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
Overview
- Effective measures for the primary prevention of sudden cardiac death (SCD) in individuals who are at risk of SCD but have not yet experienced an aborted cardiac arrest or life-threatening arrhythmias include implantable cardioverter defibrillator (ICD) based on the guideline.
- Secondary prevention strategy following aborted sudden cardiac death include revascularization in patients with ischemic heart disease and ICD implantation in patients with reduced left ventricular ejection fraction who had an experience of lethal arrhythmia.
- In absence of noncardiac or reversible causes, an implantable cardioverter-defibrillator (ICD) is recommended because of the high risk of recurrent lethal ventricular arrhythmias. Adjunctive therapy (eg, amiodarone, catheter ablation) and lifestyle modifications for certain genetic arrhythmia syndromes may reduce ventricular arrhythmia recurrence after ICD placement.
Prevention
Primary prevention:
- Effective measures for the primary prevention of sudden cardiac death in individuals who are at risk of SCD but have not yet experienced an aborted cardiac arrest or life-threatening arrhythmias include ICD implantation based on the guideline.[1]
- Secondary prevention strategy following aborted sudden cardiac death include revascularization, ICD implantation.
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.[2],[3]
- 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.[2][1][4]
- 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.[5]
- 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.[6]
- After exclusion of non-cardiac or reversible causes are excluded, sudden cardiac arrest survivors who remain at high risk of recurrent ventricular arrhythmias.[7] ICD implants as secondary prevention is indicated,[8][9][10] 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.[11],[12]
Other methods for secondary prevention:
Adjunctive pharmacotherapy, especially amiodarone,[13],[14] or catheter ablation[13],[15],[16] 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.[17]
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.[2],[18]
- CPVT patients should avoid strenuous exercise and high psychological stress due to increased adrenergic activity.
| 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 [2]
| Recommendations for risk stratification and primary prevention of sudden cardiac death |
| Class I (Level of Evidence: C) |
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| Class I (Level of Evidence: A) |
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| Class IIa (Level of Evidence: B) |
| Class IIa (Level of Evidence: B) |
| Class III (Level of Evidence: A) |
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| Recommendations for primary prevention of sudden cardiac death in arrhythmogenic right ventricular cardiomyopathy |
| Class IIa (Level of Evidence: B) |
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| Class IIa (Level of Evidence: C) |
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| Class IIa (Level of Evidence: C) |
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| Class IIb (Level of Evidence: C) |
| Recommendations for risk stratification and primary prevention of sudden cardiac death |
| Class I (Level of Evidence: C) |
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| Class I (Level of Evidence: A) |
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| Class IIa (Level of Evidence: B) |
| Class IIa (Level of Evidence: B) |
| Class III (Level of Evidence: A) |
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| Recommendations for risk stratification and primary prevention of sudden cardiac death in hypertrophic cardiomyopathy |
| Class I (Level of Evidence: C) |
| Class I (Level of Evidence: B) |
| Class IIa (Level of Evidence: B) |
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| Class IIa (Level of Evidence: B) |
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| 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) |
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| Class I (Level of Evidence: B) |
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| Class IIa (Level of Evidence: B) |
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| Class IIa (Level of Evidence: C) |
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| Class IIa (Level of Evidence: C) |
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| Class IIa (Level of Evidence: C) |
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| Class IIb (Level of Evidence: B) |
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| 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) |
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| Class IIa (Level of Evidence: B) |
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| Class IIa (Level of Evidence: C) |
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| Recommendations for secondary prevention of sudden cardiac death and treatment of ventricular arrhythmias in ARVC |
| Class I (Level of Evidence: B) |
| Class I (Level of Evidence: C) |
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| Class IIa (Level of Evidence: C) |
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| Class IIa (Level of Evidence: B) |
| Class IIa (Level of Evidence: C) |
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| Class IIa (Level of Evidence: C) |
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| Recommendations for secondary prevention of sudden cardiac death and treatment of ventricular arrhythmias in hypertrophic cardiomyopathy |
| Class I (Level of Evidence: B) |
| Class IIa (Level of Evidence: C) |
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| Class IIa (Level of Evidence: C) |
| Class IIb (Level of Evidence: B) |
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Implantable Cardioverter Defibrillator
| Recommendations for implantable cardioverter defibrillator implantation (general aspects) |
| Class I (Level of Evidence: C) |
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| Class III (Level of Evidence: C) |
| Recommendations for subcutaneous implantable cardioverter defibrillator |
| Class IIa (Level of Evidence: B) |
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| Class III (Level of Evidence: C) |
| Recommendations for implantable cardioverter defibrillator implantation in left ventricular non-compaction |
| Class IIa (Level of Evidence: C) |
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| Recommendations for implantable cardioverter defibrillator implantation in patients with cardiac amyloidosis |
| Class IIa (Level of Evidence: C) |
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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): |
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❑ 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 |
| ICD implantation (Class I, Level of Evidence B) : |
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❑ 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) |
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❑ 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) |
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❑ 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 | ||||||||||||||||||||||||||||||||||||||||||||
Timing of Sudden Cardiac Death Following ST-elevation MI
Patients with STEMI are at risk of sudden cardiac death. The timing of sudden cardiac death following STEMI is as follows:
- In the first 3 months after STEMI, one-quarter of sudden cardiac deaths occur. This statistic is critical in so far as implantable cardiac defibrillators are often not implanted in the first three months. It is for this reason that wearable defibrillators are sometimes used in patients with a large MI and reduced ejection fraction.
- In the first year following STEMI, one-half of the sudden cardiac deaths occur.
- Beyond one year, there is still an increased risk of sudden cardiac death for a prolonged period of time.
Medical Therapy to Prevent Sudden Death Following STEMI
- Therapies aimed to reduce disease progression, stabilize plaque, improve left ventricular function, and reduce ischemia may minimize the risk of sudden cardiac death. These therapies include beta blockade, ACE inhibition, and statins.
- Beta blocker administration has been associated with a reduction in sudden cardiac death. [19]. The reduction in SCD was greatest among patients with congestive heart failure.
- Among patients with an ICD, beta blocker administration has been associated with an additional reduction in mortality in MADIT II and a lower frequency of ICD discharge [20].
- ACE inhibitor administration has been associated with reduction in the risk of SCD.[21] .
Angiotensin II Receptor Blockers (ARBs)
- If a patient is intolerant to ACE inhibitor, an ARB can be administered.
- Valsartan is non-inferior to captopril in reducing post MI mortality, and may therefore confer similar benefits in SCD [22].
Statin Therapy
- Among patients with an ICD implanted, statin administration has been associated with a reduction in documented arrhythmias post-MI.[23] [24].
- In the EPHESUS trial, among the specific subgroup of post MI patients who have left ventricular dysfunction and / or diabetes, eplerenone administration was associated with reduction in all cause and SCD mortality (4.9% vs 6.1%)[25].
- Despite the intuitive benefits of anti-arrhythmic treatments, antiarrhythmics have not shown a reduction in all-cause mortality in the management of post MI SCD.
- Amiodarone was associated with a reduction in arrhythmic death among patients with an LVEF of <40% following STEMI, but all cause mortality was not improved in the CAMIAT [26] [27] trial.
- Anti-arrhythmics such as amiodarone may be useful in reducing the frequency of shocks in patients with an ICD who have excessively frequent shocks. Flecainide and *propafenone should not be administered as these Class I C agents are proarrhythmic in patients with coronary artery disease [28].
Induced Hypothermia to Improve Neurological Outcome
- A systematic review by the Cochrane Collaboration suggests benefit.[30]
- A second systematic review focusing on survivors of non-shockable rhythms suggests benefit.[31]
- Patients surviving cardiac arrest who cannot follow commands or who are comatose may have increased chance of favorable neurological outcome if their body temperature is cooled to 32 to 34 degrees centigrade. [32] [33],
Prevention of Sudden Death and Implantable Cardioverter Defibrillators Following STEMI
- 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.
- Patients should also be treated with beta-blockers, ACE inhibitors, and statins.
- Patients undergoing ICD implantation should not have a limited life expectancy due to non-cardiovascular causes.
Role of Electrophysiology Testing
- Inducibiity and pharmacologic suppression of VT/VF on electrophysiologic studies is no longer deemed to be relevant based upon the MUSTT study [34] and the MADITT I study [35].
- Importantly, lack of inducibility on electrophysiological testing should not preclude implantation of an ICD.
- In both SCD-HeFT and MADIT II, the reduction in SCD was greater in patients with a QRS duration > 120 msec.
Wearable Defibrillators
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:
- Symptomatic NYHA Class III or IV congestive heart failure
- A left ventricular ejection fraction < 35%
- Evidence of left ventricular dyssynchrony with a QRS > 120 msec
See also
- Sudden cardiac death
- Sudden cardiac death post arrest care and prevention
- Post cardiac arrest syndrome care pathway
- Therapeutic hypothermia
References
- ↑ 1.0 1.1 Al-Khatib, Sana M.; Stevenson, William G.; Ackerman, Michael J.; Bryant, William J.; Callans, David J.; Curtis, Anne B.; Deal, Barbara J.; Dickfeld, Timm; Field, Michael E.; Fonarow, Gregg C.; Gillis, Anne M.; Granger, Christopher B.; Hammill, Stephen C.; Hlatky, Mark A.; Joglar, José A.; Kay, G. Neal; Matlock, Daniel D.; Myerburg, Robert J.; Page, Richard L. (2018). "2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death". Circulation. 138 (13). doi:10.1161/CIR.0000000000000549. ISSN 0009-7322.
- ↑ 2.0 2.1 2.2 2.3 2.4 Zeppenfeld K, Tfelt-Hansen J, de Riva M, Winkel BG, Behr ER, Blom NA; et al. (2022). "2022 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death". Eur Heart J. 43 (40): 3997–4126. doi:10.1093/eurheartj/ehac262. PMID 36017572 Check
|pmid=value (help). - ↑ Antiarrhythmics versus Implantable Defibrillators (AVID) Investigators. A comparison of antiarrhythmic-drug therapy with implantable defibrillators in patients resuscitated from near-fatal ventricular arrhythmias. N Engl J Med. 1997;337(22):1576-1583. doi:10.1056/ NEJM199711273372202
- ↑ Stout KK, Daniels CJ, Aboulhosn JA, et al. 2018 AHA/ACC Guideline for the management of adults with congenital heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2019;139(14):e698-e800.
- ↑ Dezfulian C, Orkin AM, Maron BA, et al; American Heart Association Council on Cardiopulmonary, Critical Care, Perioperative and Resuscitation; Council on Arteriosclerosis, Thrombosis and Vascular Biology; Council on Cardiovascular and Stroke Nursing; Council on Quality of Care and Outcomes Research;and Council on Clinical Cardiology. Opioid-associated out-of-hospital cardiac arrest: distinctive clinical features and implications for health care and public responses: a scientific statement from the American Heart Association. Circulation. 2021;143 (16):e836-e870. doi:10.1161/CIR. 0000000000000958
- ↑ Ficker DM, So EL, Shen WK, et al. Population-based study of the incidence of sudden unexplained death in epilepsy. Neurology. 1998;51 (5):1270-1274. doi:10.1212/WNL.51.5.1270
- ↑ van der Lingen ACJ, Becker MAJ, Kemme MJB, et al. Reversible cause of cardiac arrest and secondary prevention implantable cardioverter defibrillators in patients with coronary artery disease: value of complete revascularization and LGE-CMR.JAmHeartAssoc.2021;10(8):e019101. doi:10.1161/JAHA.120.019101
- ↑ Antiarrhythmics versus Implantable Defibrillators (AVID) Investigators. A comparison of antiarrhythmic-drug therapy with implantable defibrillators in patients resuscitated from near-fatal ventricular arrhythmias. N Engl J Med.1997;337(22):1576-1583. doi:10.1056/ NEJM199711273372202
- ↑ Connolly SJ, Gent M, Roberts RS, et al. Canadian implantable defibrillator study (CIDS): a randomizedtrial of the implantable cardioverter defibrillator against amiodarone. Circulation. 2000; 101(11):1297-1302. doi:10.1161/01.CIR.101.11.1297
- ↑ Kuck KH, Cappato R, Siebels J, Rüppel R. Randomized comparison of antiarrhythmic drug therapy with implantable defibrillators in patients resuscitated from cardiac arrest: the Cardiac Arrest Study Hamburg(CASH).Circulation. 2000;102(7): 748-754. doi:10.1161/01.CIR.102.7.748
- ↑ Pappone C, Vicedomini G, Manguso F, et al. Wolff-Parkinson-White syndrome in the era of catheter ablation: insights from a registry study of 2169 patients. Circulation. 2014;130(10):811-819. doi:10.1161/CIRCULATIONAHA.114.011154
- ↑ Weiss R, Knight BP, El-Chami M, et al. Impact of age on subcutaneous implantable cardioverter-defibrillator in a large patient cohort: mid-term follow-up. JACC Clin Electrophysiol. 2023; 9(10):2132-2145. doi:10.1016/j.jacep.2023.06.013
- ↑ 13.0 13.1 Kheiri B, Barbarawi M, Zayed Y, et al. Antiarrhythmic drugs or catheter ablation in the management of ventricular tachyarrhythmias in patients with implantable cardioverter defibrillators: a systematic review and meta-analysis of randomized controlled trials. Circ ArrhythmElectrophysiol. 2019;12(11):e007600. doi:10.1161/CIRCEP.119.007600
- ↑ Connolly SJ, Dorian P, Roberts RS, et al; Optimal Pharmacological Therapy in Cardioverter Defibrillator Patients (OPTIC) Investigators. Comparison of beta-blockers, amiodarone plus beta-blockers, or sotalol for prevention of shocks fromimplantable cardioverter defibrillators: the OPTIC Study:a randomized trial. JAMA.2006;295 (2):165-171. doi:10.1001/jama.295.2.165
- ↑ Kuck KH, Tilz RR, Deneke T, et al; SMS Investigators. Impact of substrate modification by catheter ablation on implantable cardioverter-defibrillator interventions in patients with unstable ventricular arrhythmias and coronary artery disease: results from the multicenter randomizedcontrolled SMS (Substrate Modification Study). Circ Arrhythm Electrophysiol. 2017;10(3): e004422.doi:10.1161/CIRCEP.116.004422
- ↑ Sapp JL, Wells GA, Parkash R, et al.Ventricular tachycardia ablation versus escalation of antiarrhythmic drugs. N Engl J Med.2016;375(2): 111-121. doi:10.1056/NEJMoa1513614
- ↑ Zaman S, Sivagangabalan G, Chik W, et al. Ventricular tachyarrhythmia recurrence in primary versus secondary implantable cardioverter defibrillator patients and role of electrophysiology study. J Interv Card Electrophysiol. 2014;41(3): 195-202. doi:10.1007/s10840-014-9941-8
- ↑ Adler A,Topaz G,Heller K,et al.Fever-induced Brugada pattern: how common is it and what does it mean?HeartRhythm.2013;10(9):1375-1382. doi:10.1016/j.hrthm.2013.07.030
- ↑ Nuttall SL, Toescu V, Kendall MJ (2000). "beta Blockade after myocardial infarction. Beta blockers have key role in reducing morbidity and mortality after infarction". BMJ (Clinical Research Ed.). 320 (7234): 581. PMC 1117610. PMID 10688573. Retrieved 2011-02-06. Unknown parameter
|month=ignored (help) - ↑ Brodine WN, Tung RT, Lee JK, Hockstad ES, Moss AJ, Zareba W, Hall WJ, Andrews M, McNitt S, Daubert JP (2005). "Effects of beta-blockers on implantable cardioverter defibrillator therapy and survival in the patients with ischemic cardiomyopathy (from the Multicenter Automatic Defibrillator Implantation Trial-II)". The American Journal of Cardiology. 96 (5): 691–5. doi:10.1016/j.amjcard.2005.04.046. PMID 16125497. Retrieved 2011-02-06. Unknown parameter
|month=ignored (help) - ↑ Domanski MJ, Exner DV, Borkowf CB, Geller NL, Rosenberg Y, Pfeffer MA (1999). "Effect of angiotensin converting enzyme inhibition on sudden cardiac death in patients following acute myocardial infarction. A meta-analysis of randomized clinical trials". Journal of the American College of Cardiology. 33 (3): 598–604. PMID 10080457. Retrieved 2011-02-06. Unknown parameter
|month=ignored (help) - ↑ Pfeffer MA, McMurray JJ, Velazquez EJ, Rouleau JL, Køber L, Maggioni AP, Solomon SD, Swedberg K, Van de Werf F, White H, Leimberger JD, Henis M, Edwards S, Zelenkofske S, Sellers MA, Califf RM (2003). "Valsartan, captopril, or both in myocardial infarction complicated by heart failure, left ventricular dysfunction, or both". The New England Journal of Medicine. 349 (20): 1893–906. doi:10.1056/NEJMoa032292. PMID 14610160. Retrieved 2011-02-06. Unknown parameter
|month=ignored (help) - ↑ Mitchell LB, Powell JL, Gillis AM, Kehl V, Hallstrom AP (2003). "Are lipid-lowering drugs also antiarrhythmic drugs? An analysis of the Antiarrhythmics versus Implantable Defibrillators (AVID) trial". Journal of the American College of Cardiology. 42 (1): 81–7. PMID 12849664. Retrieved 2011-02-06. Unknown parameter
|month=ignored (help) - ↑ Dickinson MG, Ip JH, Olshansky B, Hellkamp AS, Anderson J, Poole JE, Mark DB, Lee KL, Bardy GH (2007). "Statin use was associated with reduced mortality in both ischemic and nonischemic cardiomyopathy and in patients with implantable defibrillators: mortality data and mechanistic insights from the Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT)". American Heart Journal. 153 (4): 573–8. doi:10.1016/j.ahj.2007.02.002. PMID 17383296. Retrieved 2011-02-06. Unknown parameter
|month=ignored (help) - ↑ Pitt B, Remme W, Zannad F, Neaton J, Martinez F, Roniker B, Bittman R, Hurley S, Kleiman J, Gatlin M (2003). "Eplerenone, a selective aldosterone blocker, in patients with left ventricular dysfunction after myocardial infarction". The New England Journal of Medicine. 348 (14): 1309–21. doi:10.1056/NEJMoa030207. PMID 12668699. Retrieved 2011-02-06. Unknown parameter
|month=ignored (help) - ↑ Cairns JA, Connolly SJ, Roberts R, Gent M (1997). "Randomised trial of outcome after myocardial infarction in patients with frequent or repetitive ventricular premature depolarisations: CAMIAT. Canadian Amiodarone Myocardial Infarction Arrhythmia Trial Investigators". Lancet. 349 (9053): 675–82. PMID 9078198. Retrieved 2011-02-04. Unknown parameter
|month=ignored (help) - ↑ Farré J, Romero J, Rubio JM, Ayala R, Castro-Dorticós J (1999). "Amiodarone and "primary" prevention of sudden death: critical review of a decade of clinical trials". The American Journal of Cardiology. 83 (5B): 55D–63D. PMID 10089841. Unknown parameter
|month=ignored (help);|access-date=requires|url=(help) - ↑ Echt DS, Liebson PR, Mitchell LB, Peters RW, Obias-Manno D, Barker AH, Arensberg D, Baker A, Friedman L, Greene HL (1991). "Mortality and morbidity in patients receiving encainide, flecainide, or placebo. The Cardiac Arrhythmia Suppression Trial". The New England Journal of Medicine. 324 (12): 781–8. doi:10.1056/NEJM199103213241201. PMID 1900101. Retrieved 2011-02-07. Unknown parameter
|month=ignored (help) - ↑ ECC Committee, Subcommittees and Task Forces of the American Heart Association (2005). "2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care". Circulation. 112 (24 Suppl): IV1–203. doi:10.1161/CIRCULATIONAHA.105.166550. PMID 16314375.
- ↑ Arrich J, Holzer M, Havel C, Müllner M, Herkner H (2012). "Hypothermia for neuroprotection in adults after cardiopulmonary resuscitation". Cochrane Database Syst Rev. 9: CD004128. doi:10.1002/14651858.CD004128.pub3. PMID 22972067.
- ↑ Kim YM, Yim HW, Jeong SH, Klem ML, Callaway CW (2012). "Does therapeutic hypothermia benefit adult cardiac arrest patients presenting with non-shockable initial rhythms?: A systematic review and meta-analysis of randomized and non-randomized studies". Resuscitation. 83 (2): 188–96. doi:10.1016/j.resuscitation.2011.07.031. PMID 21835145.
- ↑ Hypothermia after Cardiac Arrest Study Group (2002). "Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest". N Engl J Med. 346 (8): 549–56. doi:10.1056/NEJMoa012689. PMID 11856793. Review in: ACP J Club. 2002 Sep-Oct;137(2):46 Review in: Evid Based Nurs. 2002 Oct;5(4):111
- ↑ Bernard SA, Gray TW, Buist MD, Jones BM, Silvester W, Gutteridge G; et al. (2002). "Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia". N Engl J Med. 346 (8): 557–63. doi:10.1056/NEJMoa003289. PMID 11856794.
- ↑ Buxton AE, Lee KL, Fisher JD, Josephson ME, Prystowsky EN, Hafley G (1999). "A randomized study of the prevention of sudden death in patients with coronary artery disease. Multicenter Unsustained Tachycardia Trial Investigators". The New England Journal of Medicine. 341 (25): 1882–90. doi:10.1056/NEJM199912163412503. PMID 10601507. Retrieved 2011-02-06. Unknown parameter
|month=ignored (help) - ↑ Moss AJ, Hall WJ, Cannom DS, Daubert JP, Higgins SL, Klein H, Levine JH, Saksena S, Waldo AL, Wilber D, Brown MW, Heo M (1996). "Improved survival with an implanted defibrillator in patients with coronary disease at high risk for ventricular arrhythmia. Multicenter Automatic Defibrillator Implantation Trial Investigators". The New England Journal of Medicine. 335 (26): 1933–40. doi:10.1056/NEJM199612263352601. PMID 8960472. Retrieved 2011-02-06. Unknown parameter
|month=ignored (help)