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==Prevention of Sudden Cardiac Death==
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With positive outcomes following cardiac arrest so unlikely, a great deal of effort has been spent in finding effective strategies to prevent cardiac arrest.


As noted above, one of the prime causes of cardiac arrest outside of hospital is [[ischemic heart disease]]. Vast resources have been put into trying to reduce cardiovascular risks across much of the developed world. In particular schemes have been put in place to promote a [[healthy diet]] and [[exercise]]. For people considered to be particularly at risk of heart disease, measures such as [[blood pressure]] control, prescription of [[cholesterol]] lowering medications, and other medico-therapeutic interventions, have been widely used. A [[magnesium deficiency (medicine)|magnesium deficiency]], or lower levels of [[magnesium]], can contribute to heart disease and a [[healthy diet]] that contains adequte [[magnesium]] may help prevent heart disease.<ref name="pmid15466951">{{cite journal |author=Rosanoff A, Seelig MS |title=Comparison of mechanism and functional effects of magnesium and statin pharmaceuticals |journal=J Am Coll Nutr |volume=23 |issue=5 |pages=501S–505S |year=2004 |month=October |pmid=15466951 |doi= |url=http://www.jacn.org/cgi/pmidlookup?view=long&pmid=15466951}}</ref> [[Magnesium]] can be used to enhance long term treatment, so it may be effective in long term prevention.<p>
{{SI}}


Patients in hospital are far less likely to have a cardiac arrest caused of primary cardiac origin, and hence present in Asystole or PEA, and have bleak outcomes. Extensive research has shown that patients in general wards often deteriorate for several hours or even days before a cardiac arrest occurs <ref name="pmid15325446">{{cite journal |author=Kause J, Smith G, Prytherch D, Parr M, Flabouris A, Hillman K |title=A comparison of antecedents to cardiac arrests, deaths and emergency intensive care admissions in Australia and New Zealand, and the United Kingdom--the ACADEMIA study |journal=Resuscitation |volume=62 |issue=3 |pages=275–82 |year=2004 |month=September |pmid=15325446 |doi=10.1016/j.resuscitation.2004.05.016 |url=}}</ref>. This has been attributed to a lack of knowledge and skill amongst ward based staff, in particular a failure to carry out measurement of the [[Respiratory rate]], which is often the major predictor of a deterioration and can often change up to 48 hours prior to a cardiac arrest. In response to this, many hospitals now have increased training for ward based staff. A number of "early warning" systems also exist which aim to quantify the risk which patients are at of deterioration based on their [[vital signs]] and thus provide a guide to staff. In addition, specialist staff are being utilised more effectively in order to augment the work already being done at ward level. These include:
{{CMG}}
* '''Crash teams''' (also known as '''Code teams''') - These are designated staff members who have particular expertise in resuscitation, who are called to the scene of all arrests within the hospital.
 
* '''Medical Emergency Teams''' - These teams respond to all emergencies, with the aim of treating the patient in the acute phase of their illness in order to prevent a cardiac arrest.
==Timing of Sudden Cardiac Death Following ST elevation MI ==
* '''Critical care outreach''' - As well as providing the services of the other two types of team, these teams are also responsible for educating non-specialist staff. In addition, they help to facilitate transfers between [[Intensive care unit|intensive care/high dependency units]] and the general hospital wards. This is particularly important, as many studies have shown that a significant percentage of patients discharged from critical care environments quickly deteriorate and are re-admitted - the outreach team offers support to ward staff to prevent this from happening.
 
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 Blockers===
 
[[Beta blocker]] administration has been associated with a reduction in sudden cardiac death from  5.0% to 3.3% in a review of 13 trials <ref name="pmid10688573">{{cite journal | author = Nuttall SL, Toescu V, Kendall MJ | title = beta Blockade after myocardial infarction. Beta blockers have key role in reducing morbidity and mortality after infarction | journal = [[BMJ (Clinical Research Ed.)]] | volume = 320 | issue = 7234 | pages = 581 | year = 2000 | month = February | pmid = 10688573 | pmc = 1117610 | doi = | url = http://bmj.com/cgi/pmidlookup?view=long&pmid=10688573 | issn = | accessdate = 2011-02-06}}</ref>.  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 (hazard ratio of 0.42 to 0.44) and a lower frequency of ICD discharge (hazard ratio of 0.48) <ref name="pmid16125497">{{cite journal | author = Brodine WN, Tung RT, Lee JK, Hockstad ES, Moss AJ, Zareba W, Hall WJ, Andrews M, McNitt S, Daubert JP | title = 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) | journal = [[The American Journal of Cardiology]] | volume = 96 | issue = 5 | pages = 691–5 | year = 2005 | month = September | pmid = 16125497 | doi = 10.1016/j.amjcard.2005.04.046 | url = http://linkinghub.elsevier.com/retrieve/pii/S0002-9149(05)00942-2 | issn = | accessdate = 2011-02-06}}</ref>.
===ACE inhibition===
 
[[ACE inhibitor]] administration has been associated with a 20% relative and a 1.4% absolute reduction in the risk of SCD in a metanalysis of randomized trials<ref name="pmid10080457">{{cite journal | author = Domanski MJ, Exner DV, Borkowf CB, Geller NL, Rosenberg Y, Pfeffer MA | title = Effect of angiotensin converting enzyme inhibition on sudden cardiac death in patients following acute myocardial infarction. A meta-analysis of randomized clinical trials | journal = [[Journal of the American College of Cardiology]] | volume = 33 | issue = 3 | pages = 598–604 | year = 1999 | month = March | pmid = 10080457 | doi = | url = http://linkinghub.elsevier.com/retrieve/pii/S0735-1097(98)00609-3 | issn = | accessdate = 2011-02-06}}</ref> .
 
===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 <ref name="pmid14610160">{{cite journal | author = 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 | title = Valsartan, captopril, or both in myocardial infarction complicated by heart failure, left ventricular dysfunction, or both | journal = [[The New England Journal of Medicine]] | volume = 349 | issue = 20 | pages = 1893–906 | year = 2003 | month = November | pmid = 14610160 | doi = 10.1056/NEJMoa032292 | url = http://dx.doi.org/10.1056/NEJMoa032292 | issn = | accessdate = 2011-02-06}}</ref>.
 
===Statin Therapy===
 
Among patients with an ICD implanted, statin administration has been associated with a reduction in documented arrhythmias post-MI in observation studies <ref name="pmid12849664">{{cite journal | author = Mitchell LB, Powell JL, Gillis AM, Kehl V, Hallstrom AP | title = Are lipid-lowering drugs also antiarrhythmic drugs? An analysis of the Antiarrhythmics versus Implantable Defibrillators (AVID) trial | journal = [[Journal of the American College of Cardiology]] | volume = 42 | issue = 1 | pages = 81–7 | year = 2003 | month = July | pmid = 12849664 | doi = | url = http://linkinghub.elsevier.com/retrieve/pii/S0735109703004984 | issn = | accessdate = 2011-02-06}}</ref> <ref name="pmid17383296">{{cite journal | author = Dickinson MG, Ip JH, Olshansky B, Hellkamp AS, Anderson J, Poole JE, Mark DB, Lee KL, Bardy GH | title = 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) | journal = [[American Heart Journal]] | volume = 153 | issue = 4 | pages = 573–8 | year = 2007 | month = April | pmid = 17383296 | doi = 10.1016/j.ahj.2007.02.002 | url = http://linkinghub.elsevier.com/retrieve/pii/S0002-8703(07)00122-6 | issn = | accessdate = 2011-02-06}}</ref>.
 
===Aldosterone antagonists===
 
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%)<ref name="pmid12668699">{{cite journal | author = Pitt B, Remme W, Zannad F, Neaton J, Martinez F, Roniker B, Bittman R, Hurley S, Kleiman J, Gatlin M | title = Eplerenone, a selective aldosterone blocker, in patients with left ventricular dysfunction after myocardial infarction | journal = [[The New England Journal of Medicine]] | volume = 348 | issue = 14 | pages = 1309–21 | year = 2003 | month = April | pmid = 12668699 | doi = 10.1056/NEJMoa030207 | url = http://dx.doi.org/10.1056/NEJMoa030207 | issn = | accessdate = 2011-02-06}}</ref>.


===Prevention of Sudden Death and Implantable Cardioverter Defibrillators Following STEMI===
===Prevention of Sudden Death and Implantable Cardioverter Defibrillators Following STEMI===

Revision as of 01:43, 7 February 2011

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]

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 Blockers

Beta blocker administration has been associated with a reduction in sudden cardiac death from 5.0% to 3.3% in a review of 13 trials [1]. 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 (hazard ratio of 0.42 to 0.44) and a lower frequency of ICD discharge (hazard ratio of 0.48) [2].

ACE inhibition

ACE inhibitor administration has been associated with a 20% relative and a 1.4% absolute reduction in the risk of SCD in a metanalysis of randomized trials[3] .

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 [4].

===Statin Therapy===

Among patients with an ICD implanted, statin administration has been associated with a reduction in documented arrhythmias post-MI in observation studies [5] [6].

Aldosterone antagonists

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%)[7].

Prevention of Sudden Death and Implantable Cardioverter Defibrillators Following STEMI

  • The majority, but not all trials indicate that there is a benefit to placement of an ICD after the first three months of survival following STEMI in patients with a reduced LVEF at 3 months.
  • The DINAMIT [8] and IRIS [9] trials did not show a benefit of ICD placement during the first 3 months after STEMI.
  • Likewise, it should be noted that MADITT II [10] excluded patients who had an MI or revascularization within the preceding 40 days.
  • Amiodarone was associated with a reduction in arrhythmic death among patients with an LVEF of <40% following STEMI, but all cause mortality was not imprlved in the CAMIAT [11] [12] trial.
  • An external cardiac defibrillator vest can be prescribed in high risk patients with a low ejection fraction while the patient is awaiting assessment of their LVEF at 3 months.

Wearable Defibrillators

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

Prevention of Sudden Cardiac Death

ACC / AHA Guidelines- Recommendations for Implantable Cardioverter Defibrillators (DO NOT EDIT) [13]

Class I

1. ICD therapy is indicated in patients who are survivors of cardiac arrest due to VF or hemodynamically unstable sustained VT after evaluation to define the cause of the event and to exclude any completely reversible causes. (Level of Evidence: A)

2. ICD therapy is indicated in patients with structural heart disease and spontaneous sustained VT, whether hemodynamically stable or unstable. (Level of Evidence: B)

3. ICD therapy is indicated in patients with syncope of undetermined origin with clinically relevant, hemodynamically significant sustained VT or VF induced at electrophysiological study. (Level of Evidence: B)

4. ICD therapy is indicated in patients with LVEF less than 35% due to prior MI who are at least 40 days post-MI and are in NYHA functional Class II or III. (Level of Evidence: A)

5. ICD therapy is indicated in patients with nonischemic DCM who have an LVEF less than or equal to 35% and who are in NYHA functional Class II or III. (Level of Evidence: B)

6. ICD therapy is indicated in patients with LV dysfunction due to prior MI who are at least 40 days post-MI, have an LVEF less than 30%, and are in NYHA functional Class I. (Level of Evidence: A)

7. ICD therapy is indicated in patients with nonsustained VT due to prior MI, LVEF less than 40%, and inducible VF or sustained VT at electrophysiological study. (Level of Evidence: B)

Class IIa

1. ICD implantation is reasonable for patients with unexplained syncope, significant LV dysfunction, and nonischemic DCM. (Level of Evidence: C)

2. ICD implantation is reasonable for patients with sustained VT and normal or near-normal ventricular function. (Level of Evidence: C)

3. ICD implantation is reasonable for patients with HCM who have 1 or more major{dagger} risk factors for SCD. (Level of Evidence: C)

4. ICD implantation is reasonable for the prevention of SCD in patients with ARVD/C who have 1 or more risk factors for SCD. (Level of Evidence: C)

5. ICD implantation is reasonable to reduce SCD in patients with long-QT syndrome who are experiencing syncope and/or VT while receiving beta blockers. (Level of Evidence: B)

6. ICD implantation is reasonable for non hospitalized patients awaiting transplantation. (Level of Evidence: C)

7. ICD implantation is reasonable for patients with Brugada syndrome who have had syncope. (Level of Evidence: C)

8. ICD implantation is reasonable for patients with Brugada syndrome who have documented VT that has not resulted in cardiac arrest. (Level of Evidence: C)

9. ICD implantation is reasonable for patients with catecholaminergic polymorphic VT who have syncope and/or documented sustained VT while receiving beta blockers. (Level of Evidence: C)

10. ICD implantation is reasonable for patients with cardiac sarcoidosis, giant cell myocarditis, or Chagas disease. (Level of Evidence: C)

Class IIb

1. ICD therapy may be considered in patients with nonischemic heart disease who have an LVEF of less than or equal to 35% and who are in NYHA functional Class I. (Level of Evidence: C)

2. ICD therapy may be considered for patients with long-QT syndrome and risk factors for SCD. (Level of Evidence: B)

3. ICD therapy may be considered in patients with syncope and advanced structural heart disease in whom thorough invasive and noninvasive investigations have failed to define a cause. (Level of Evidence: C)

4. ICD therapy may be considered in patients with a familial cardiomyopathy associated with sudden death. (Level of Evidence: C)

5. ICD therapy may be considered in patients with LV noncompaction. (Level of Evidence: C)

Class III

1. ICD therapy is not indicated for patients who do not have a reasonable expectation of survival with an acceptable functional status for at least 1 year, even if they meet ICD implantation criteria specified in the Class I, IIa, and IIb recommendations above. (Level of Evidence: C)

2. ICD therapy is not indicated for patients with incessant VT or VF. (Level of Evidence: C)

3. ICD therapy is not indicated in patients with significant psychiatric illnesses that may be aggravated by device implantation or that may preclude systematic follow-up. (Level of Evidence: C)

4. ICD therapy is not indicated for NYHA Class IV patients with drug-refractory congestive heart failure who are not candidates for cardiac transplantation or CRT-D. (Level of Evidence: C)

5. ICD therapy is not indicated for syncope of undetermined cause in a patient without inducible ventricular tachyarrhythmias and without structural heart disease. (Level of Evidence: C)

6. ICD therapy is not indicated when VF or VT is amenable to surgical or catheter ablation (e.g., atrial arrhythmias associated with the Wolff-Parkinson-White syndrome, RV or LV outflow tract VT, idiopathic VT, or fascicular VT in the absence of structural heart disease). (Level of Evidence: C)

7. ICD therapy is not indicated for patients with ventricular tachyarrhythmias due to a completely reversible disorder in the absence of structural heart disease (e.g., electrolyte imbalance, drugs, or trauma). (Level of Evidence: B)

ACC / AHA Guidelines- Recommendations for Implantable Cardioverter-Defibrillators in Pediatric Patients and Patients With Congenital Heart Disease (DO NOT EDIT) [13]

Class I

1. ICD implantation is indicated in the survivor of cardiac arrest after evaluation to define the cause of the event and to exclude any reversible causes. (Level of Evidence: B)

2. ICD implantation is indicated for patients with symptomatic sustained VT in association with congenital heart disease who have undergone hemodynamic and electrophysiological evaluation. Catheter ablation or surgical repair may offer possible alternatives in carefully selected patients. (Level of Evidence: C)

Class IIa

1. ICD implantation is reasonable for patients with congenital heart disease with recurrent syncope of undetermined origin in the presence of either ventricular dysfunction or inducible ventricular arrhythmias at electrophysiological study. (Level of Evidence: B)

Class IIb

1. ICD implantation may be considered for patients with recurrent syncope associated with complex congenital heart disease and advanced systemic ventricular dysfunction when thorough invasive and noninvasive investigations have failed to define a cause. (Level of Evidence: C)

Class III

1. All Class III recommendations found in Section 3, "Indications for Implantable Cardioverter-Defibrillator Therapy," apply to pediatric patients and patients with congenital heart disease, and ICD implantation is not indicated in these patient populations. (Level of Evidence: C)

References

  1. 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)
  2. 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)
  3. 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)
  4. 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)
  5. 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)
  6. 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)
  7. 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)
  8. Hohnloser SH, Kuck KH, Dorian P, Roberts RS, Hampton JR, Hatala R, Fain E, Gent M, Connolly SJ (2004). "Prophylactic use of an implantable cardioverter-defibrillator after acute myocardial infarction". The New England Journal of Medicine. 351 (24): 2481–8. doi:10.1056/NEJMoa041489. PMID 15590950. Retrieved 2011-02-04. Unknown parameter |month= ignored (help)
  9. Steinbeck G, Andresen D, Seidl K, Brachmann J, Hoffmann E, Wojciechowski D, Kornacewicz-Jach Z, Sredniawa B, Lupkovics G, Hofgärtner F, Lubinski A, Rosenqvist M, Habets A, Wegscheider K, Senges J (2009). "Defibrillator implantation early after myocardial infarction". The New England Journal of Medicine. 361 (15): 1427–36. doi:10.1056/NEJMoa0901889. PMID 19812399. Retrieved 2011-02-04. Unknown parameter |month= ignored (help)
  10. Moss AJ, Zareba W, Hall WJ, Klein H, Wilber DJ, Cannom DS, Daubert JP, Higgins SL, Brown MW, Andrews ML (2002). "Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction". The New England Journal of Medicine. 346 (12): 877–83. doi:10.1056/NEJMoa013474. PMID 11907286. Retrieved 2011-02-04. Unknown parameter |month= ignored (help)
  11. 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)
  12. 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)
  13. 13.0 13.1 Epstein AE, DiMarco JP, Ellenbogen KA; et al. (2008). "ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices): developed in collaboration with the American Association for Thoracic Surgery and Society of Thoracic Surgeons". Circulation. 117 (21): e350–408. PMID 18483207. Text "doi:10.1161/CIRCUALTIONAHA.108.189742 " ignored (help); Unknown parameter |month= ignored (help)

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