eMedicine Specialties > Cardiology > Arrhythmias

Ventricular Fibrillation: Treatment & Medication

Author: Michael E Zevitz, MD, Assistant Professor of Medicine, Finch University of the Health Sciences, The Chicago Medical School; Consulting Staff, Private Practice
Contributor Information and Disclosures

Updated: Jul 18, 2006

Treatment

Medical Care

  • Advanced cardiac life support (ACLS): In the event of cardiac arrest, the immediate implementation of ACLS guidelines is indicated. Interest in improving rates of public ACLS training—with a special emphasis on use of early defibrillation by public service personnel (eg, police, fire, airline)—is widespread. These measures can help achieve the greatest public health benefits in the fight against sudden death.
  • Defibrillation
    • External electrical defibrillation remains the most successful treatment of VF. A shock is delivered to the heart in order to uniformly and simultaneously depolarize a critical mass of the excitable myocardium. The objectives are to interfere with all reentrant arrhythmia and to allow any intrinsic cardiac pacemakers to assume the role of primary pacemaker.
    • Successful defibrillation largely depends on 2 key factors: duration between onset of VF and defibrillation and the metabolic condition of the myocardium. VF waveform usually begins with a relatively high amplitude and frequency; it then degenerates to smaller and smaller amplitude until asystole after approximately 15 minutes, possibly from depletion of the heart's energy reserves. Consequently, early defibrillation is vital; emergency response teams can perform defibrillation before arrival at the ED.
    • Defibrillation success rates decrease 5-10% for each minute after onset of VF. Success rates of 85% have been reported in strictly monitored settings where defibrillation was most rapid.
    • Factors that increase the energy required for successful defibrillation include the following:
      • Time before defibrillation begins
      • Paddle size
      • Paddle-to-myocardium distance (eg, obesity, mechanical ventilation)
      • Use of conduction fluid (eg, disposable pads, electrode paste/jelly)
      • Contact pressure
      • Elimination of stray conductive pathways (eg, electrode jelly bridges on skin)
      • Previous shocks, which decrease defibrillation threshold
    • The goal is to use the minimum amount of energy required to overcome the threshold of defibrillation. Excessive energy can cause myocardial injury and arrhythmias.
    • Larger paddles result in lower impedance, which allows the use of lower-energy shocks. Approximate optimal sizes are 8-12.5 cm for an adult, 8-10 cm for a child, and 4.5-5 cm for an infant. Position one paddle below the outer half of the right clavicle and one over the apex (V4 -V5).
    • Artificial pacemakers or ICDs necessitate the use of anteroposterior paddle placement.
    • Before any defibrillation, remove all patches and ointments from the chest wall because they create a risk of fire or explosion.
    • Patient must be dry and not in contact with metallic objects. Rescuers must remember to ensure the safety of everyone around the patient before each shock is applied.
    • If contraction is reestablished following defibrillation, a period of low cardiac output (ie, postcountershock myocardial depression) may occur. Cardiac output recovery may take minutes to hours.
    • Defibrillation causes serum creatine phosphokinase levels to increase proportionate to the amount of electric energy delivered. If customary voltage is used to defibrillate a patient, the proportion of myocardial fraction (CK-MB) should remain within reference ranges unless an infarction has caused myocardial injury.
    • Although precordial thump is less appropriate for VF than for VT, it really is appropriate in neither. Use it only for witnessed monitored arrests in which no defibrillator is immediately available.
  • Algorithm
    • Activate emergency response system.
    • Initiate CPR.
    • Verify that the patient is in VF as soon as possible (ie, AED, quick look with paddles).
    • Defibrillate the patient (adult, 200 J; child, 2 J/kg or equivalent biphasic energy).
    • Defibrillate the patient (adult, 200-300 J; child, 2-3 J/kg or equivalent biphasic energy).
    • Defibrillate the patient (adult, maximum 360 J; child, 4 J/kg child; maximum biphasic energy varies with manufacturer).
    • Check for pulses/rhythm.
    • Perform CPR for 1 minute with attention to the following:
      • Properly positioning the electrode
      • Attempting tracheal intubation and IV access
      • Administering epinephrine every 3 minutes
    • Correct the following if necessary and/or possible:
      • Hypoxia
      • Hypovolemia
      • Hyperkalemia/hypokalemia and metabolic disorders
      • Tension pneumothorax
      • Tamponade
      • Toxic/therapeutic substances
      • Thromboembolic/mechanical obstruction
    • Defibrillate the patient (adult, 360 J; child, 4 J/kg or maximum biphasic).
    • Administer amiodarone (300 mg IV). If not available, use lidocaine (1-1.5 mg/kg bolus).
    • Defibrillate the patient (adult, 360 J; child, 4 J/kg or maximum biphasic).
    • Administer lidocaine (1 mg/kg IV) if amiodarone was used in the first round.
  • Other options are as follows: If not used in the first round, administer amiodarone (300 mg IV) now, and repeat lidocaine.
    • Administer amiodarone IV bolus only once.
    • Defibrillate the patient (adult, 360 J; child, 4 J/kg or maximum biphasic).
    • If no response, administer epinephrine 1 mg IV push or vasopressin (40 U IV push). Vasopressin can be used only once. Wait 10 minutes after vasopressin administration before giving epinephrine.
    • Administer a procainamide infusion (50 mg/min IV) to a total of 1 g.
    • Following the third shock, intervals between consecutive jolts should not exceed 1 minute.
    • Assess use of the following in conjunction with subsequent defibrillation attempts, and administer a shock 30 seconds after each dose of the indicated drug:
      • Lidocaine (1-1.5 mg/kg IV; maximum 3 mg/kg total)
      • Amiodarone (0.5 mg/min following bolus dosing above or IV loading protocol below)
      • Epinephrine (0.1-0.2 mg/kg IV): For adults, 1 mg IV every 3 minutes is typically used; alternative dosing regimens are advocated (ie, high, intermediate, escalating).
      • Procainamide (30 mg/min IV; maximum 17 mg/kg total in refractory VF)
      • Magnesium sulfate (1-2 g IV push) in cases of probable hypomagnesemia or refractory VF
      • Sodium bicarbonate (1 mEq/kg IV push) in cases of known preexistent hyperkalemia or known tricyclic antidepressant overdose
    • Three initial defibrillation attempts take precedence over CPR as soon as a defibrillator or AED is available.
    • Lidocaine and epinephrine can be administered through an endotracheal tube if IV attempts fail. Use 2.5 times the IV dose.
  • Refractory VF
    • Lack of response to standard defibrillation algorithms is challenging. Addition of magnesium and/or procainamide is often ineffective.
    • If not used earlier, consider the following amiodarone-loading protocol: 15 mg/min for 10 minutes, followed by 1 mg/min for 6 hours, then 0.5 mg/min for 18 hours.
    • Such reported alternatives as transesophageal and intracardiac defibrillation or thoracotomy with internal defibrillation are generally impractical because of limited experience and availability of equipment and trained personnel.
  • Postresuscitative care
    • Continue successfully used antiarrhythmics. Maintain lidocaine at 1-4 mg/min, bretylium at 1-2 mg/min, and amiodarone at 0.5 mg/min.
    • Control any hemodynamic instability.
    • Administer vasopressors as indicated.
      • Postdefibrillation arrhythmias (mainly AV blocks) have been reported in up to 24% of patients. The incidence is related to the amount of energy used for defibrillation.
      • Check for complications (eg, aspiration pneumonia, CPR-related injuries).
      • Establish the need for emergent interventions (eg, thrombolytics, antidotes, decontamination).
  • Medical stabilization: Careful postresuscitative care is essential to survival because studies have shown a 50% repeat in-hospital arrest rate for people admitted after a VF event. Treatment of myocardial ischemia, heart failure, and electrolyte disturbances are all justified by the results of multiple randomized trials investigating acute MI and CHF. Empiric beta-blockers are reasonable in many circumstances because of favorable properties discussed in Causes. Empiric antiarrhythmics, including amiodarone, should not supersede ICD placement unless control of recurrent VT is needed while the patient is hospitalized.

Surgical Care

Most survivors of VF should be treated with ICDs. Transvenous ICDs can be placed with minimal morbidity and mortality.

  • Radiofrequency ablation: Now routinely available, radiofrequency ablation is indicated for patients with AV bypass tracts, bundle-branch block VT, RVOT tachycardia, idiopathic LV tachycardia, and more rare forms of automatic foci VT (which almost never cause VF). Unfortunately, most cases of VF are not amenable to radiofrequency ablation and require ICD placement. VF is an exception because of preexcited tachycardias in patients with WPW syndrome. In these patients, successful catheter ablation of the accessory pathway(s) is the appropriate therapy.
  • Several multicenter trials have examined the prophylactic use of ICD therapy in patients at high risk for VF.
    • The annual VF rate in patients with these devices has been reduced from 25% to 1-2%. ICD placement is beneficial in high-risk patients in whom electrophysiologic-guided therapy with antiarrhythmics has failed. In several studies comparing ICD placement with antiarrhythmic therapy in patients with VT/VF and/or prior cardiac arrest, ICD placement has been shown to be associated with significantly decreased mortality rate (Myerburg, 1997; Cappato, 1999; Domanski, 1999).
    • The use of ICDs as primary prevention for VF is still being investigated in ongoing trials. Newer ICDs have pacing capabilities and have addressed bradyarrhythmias either causing or complicating VT or VF.
    • Currently, the transvenous approach to implantation is universally applied and favored over the thoracotomy implants. In the Multicenter Automatic Defibrillation Implantation Trial (MADIT) 1, prophylactic use of ICDs in patients with a history of MI, LVEF of less than 35%, documented episode of nonsustained VT, and inducible nonsuppressible VT had a 54% reduction in mortality during any follow-up interval compared with patients treated with conventional medical therapy. In MADIT 2, the ICD conferred a 31% reduction in mortality in patients with prior MI and LVEF of 30% or less. In MADIT 2, there was no requirement for nonsustained VT or EPS (Moss, 1996; Moss, 2002).
  • Cardiac surgery can be a primary treatment for VF via a variety of strategies.
    • Surgical treatment in patients with ventricular arrhythmias and ischemic heart disease includes coronary artery bypass grafting (CABG). The CASS study illustrated that patients with significant CAD and operable vessels who underwent CABG had a decrease in the incidence of VT/VF arrest compared with patients on conventional medical treatment. The reduction was most evident in patients who had 3-vessel disease and CHF (Holmes, 1989). By itself, CABG only prevents recurrent VF if the ejection fraction is normal and ischemia was the cause of the arrest. Even in these patients, ICDs are frequently placed after CABG.
    • Surgical treatment of ventricular arrhythmias in patients with nonischemic heart disease includes excision of VT foci after endocardial mapping and excision of LV aneurysms. This is practiced very infrequently, however, given the efficacy of ICDs.
    • Aortic valve replacement is associated with improved outcome in patients with hemodynamically significant valvular stenosis and well-preserved ventricular function. In patients with MVP associated with significant valvular regurgitation and LV dysfunction, malignant tachyarrhythmias, such as VT and VF, have been reported. These patients are candidates for mitral valve replacement.
    • Orthotopic heart transplantation is indicated in patients with SCD and refractory heart failure, in whom significant improvement in actuarial survival is expected. Given a limited donor service, this form of treatment is expected to be beneficial for very few people who survive VF.
    • Patients with long QT syndrome who do not respond to beta-blockers are candidates for ICD placement or high thoracic left sympathectomy.

Consultations

  • A cardiologist should always participate in the care of these patients. Cardiac electrophysiologists should also be involved in the care of these patients, which generally involves ICD placement.
  • Other consultants include an interventional cardiologist and cardiac surgeon. Such consultations are made on a case-by-case basis.

Diet

  • Patients with CAD are advised to follow a diet low in fat and cholesterol. Patients with severe heart failure should monitor their fluid and sodium intake.

Medication

Medications (eg, vasopressin, epinephrine, amiodarone) are used after 3 defibrillation attempts are performed to restore normal rhythm.

Amiodarone can also be used on a long-term basis in patients who refuse ICDs or who are not candidates for ICDs.

Antiarrhythmic agents

Can raise fibrillation and defibrillation thresholds, but amiodarone can restore normal cardiac rhythm.


Amiodarone (Cordarone)

Class III antiarrhythmic. First-line drug of choice for VF. May inhibit AV conduction and sinus node function. Prolongs action potential and refractory period in myocardium and inhibits adrenergic stimulation.

Adult

300 mg IV bolus; may repeat 150 mg IV bolus q5min; not to exceed 2.2 g over 24 h

Pediatric

10-15 mg/kg/d or 600-800 mg/1.73 m2/d PO for 4-14 d or until adequate control of arrhythmia is attained

Increases effect and blood levels of theophylline, quinidine, procainamide, phenytoin, methotrexate, flecainide, digoxin, cyclosporine, beta-blockers, and anticoagulants; cardiotoxicity is increased by ritonavir, sparfloxacin, and disopyramide; coadministration with calcium channel blockers may cause an additive effect and decrease myocardial contractility further; cimetidine may increase levels

In the setting of VF, no absolute contraindications exist

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Caution in thyroid or liver disease; may cause bradycardia and hypotension


Lidocaine (Dilocaine, Xylocaine)

Second-line drug of choice for VF. Class I-B antiarrhythmic that increases electrical stimulation threshold of the ventricle, suppressing automaticity of conduction through the tissue.

Adult

Loading dose: 1-1.5 mg/kg IV bolus, followed by 1-2 mg/min IV infusion; repeat bolus doses of 0.5-0.75 mg/kg in 5-10 min to a total of 3 mg/kg

Pediatric

Loading dose: 1 mg/kg IV, followed by continuous infusion of 20-50 mcg/kg/min IV; repeat bolus in 10-15 min for 2 doses

Coadministration with cimetidine or beta-blockers increases toxicity; coadministration with procainamide and tocainide may result in additive cardiodepressant action; may increase effects of succinylcholine

In the setting of VF, no absolute contraindications exist; relative contraindications include documented hypersensitivity to amide-type local anesthetics, Adams-Stokes syndrome, WPW syndrome, severe sinoatrial, AV or intraventricular block; if artificial pacemaker not in place, idioventricular rhythm (may evolve into asystole because of suppression of ectopic ventricular depolarizations)

Pregnancy

B - Usually safe but benefits must outweigh the risks.

Precautions

Use a solution without preservatives; caution in heart failure, hepatic disease, hypoxia, hypovolemia or shock, respiratory-depression, and bradycardia; may increase risk of CNS and cardiac adverse effects in elderly persons; high plasma concentrations can cause seizures, heart block, and AV conduction abnormalities


Procainamide (Pronestyl)

Third-line drug of choice for VF. Long loading time to prevent recurrences of VF only. This drug is generally not recommended for VF patients. Class I-A antiarrhythmics increase refractory periods of the atria and ventricles. Myocardiac excitability is reduced by an increase in threshold for excitation and inhibition of ectopic pacemaker activity.

Adult

20 mg/min IV continuous infusion until arrhythmia is suppressed, patient becomes hypotensive, QRS widens 50% above baseline, or a maximum dose of 17 mg/kg is administered; once arrhythmia is suppressed, may infuse at a continuous rate of 1-4 mg/min; in refractory VT/VF, may administer 100 mg IV push q5min

Pediatric

Not established; the following doses have been suggested: 15-50 mg/kg/d PO divided q3-6h; not to exceed 4 g/d

20-30 mg/kg/d IM divided q4-6h; not to exceed 4 g/d

3-6 mg/kg/dose IV infused over 5 min

Maintenance: 20-80 mcg/kg/min IV administered as continuous infusion; not to exceed 100 mg/dose or 2 g/d

Can expect increased levels of procainamide metabolite NAPA in patients taking cimetidine, ranitidine, beta-blockers, amiodarone, trimethoprim and quinidine; may increase effect of skeletal muscle relaxants, quinidine, lidocaine, and neuromuscular blockers; ofloxacin inhibits tubular secretion of procainamide and may increase bioavailability; when taken concurrently with sparfloxacin, may increase risk of cardiotoxicity

Patients diagnosed with complete heart block or second- or third-degree heart block, if a pacemaker is not in place; torsade de pointes; documented hypersensitivity; systemic lupus erythematosus

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Monitor for hypotension; plasma concentrations of procainamide and active metabolite, NAPA, may increase in renal failure; high or toxic concentrations may induce AV block or abnormal automaticity; caution in complete AV block, digitalis intoxication, organic heart disease, renal disease, and hepatic insufficiency


Magnesium sulfate

Acts as anti-arrhythmic agent and diminishes frequency of PVCs, particularly when secondary to acute ischemia. Clinical trials have been inconclusive in demonstrating its ability to improve mortality rates in the setting of refractory VF.

Adult

2-4 g IV once

Pediatric

Not established

Concurrent use with nifedipine may cause hypotension and neuromuscular blockade; may increase neuromuscular blockade observed with aminoglycosides and potentiate neuromuscular blockade produced by tubocurarine, vecuronium, and succinylcholine; may increase CNS effects and toxicity of CNS depressants, betamethasone, and cardiotoxicity of ritodrine

In the setting of VF, no absolute contraindications exist; relative contraindications include heart block, Addison disease, myocardial damage, or severe hepatitis

Pregnancy

A - Safe in pregnancy

Precautions

May alter cardiac conduction leading to heart block in digitalized patients; respiratory rate, deep tendon reflex, and renal function should be monitored when electrolyte is administered parenterally; caution when administering because may produce significant hypotension or asystole; in overdose, calcium gluconate, 10-20 mL IV of 10% solution, can be administered as antidote for clinically significant hypermagnesemia

Anticholinergic agents

Improve conduction through the AV node by reducing vagal tone via muscarinic receptor blockade.


Atropine sulfate

Use in asystole. Antimuscarinic agent that improves sinus node conduction by inhibiting vagal activity. To date, large randomized trials have not demonstrated benefit from atropine in the treatment of asystole.

Adult

1 mg IV push q3-5min; not to exceed 3-mg dose

Pediatric

Not established

Coadministration with other anticholinergics has additive effects; pharmacologic effects of atenolol and digoxin may increase with atropine; antipsychotic effects of phenothiazines may decrease; tricyclic antidepressants with anticholinergic activity may increase effects

In the setting of asystole, no absolute contraindications exist

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Caution in Down syndrome and/or children with brain damage to prevent hyperreactive response; caution in coronary heart disease, tachycardia, CHF, cardiac arrhythmias, hypertension, peritonitis, ulcerative colitis, hepatic disease, and hiatal hernia with reflux esophagitis; in prostatic hypertrophy, prostatism can have dysuria and may require catheterization

Vasopressor agents

Augment both coronary and cerebral blood flow present during the low flow state associated with CPR. Use has resulted in short-term resuscitation benefits in the setting of prolonged out-of-hospital CPR for VF in adults.


Epinephrine (Adrenalin)

The most useful and efficacious drug in cardiac arrest. Increases coronary perfusion pressure.

Adult

1 mg (10 mL of 1:10,000 solution) IV push q3-5min or 0.1 mg/kg IV push q3-5min; intermediate doses of 2- to 5-mg IV push q3-5min may also be used; dose may be increased as follows: 1-, 3-, and 5-mg IV push administered at 3-min intervals; higher doses do not improve survival or neurologic outcome; endotracheal administration requires 2-2.5 times IV dose

Pediatric

0.1 mcg/kg/min SC q15min for 2 doses, then q4h with increments of 0.1 mcg/kg/min prn; not to exceed 1.5 µg/kg/min

Increases toxicity of beta- and alpha-blocking agents and that of halogenated inhalational anesthetics

In the setting of VF, no absolute contraindications exist; relative contraindications include documented hypersensitivity; angle-closure glaucoma; local anesthesia in areas such as fingers or toes because vasoconstriction may produce sloughing of tissue; during labor (may delay second stage of labor)

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Caution in elderly patients, prostatic hypertrophy, hypertension, cardiovascular disease, diabetes mellitus, hyperthyroidism, and cerebrovascular insufficiency; rapid IV infusions may cause death from cerebrovascular hemorrhage or cardiac arrhythmias


Vasopressin (Pitressin)

May improve vital organ blood flow, cerebral oxygen delivery, ability to be resuscitated, and neurologic recovery.

Adult

40 U IV once

Pediatric

Not established

Lithium, epinephrine, demeclocycline, heparin, and alcohol may decrease effects; chlorpropamide, urea, fludrocortisone, and carbamazepine may potentiate effects

In the setting of VF, no absolute contraindications exist; relative contraindications include CAD

Pregnancy

B - Usually safe but benefits must outweigh the risks.

Precautions

Caution in cardiovascular disease, seizure disorders, nitrogen retention, asthma, or migraine; excessive doses may result in hyponatremia

More on Ventricular Fibrillation

Overview: Ventricular Fibrillation
Differential Diagnoses & Workup: Ventricular Fibrillation
Treatment & Medication: Ventricular Fibrillation
Follow-up: Ventricular Fibrillation
Multimedia: Ventricular Fibrillation
References
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Further Reading

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Keywords

ventricular fibrillation, VFib, VF, sudden cardiac death, SCD, ventricular flutter, ventricular arrhythmia, automatic external defibrillators, AEDs, coronary artery disease, CAD, myocardial infarction, MI, premature ventricular contractions, PVCs, congestive heart failure, CHF, anoxic encephalopathy, smoking, dyslipidemia, hypertension, diabetes, obesity, sedentary lifestyle, atherosclerosis, dilated cardiomyopathy, DCM, hypertrophic cardiomyopathy, HCM, arrhythmogenic right ventricular dysplasia, valvular heart disease, aortic stenosis, cystic medial necrosis, sinus node artery obstruction, commotio cordis, torsade de pointes, syncope, Brugada syndrome, implantable cardioverter-defibrillator, ICD, right ventricular outflow tract tachycardia, RVOT tachycardia, exercise-induced ventricular tachycardia, adenosine-sensitive ventricular tachycardia, repetitive monomorphic ventricular tachycardia, radiofrequency catheter ablation, Marfan syndrome, Ehlers-Danlossyndrome, aortic cystic medialnecrosis,wall-motionabnormalities, WMAs, revascularization, cardiopulmonary resuscitation, CPR, advanced cardiac life support, ACLS, coronary artery bypass grafting, CABG

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Contributor Information and Disclosures

Author

Michael E Zevitz, MD, Assistant Professor of Medicine, Finch University of the Health Sciences, The Chicago Medical School; Consulting Staff, Private Practice
Michael E Zevitz, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Medical Association, and Michigan State Medical Society
Disclosure: Nothing to disclose.

Medical Editor

Robert E Fowles, MD, Clinical Professor of Medicine, University of Utah College of Medicine; Consulting Staff, LDS Hospital; Director and Consulting Staff, Department of Cardiology, Salt Lake Clinic
Robert E Fowles, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, and American Heart Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Brian Olshansky, MD, Professor of Medicine, Department of Internal Medicine, University of Iowa College of Medicine
Brian Olshansky, MD is a member of the following medical societies: American Autonomic Society, American College of Cardiology, American College of Chest Physicians, American College of Physicians, American College of Sports Medicine, American Federation for Clinical Research, American Heart Association, Cardiac Electrophysiology Society, Heart Rhythm Society, and New York Academy of Sciences
Disclosure: Guidant/Boston Scientific Honoraria Speaking and teaching; Medtronic Honoraria Speaking and teaching; Guidant/Boston Scientific Consulting fee Consulting; Reliant Grant/research funds Other; Novartis Honoraria Speaking and teaching; Novartis Consulting fee Consulting

CME Editor

Amer Suleman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital
Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

Chief Editor

Leonard Ganz, MD, Associate Professor of Medicine, Temple University School of Medicine; Cardiac Electrophysiologist, Children's Hospital of Pittsburgh, University of Pittsburgh Medical Cent, West Penn Hospital
Disclosure: Nothing to disclose.

 
 
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