommendations for primary prevention of sudden cardiac death in arrhythmogenic right ventricular cardiomyopathy
Class IIa (Level of Evidence: B)
Class IIa (Level of Evidence: C)
Class IIa (Level of Evidence: C)
Class IIb (Level of Evidence: C)
Recommendations for risk stratification and primary prevention of sudden cardiac death
Class I (Level of Evidence: C)
Class I (Level of Evidence: A)
Class IIa (Level of Evidence: B)
Class IIa (Level of Evidence: B)
Class III (Level of Evidence: A)
Recommendations for risk stratification and primary prevention of sudden cardiac death in hypertrophic cardiomyopathy
Class I (Level of Evidence: C)
  • It is recommended that the 5-year risk of SCD is assessed at first evaluation and at 1-3 year intervals, or when there is a change in clinical status.
Class I (Level of Evidence: B)
Class IIa (Level of Evidence: B)
Class IIa (Level of Evidence: B)
Class IIb (Level of Evidence: B)
Class IIb (Level of Evidence: B)
Recommendations for secondary prevention of sudden cardiac death and treatment of ventricular arrhythmias
Class I (Level of Evidence: A)
Class I (Level of Evidence: B)
Class IIa (Level of Evidence: B)
Class IIa (Level of Evidence: C)
Class IIa (Level of Evidence: C)
Class IIa (Level of Evidence: C)
Class IIb (Level of Evidence: B)
Recommendations for secondary prevention of sudden cardiac death and treatment of ventricular arrhythmias
Class I (Level of Evidence: B)
Class IIa (Level of Evidence: C)
Class IIa (Level of Evidence: B)
Class IIa (Level of Evidence: C)
Recommendations for secondary prevention of sudden cardiac death and treatment of ventricular arrhythmias in ARVC
Class I (Level of Evidence: B)
  • ICD [[[implantation]] is recommended in [[[ARVC]] patients with hemodynamically not-tolerated VT or VF.
Class I (Level of Evidence: C)
Class IIa (Level of Evidence: C)
Class IIa (Level of Evidence: B)
Class IIa (Level of Evidence: C)
Class IIa (Level of Evidence: C)
Recommendations for secondary prevention of sudden cardiac death and treatment of ventricular arrhythmias in hypertrophic cardiomyopathy
Class I (Level of Evidence: B)
  • ICD [[[implantation]] is recommended in HCM patients with hemodynamically not-tolerated VT or VF.
Class IIa (Level of Evidence: C)
Class IIa (Level of Evidence: C)
Class IIb (Level of Evidence: B)

Implantable Cardioverter Defibrillator

Recommendations for implantable cardioverter defibrillator implantation (general aspects)
Class I (Level of Evidence: C)
Class III (Level of Evidence: C)
Recommendations for subcutaneous implantable cardioverter defibrillator
Class IIa (Level of Evidence: B)
Class III (Level of Evidence: C)
Recommendations for implantable cardioverter defibrillator implantation in left ventricular non-compaction
Class IIa (Level of Evidence: C)
Recommendations for implantable cardioverter defibrillator implantation in patients with cardiac amyloidosis
Class IIa (Level of Evidence: C)
Recommendation for diagnosis and management of ventricular arryhthmia in neuromuscular diseases
Class I (Level of Evidence: C)
Class I (Level of Evidence: C)
Class IIa (Level of Evidence: B)
Class IIa (Level of Evidence: B)
Class IIa (Level of Evidence: C)
Class IIa (Level of Evidence: C)
Class IIa (Level of Evidence: C)
Class IIb (Level of Evidence: C)
Class IIb (Level of Evidence: C)
Class III (Level of Evidence: C)

2017AHA/ACC/HRS Guideline for management of sudden cardiac arrest and ventricular arrhythmia

Abbreviations: MI: Myocardial infarction; VT: Ventricular tachycardia; VF: Ventricular fibrillation; LVEF: Left ventricular ejection fraction; ICD: Implantable cardioverter defibrillator; NYHA: New York Heart Association functional classification; LVAD: Left ventricular assist device; EPS: Electrophysiology study

Recommendations for primary prevention of sudden cardiac death in ischemic heart disease
ICD implantation (Class I, Level of Evidence A):

❑ In patients with LVEF≤ 35% and NYHA class 2,3 heart failure despite medical therapy, at least 40 days post MI or 90 days post revascularization with life expectancy > 1 year
1 year

ICD implantation (Class I, Level of Evidence B) :

❑ In patients with LVEF ≤ 40% and nonsustained VT due to prior MI or VT ,VF inducible in EPS with life expectancy >1 year

ICD implantation : (Class IIa, Level of Evidence B)

❑ In patients with NYHA class 4 who are candidates for cardiac transplantation or LVAD with life expectancy > 1 year

(Class III, Level of Evidence C)

ICD is not beneficial in patients with NYHA class 4 despite optimal medical therapy who are not candidates for cardiac transplantation or LVAD


 
 
 
 
 
 
Secondary prevention in patients with IHD
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
SCA survivor or sustained monomorph VT
 
 
 
Cardiac syncope
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Ischemia
 
 
 
LVEF≤35%
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Yes: revascularization, reassessment about SCD risk (class1)
 
NO:ICD candidate
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Yes:ICD (class1)
 
NO: medical therapy (class1)
 
 
Yes:ICD (CLASS1)
 
NO:EP study (class 2a)
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Ventriculat arrhythmia induction
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Yes: ICD (class1)
 
NO: monitoring
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 


Patients with STEMI are at risk of sudden cardiac death. The timing of sudden cardiac death following STEMI is as follows:

Medical Therapy to Prevent Sudden Death Following STEMI

Angiotensin II Receptor Blockers (ARBs)

Statin Therapy

Induced Hypothermia to Improve Neurological Outcome

[48]

Role of Electrophysiology Testing

The Benefit of ICD Implantation May Be Greater in Patients with a QRS Duration > 120 msec

  • In both SCD-HeFT and MADIT II, the reduction in SCD was greater in patients with a QRS duration > 120 msec.

In patients with a large MI with a low EF who are awaiting permanent ICD implantation, the use of a wearable defibrillator is a reasonable strategy.

Cardiac resynchronization therapy (CRT) Combined with ICD Placement

Based upon the results of the COMPANION trial it is reasonable to place a combined ICD / CRT device in patients with the following:

See also

References

  1. 1.0 1.1 PCAC2025">Hirsch KG, Amorim E, Coppler PJ, et al. (2025). "Part 11: Post-Cardiac Arrest Care: 2025 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care". Circulation. 152 (16suppl2): S673–S718. doi:10.1161/CIR.0000000000001375.
  2. 2.0 2.1 2.2 2.3 2.4 2.5 2.6 Del Rios M, Bartos JA, Panchal AR, et al. (2025). "Part 1: Executive Summary: 2025 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care". Circulation. 152 (16suppl2): S284–S312. doi:10.1161/CIR.0000000000001372. PMID 41122893 Check |pmid= value (help).
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