Ventricular tachycardia medical therapy

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Sara Zand, M.D.[2] Cafer Zorkun, M.D., Ph.D. [3], Avirup Guha, M.B.B.S.[4]

Overview

The mainstay of medical therapy in hemodynamic stable VT is suppression of tachyarrhythmia with antiarrhythmic medications such as amiodarone, sotalol, lidocaine, betablocker alongside with correction of hypokalemia, hypomagnesemia and hypocalcemia. In addition, treatment the underlying cause of VT including IHD or decompensated heart failure should be warranted.

Medical Therapy

Common medications for treatment of VT include:^[1]

Antiarrhythmic medications

^[2]

Sodium channel blocker

In patients with ischemic heart disease, chronic use of sodium channel blocker increased risk of mortality.
Some sodium channel blockers that are benefit in special setting include the following:

Lidocaine (class1) for patients with refractory VT, cardiac arrest (especially witnessed) ^[3]
Oral mexiletine for congenital long QT syndrome^[4]
Quinidine for patients with Brugada syndrome
Flecainide for patients with catecholaminergic polymorphic ventricular tachycardia^[5]

Theses medications are useful in ICD patients with drug and ablation refractory VT.

Ranolazine

A new antiangina drug approved by FDA with antiarrhythmic efficacy.
Mechanism of action is late sodium channel current blockade , blockade of the phase 3 repolarizing potassium current.
Reducing ICD shocks in drug resistant VT, VF^[1]

Reducing VT in the first days after NSTMI according to MERLIN TIMI-36.^[6]

NO efficacy in reduction the fist VT, VF in high risk patients, but significant reduction of recurrent VT, VF requiring ICD implantation.^[7]

Beta blocker

First line therapy for the most of ventricular arrhythmia such as PVC, VT due to safety and efficacy^[8]

Supression of ventricular arrhythmia in structurally normal heart.
Reduction of all-cause mortality and SCD in patients with heart failure with reduced EF^[9]
Reduction of mortality after MI
Increased mortality and risk of cardiogenic shock after MI in the presence of >70 years of age, symptoms <12 hours ST-elevation MI patients, systolic blood pressure <120 mm Hg, heart rate >110 beat/min ^[10]
Increased antiarrhythmic effect of membrane stabilizing drug in malignant VT^[11]
Nadolol, propranolol: first-line therapy for some cardiac channelopathies such as long QT syndrome, catecholaminergic polymorphic ventricular tachycardia

Amiodarone, sotalol

Amiodarone is a multichannel blocker by blockade of beta receptors, sodium, calcium, potassium currents
NO survival benefit from amiodarone compared with placebo in patients with LV dysfunction due to prior MI and non ischemic cardiomyopathy according to SCD-HeFT^[12]
Use of amiodarone after MI in patients with NYHA 3 symptoms was associated with increased risk of mortality.^[13]
In patients with nonischemic cardiomyopathy (LVEF<40%), use of amiodarone reduced the risk of SCD (with low quality of support of article), but there was NO benefit of using amiodarone for secondary prevention.^[14]

Infused amiodarone during cardiopulmonary resucitation prevents recurrent VT, VF.^[15]
Amiodarone decreased risk of SCD and all-cause mortality compared with betablocker or sotalol.^[14]
Chronic use of amiodarone has adverse effect on lung, liver, thyroid, skin, and nervous system.^[14]
ECG, liver function tests, thyroid function tests, chest x-ray, and pulmonary function tests (including diffusing capacity of the lungs for carbon monoxide) is needed before administration of amiodarone. In case of pulmonary toxicity, chest CT scan should be done.^[16]
Although sotalol suppressed ventricular arrhythmia, it was associated with increased risk of mortality in heart failure patients.^[17]
Sotalol may decrease defibrillation threshold and should be avoided in patients with LVEF< 20% due to decompensation of heart failure.^[18]

Calcium channel blocker

Non-dihydropyridines calcium channel blockers have no role in the treatment of most ventricular arrhythmias.
In patients with prior MI, administration of intravenous verapamil for sustained VT has been associated with hemodynamic collapse .^[19]
Verapamil and diltiazem can be used for suppression of some VT originated outflow tract.^[20]
Oral and intravenous verapamil is effective for the treatment of idiopathic interfascicular reentrant left VT in patients with normal structurally heart.^[21]
Non-dihydropyridines Calcium channel blockers should be avoided for converting VT in heart failure reduced EF.

Arrhythmiac medication, class, dose	Indication	Receptor target	Electrophysiologic effect	Pharmacological characteristics	Common advers effects
Acebutolol PO 200–1200 mg daily, up to 600 mg bid	VT, PVC	B1, mild internistic sympathetic activity	Slowing sinus rate, increasing AV nodal refractoriness	Prolonged haft life in renal impairment, metabolism: hepatic	Bradycardia, hypotension, HF, AV block, Dizziness, fatigue, anxiety, impotence, hyperesthesia,hypoesthesia
Amiodarone (III) IV:VF/pulseless VT arrest: 300 mg bolus, stable VT: 150-mg bolus then 1 mg/min x 6 h, then 0.5 mg/min x 18 h PO: 400 mg q 8 to 12 h for 1–2 wk, then 300–400 mg daily; reduce dose to 200 mg daily if possible	VT, VF, PVC	INa, ICa, IKr, IK1, IKs, Ito, Beta receptor, Alpha receptor, nuclear T3 recepto	Slowed sinus rate, QRS prolongation, QTc prolongation, increased AV nodal refractoriness ,increased defibrilation threshold	Metabolism: hepatic, half life: 26-107 days	Hypotension, bradycardia, AV block, TdP, slowing VT below programmed ICD detection rate, increased defibrillation threshold, corneal microdeposits, thyroid abnormalities, ataxia, nausea, emesis, constipation, photosensitivity, skin discoloration, ataxia, dizziness, peripheral neuropathy, tremor, hepatitis, cirrhosis, pulmonary fibrosis, pneumonitis
Atenolol (II) PO: 25–100 mg qd or bid	VT, PVC, ARVC, LQTS	Beta 1	Slowed sinus rate , increased AV nodal refractoriness	Metabolism: hepatic	Bradycardia, hypotension, heart failure, AV block, dizziness, fatigue, depression, impotence
Bisoprolol (II) PO: 2.5–10 mg once daily	VT, PVC	Beta 1 receptor	Slowed sinus rate, increased AV nodal refractoriness	Metabolism: hepatic	Chest pain, bradycardia, AV block, Fatigue, insomnia, diarrhea
Carvedilol (II) PO: 3.125–25 mg q 12 h	VT, PVC	Beta 1, Beta 2, Alpha	Slowed sinus rate, increased AV nodal refractoriness	Metabolism: hepatic	Bradycardia, hypotension, AV block, edema, syncope, Hyperglycemia, dizziness, fatigue, diarrhea
Carvedilol (II) PO: 3.125–25 mg q 12 h	VT, PVC	Beta 1, Beta 2, Alpha	Slowed sinus rate, increased AV nodal refractoriness	Metabolism: hepatic	Bradycardia, hypotension, AV block, edema, syncope, Hyperglycemia, dizziness, fatigue, diarrhea
Diltiazem (IV) IV: 5–10 mg,qd: 15–30 min, Extended release: PO: 120–360 mg/da, PO: 3.125–25 mg q 12 h	RVOT VT, ideopathic left VT	ICa-L	Slowed sinus rate, slowed AV node conduction, PR prolongation	Metabolism: hepatic	Bradycardia, hypotension, AV block, edema, exacerbation of HF reduced EF, Headache, rash, constipation
Esmolol (II) IV: 0.5 mg/kg bolus, 0.05 mg/kg/min	VT	B1	Slowed sinus rate, increased AV node refractoriness	Metabolism: RBC	Bradycardia, hypotension, AV block, HF, dizziness, neusea
Flecainide (IC) PO: 50–200 mg q 12 h	VT, PVC (in the absence of structural heart disease), CPVT	INa, IKr, IKur	Prolonged PR interval, prolonged QRS duration, increased defibrillation threshold	Metabolism: RBC	Sinus node dysfunction, AV block, drug-induced Brugada syndrome, monomorphic VT in patients with a myocardial scar, exacerbation of HFrEF
Lidocaine (IB) IV: 1 mg/kg bolus, 1–3 mg/min, 1–1.5 mg/kg. Repeat 0.5–0.75 mg/kg bolus every 5–10 min (max cumulative dose 3 mg/kg), maintenance infusion: 1–4 mg/min or starting 0.5 mg/min	VT, VF	INa	Slightly shortening of QTc interval	Metabolism: hepatic, prolonged half life in HF, liver disease, shock, severe renal disease	Bradycardia, hemodynamic collapse, AV block, sinus arrest, delirium, psychosis, seizure, nausea, tinnitus, dyspnea, bronchospasm
Metoprolol (II) IV: 5 mg q 5 min up to 3 doses, PO: 25–100 mg Extended release qd or q 12 h	VT, PVC	B1	Slowed sinus rate, increased AV nodal refractoriness	Metabolism: None, Excretion: urine	Bradycardia, hypotension, AV block, dizziness, fatigue, diarrhea, depression, dyspnea
Metoprolol (II) IV: 5 mg q 5 min up to 3 doses, PO: 25–100 mg Extended release qd or q 12 h	VT, PVC	B1	Slowed sinus rate, increased AV nodal refractoriness	Metabolism: None, Excretion: urine	Bradycardia, hypotension, AV block, dizziness, fatigue, diarrhea, depression, dyspnea
Mexiletine (IB), PO: 150–300 mg q 8 h or q 12 h	VT, PVC, VF, Long QT3	INa	Slightly shortening of QTc interval	Metabolism: hepatic	HF, AV block, lightheaded, tremor, ataxia, paresthesias, nausea, blood dyscrasias
Nadolol (II) PO: 40–320 mg daily	VT, PVC, LQTS, CPVT	B1, B2	Slowed sinus rate, increased AV nodal refractoriness	Metabolism: none, excretion: urine	Bradycardia, hypotension, HF, AV block, edema, dizziness, cold extremities, bronchospasm
Procainamide (IA), IV: loading dose 10–17 mg/kg at 20–50 mg/min, maintenance dose: 1–4 mg/min, PO (SR preparation): 500–1250 mg q 6 h	VT, PVC, LQTS, CPVT	B1, B2	Slowed sinus rate, increased AV nodal refractoriness	Metabolism: none, excretion: urine	Bradycardia, hypotension, HF, AV block, edema, dizziness, cold extremities, bronchospasm
Propafenone (IC), PO: Immediate release 150–300 mg q 8 h, Extended release 225–425 mg q 12 h	VT, PVC (in the absence of structural heart disease]]	INa, IKr, IKur, Beta receptor, Alpha recept	Prolonged PR interval, prolonged QRS duration, increased defibrillation threshold	Metabolism: hepatic	HF, AV block, drug-induced Brugada syndrome, dizziness, fatigue, nausea, diarrhea, xerostomia, tremor, blurred vision
Propranolol (II), IV: 1–3 mg q 5 min to a total of 5 mg, PO: Immediate release 10–40 mg q 6 h; Extended release 60–160 mg q 12 h	VT, PVC, Long QT syndrome	Beta 1 , B2 , INa	Slowed sinus rate, increased AV nodal refractoriness	Metabolism: hepatic	Bradycardia, hypotension, HF, AV block, sleep disorder, dizziness, nightmares, hyperglycemia, diarrhea, bronchospasm
Quinidine (IA), PO: sulfate salt 200–600 mg q 6 h to q 12 h, gluconate salt 324–648 mg q 8 h to q 12 h, IV: loading dose: 800 mg in 50 mL infused at 50 mg/min	VT, VF, short QT syndrome, brugada	INa, Ito, IKr, M, Alpha receptor	QRS prolongation, QTc prolongation, increased defibrillation threshold	Metabolism: hepatic	[[Syncope], torsades de pointes, AV block, dizziness, diarrhea, nausea, esophagitis, emesis, tinnitus, blurred vision, rash, weakness, tremor, blood dyscrasias
Ranolazine (not classified), PO: 500–1000 mg q 12 h	VT	INa, IKr	Slowed sinus rate, QTc prolongation	Metabolism: hepatic	Bradycardia, hypotension, headache, dizziness, syncope, nausea, dyspnea
Sotalol (III), IV: 75 mg q 12 h, PO: 80–120 mg q 12 h, may increase dose every 3 d; max 320 mg/d	VT, VF, PVC	B1, B2 IKr	Slowed sinus rate, QTc prolongation, increased AV nodal refractoriness, decreased defibrillation threshold	Metabolism: none	Bradycardia, hypotension, HF, syncope, TdP, fatigue, dizziness, weakness, dyspnea, bronchitis, depression, nausea, diarrhea
Verapamil, IV: 2.5–5 mg q 15–30 min, sustained release PO: 240–480 mg/d	RVOT VT, verapamil-sensitive idiopathic Left VT	ICa-L	Slowed sinus rate,PR prolongation, slowed AV nodal conduction	Metabolism: hepatic	Hypotension, edema, HF, AV block, bradycardia, exacerbation of HF reduced EF, headache, rash, gingival hyperplasia, constipation, dyspepsia

Electrolytes

Correction of hypokalemia and hypomagnesemia is helpful for preventing of ventricular arrhythmia in the setting of myocardial infarction or diuretic therapy in heart failure patients.^[22]
Diuretic therapy in heart failure patients may lead to hypokalemia or hypomagnesemia.^[22]

Hypokalemia and hypomagnesemia may cause ventricular arrhythmia during acute myocardial infarction .
Hypokalemia and hypomagnesemia may increase the risk of torsades de pointes in patients with use of some medications with QTc prolongation effect or long QT syndrome.^[23]
Administration of intravenous magnesium in the setting of torsades de pointes as the first line therapy is recommended.^[24]

Potassium level should be kept 4.5 mmol/L and 5 mmol/L to prevent ventricular arrhythmia or sudden cardiac death.^[25]

In patients with acute MI maintaining potassium level between 3.5 mmol/L and 4.5 mmol/L was associated with lower rate of death ^[26]
Early administration of intravenous magnesium in patients with acute STEMI has not effect on short term mortality.^[27]

Fatty acids, Lipids

The role of N-3 poly-unsaturated fatty acids and statin therapies for preventing of SCD has been proposed by stabilizing bilipid myocyte membrane for maintaining electrolyte gradients. ^[28]
Among patients with recent MI using fish oil 1 g/d reduced SCD and mortality.^[29]
Another clinical trial showed using n–3 Fatty Acids was not effective in the reduction of the cardiovascular event in high risk patients.^[30]
Statin clearly reduced mortality and SCD associated ischemic heart disease.^[31]
Supressing plaque rupture or direct cardiovascular effect are two mechanisms of decrease ventricular arrhythmia by statin.
Statin is effective in prevention of ventricular arrhythmia in ischemic heart disease, however, the role of statine in reducing SCD in heart failure ICD patients is not clearly explained.^[32]

Specific recommendation

The mainstay of therapy in heart failure reduced EF for prevention of SCD and ventricular arrhythmia is the following:
Beta blockers are benefit for preventing of SCD by reducing sympathetic activity and myocardial oxygen demand or countering electrical excitability.
Angiotensin-converting enzyme inhibitors, or angiotensin-receptor blockers is effective by reducing myocardial oxygen demand, preload, afterload, prevention the formation of angiotensin II, and slowing the process of ventricular remodeling and fibrosis.^[33]
Mineralocorticoid receptor antagonists decrease potassium loss, decrease fibrosis, and increase the myocardial uptake of norepinephrine.
Chronic Beta blockers therapy in heart failure reduced EF was associated with reduced SCD, ventricular arrhythmia and all cause mortality.
Bisoprolol, carvedilol, sustained-release metoprolol succinate decrease mortality in patients with heart failure reduced EF.^[34]^[35]^[36]
ACEI and mineralocorticoid-receptor antagonists (spironolactone, eplerenone) reduce mortality and SCD in patients with severe heart failure. ^[37]

2017 ACC/AHA/HRS Guideline for management of ventricular tachycardia

^[2]

Class I
"1. In heart failure reduced EF (LVEF< 40%) for reducing the risk of SCD and all cause mortality, use of betablocker, a mineralocontocoid receptor antagonist, and either an angiotensin converting enzyme inhibitor, an angiotensin receptor blocker, or an angiotensin receptor neprilysin inhibitor is recommended. (Level of Evidence A)"

Notes

The most common cause of cardiac arrest is VF, pulseless VT, severe bradycardia, and asystole.
Survival in the presence of VF, VT is better than bradycardia, asystole manifestation.^[38]
Factors associated with better survival include rapid defibrillation and initiation of CPR for a witnessed cardiac arrest.
Survival in patients with cardiac arrest decreases rapidly after the initial 2 minutes from the onset of cardiac arrest, by 4 to 5 minutes, survival may be ≤25%, and by 10 minutes it is 0%.^[39]
Among patients with witnessed cardiac arrest due to initial shock-refractory VF or pulseless VT, administration of amiodarone improved survival to hospital discharge compared with placebo in the setting of out-of-hospital cardiac arrest.
Administration of procainamide in out-of-hospital cardiac arrest due to VF or pulseless VT was correlated with more shocks, more pharmacologic interventions, longer resuscitation times, and lower survival.^[40]
If left untreated, VF and pulseless monomorphic or polymorphic VT, causes loss of consciousness and leads to death.
A short time to direct current cardioversion is the major determinant of survival, and defibrillation should be performed as quickly as possible.
CPR should be continued until restoration a perusing rhythm.
If defibrillation failed to returning spontaneous circulation, advanced cardiovascular life support should be followed.
In unstable patients suspected coronary artery occlusion led to cardiac arrest, emergency coronary angiography should be considered rather than later in the hospital regardless the patient is comatose or awake.^[41]^[42]
Coronary lesion requiring percutaneous coronary intervention was found in one-third of patients with out-of-hospital cardiac arrest without ST elevation in ECG. The outcome was reasonable. ^[43]

In the presence of incessant VT, amiodarone was more effective than lidocaine and improved survival at 24 hours.^[44]

Procainamide is superior to lidocaine in the setting of recurrent stable hemodynamic VT, and also preferred in the absent evidence of acuteMI, or Long QTC on ECG.^[45]

lidocaine was less effective than amiodarone to improve hospital admission after out-of-hospital cardiac arrest due to shock-refractory VF or polymorphic VT, but there were no differences between the two medications in survival to hospital discharge.
Lidocaine improved survival to hospital discharge in witnessed SCA due to initial shock-refractory VF or pulseless VT.
Administration of beta blocker in patients with recent MI was associated with reduced VF and better survival.
If VT, VF storm is refractory to amiodarone, lidocaine, or frequent cardioversion, administration of betablocker has been shown improved survival and finally reducing sympathetic tone by sedation and general anesthesia are recommended.
Administration of high-dose epinephrine ( 0.1 to 0.2 mg/kg IV) in out-of-hospital cardiac arrest unresponsive to defibrillation, improved survival to hospital admission, but there was no difference compared to standard-dose epinephrine in survival to hospital discharge or long term survival compared with standard-dose epinephrine (1 mg given intravenously or intraosseously every 3 to 5 minutes).^[46]
Administration of vasopressin is no longer recommended in the most recent advanced cardiovascular life support guideline.^[47]

Intravenous magnesium is advised in the presence of hypokalemia or medication-induced torsades de pointed by suppression of early and late after depolarization, and inhibition of calcium flux into cardiomyocytes.
Using intravenous magnesium during in-hospital or out-of-hospital cardiac arrest or refractory VF was not associated with restoration of circulation or survival benefit.^[48]

Administration The lidocaine and procainamide routinely after MI for suppression of ventricular arrhythmia was associated with increased mortality, however,

use of beta blockers lessened mortality rate.^[49]

Prophylactic use of Higher dose amiodaron after MI increase mortality, whereas moderate dose amiodarone was not superior to placebo.^[50]

Every wide QRS tachycardia in the presence of structural heart disease should be presumed VT untile proven otherwise such as SVT with aberrancy.
Administration of verapamil in wide QRS tachycardia may lead to severe hypotension and syncope and should be avoided.
The specific type of VT is verapamil-sensitive VT (interfascicular reentry) with structurally normal heart, but it is important to notify that the recognition of this rhythm is difficult at initial presentation.^[19]

Sustained monomorphic VT

Hemodynamic stability

Stable

Unstable

12-Lead ECG, history, physical exam

Dirrect current cardioversion,ACLS

Notifying disease causing VT

Cardioversion(class1)

VT termination

Structural heart disease

Intravenous procainamide (class2a)

Yes, therapy of underlying heart disease

NO, cardioversion (class1)

NO, Ideopathic VT

Intravenous amiodarone or sotalole (class2b)

VT termination

Verapamil sensitive VT: Verapamil outflow tract VT: betablocker (class2a)

Effective

Non effective: cardioversion

Yes,therapy of underlying heart disease

NO, Sedation ,anesthesia, reassessing antiarrhythmic therapy, repeating cardioversion

Therapy to prevent recurrence of VT

No VT termination

Catheter ablation (class1)

Verapamil , betablocker (class2a)

The above algorithm adopted from 2017 AHA/ACC/HRS Guideline

Comments

Common antiarrhythmic medications for supression of ventricular arrhythmia include amiodarone, sotalol, and occasionally mexilletine, quinidine,ranolazine.^[1]^[51]
Amiodarone is more effective than sotalol but discontinuation may happen during 12-24 months of use due to adverse effects.^[52]
Contraindication of sotalol may include severely reduced LVEF <20% due to its negative inotropic effects and the risk of torsades de pointed.
In patients with prior MI and recurrent sustained monomorphic VT despite receiving amiodarone , catheter ablation was related to better outcome.^[53]
Recurrent VT after catheter ablation is associated with increased mortality.
Administration of encainide or flecainide for suppression of PVCs and non sustained VT in post MI period was associated with increased mortality and non fatal cardiac arrest.^[54]

In survivors of SCA use of Propafenone increased mortality in comparison with beta-blockers, amiodarone, and the ICD.
In patients with prior MI Sustained monomorphic VT is due to scar-related reentry and is not due to acute ischemia.
Antiarrhythmic medications or ablation may be needed to prevent recurrence of VT in scar-related settings.^[55]

Revascularization is recommended in the setting of ischemia for prevention of VF, polymorphic VT. ^[56]

Recommendations for treatment of recurrent ventricular tachycardia in ischemic heart disease

Medications (Class I, Level of Evidence B):

❑ In patients with IHD and recurrent symptomatic ventricular tachycardia and frequent ICD shocks despite programming, betablocker, sotalol, amiodarone is recommended for supression of arrhythmia
❑ In patients with period MI and presence of VT storm refractory to amiodarone or other antiarrhythmic drugs, catheter ablation is recommended

Catheter ablation (Class IIb, Level of Evidence C) :

❑ Catheter ablation can be the first line therapy for recurrent sustained monomorphic VT in IHD

(Class III, Level of Evidence C)

❑ Class IC antiarrhythmic drugs (flecainide, propafenone ) is harmful for supression of ventricular tachycardia in patients with perior MI
❑ In patients with incessant VT/VF, after controlling tachyarrhythmia ICD should be implanted due to avoiding of repeated ICD shocks
❑ In patients with recurrent monomorphic VT , only revascularization is ineffective for preventing of tachyarrhythmia

The above table adopted from 2017 AHA/ACC/HRS Guideline

Message

Although ICD reduced mortality, painful ICD shocks can affect on the quality of life and increased morbidity.
The frequent of ICD shocks lessened by amiodarone plus beta blocker compared with sotalol but at the expense of increased risk of amiodarone-related adverse effects.^[52]
All types of non-ischemic cardiomyopathy can produce scar-related VT especially cardiac sarcoidosis.^[57]

Cather ablation can be used for treatment of scar related VT in non-ischemic cardiomyopathy.^[58]

Recommendations for treatment of recurrent ventricular tachycardia in non-ischemic heart disease

Amiodarone, sotalol (Class IIa, Level of Evidence B):

❑ Amiodarone or sotalol is recommended in the presensence of recurrent ventricular arrhythmia and frequent ICD shocks despite optimal programming or beta blocker therapy

Catheter ablation (Class IIa, Level of Evidence B) :

❑ In the setting of frequent ventricular arrhythmia despite optimal ICD programming or failed antiarrhythmic medications, catheter ablation is recommended

The above table adopted from 2017 AHA/ACC/HRS Guideline

References

↑ ^1.0 ^1.1 ^1.2 Bunch, T. Jared; Mahapatra, Srijoy; Murdock, David; Molden, Jamie; Weiss, J. Peter; May, Heidi T.; Bair, Tami L.; Mader, Katy M.; Crandall, Brian G.; Day, John D.; Osborn, Jeffrey S.; Muhlestein, Joseph B.; Lappe, Donald L.; Anderson, Jeffrey L. (2011). "Ranolazine Reduces Ventricular Tachycardia Burden and ICD Shocks in Patients with Drug-Refractory ICD Shocks". Pacing and Clinical Electrophysiology. 34 (12): 1600–1606. doi:10.1111/j.1540-8159.2011.03208.x. ISSN 0147-8389.
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[BunchMahapatra2011-1] 1.0 ^1.1 ^1.2 Bunch, T. Jared; Mahapatra, Srijoy; Murdock, David; Molden, Jamie; Weiss, J. Peter; May, Heidi T.; Bair, Tami L.; Mader, Katy M.; Crandall, Brian G.; Day, John D.; Osborn, Jeffrey S.; Muhlestein, Joseph B.; Lappe, Donald L.; Anderson, Jeffrey L. (2011). "Ranolazine Reduces Ventricular Tachycardia Burden and ICD Shocks in Patients with Drug-Refractory ICD Shocks". Pacing and Clinical Electrophysiology. 34 (12): 1600–1606. doi:10.1111/j.1540-8159.2011.03208.x. ISSN 0147-8389.

[Al-KhatibStevenson2018-2] 2.0 ^2.1 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.

[KudenchukBrown2016-3] Kudenchuk, Peter J.; Brown, Siobhan P.; Daya, Mohamud; Rea, Thomas; Nichol, Graham; Morrison, Laurie J.; Leroux, Brian; Vaillancourt, Christian; Wittwer, Lynn; Callaway, Clifton W.; Christenson, James; Egan, Debra; Ornato, Joseph P.; Weisfeldt, Myron L.; Stiell, Ian G.; Idris, Ahamed H.; Aufderheide, Tom P.; Dunford, James V.; Colella, M. Riccardo; Vilke, Gary M.; Brienza, Ashley M.; Desvigne-Nickens, Patrice; Gray, Pamela C.; Gray, Randal; Seals, Norman; Straight, Ron; Dorian, Paul (2016). "Amiodarone, Lidocaine, or Placebo in Out-of-Hospital Cardiac Arrest". New England Journal of Medicine. 374 (18): 1711–1722. doi:10.1056/NEJMoa1514204. ISSN 0028-4793.

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