Ventricular tachycardia medical therapy
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Ventricular tachycardia Microchapters |
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Differentiating Ventricular Tachycardia from other Disorders |
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Ventricular tachycardia medical therapy On the Web |
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Risk calculators and risk factors for Ventricular tachycardia medical therapy |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2], Avirup Guha, M.B.B.S.[3]
Overview
Certain antiarrhythmics such as amiodarone, vasopressin and epinephrine may be used in addition to defibrillation in the setting of VT. Long-term anti-arrhythmic therapy may be indicated to prevent the recurrence of VT.
Medical Therapy
Common medications for treatment of VT include:[1]
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) [2]
- Oral mexiletine for congenital long QT syndrome[3]
- Quinidine for patients with Brugada syndrome
- Flecainide for patients with catecholaminergic polymorphic ventricular tachycardia[4]
- 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.
- Reduction of ICD shocks in drug resistant VT, VF[1]
- Reduction of VT in the first days after [NSTMI]] according to MERLIN TIMI-36.[5]
Beta blocker
- First line therapy for the most of ventricular arrhythmia such as PVC, VT due to safety and efficacy[7]
- Supression of ventricular arrhythmia in structurally normal heart.
- Reduction of all-cause mortality and SCD in patients with heart failure with reduced EF[8]
- 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 [9]
- Increased antiarrhythmic effect of membrane stabilizing drug in malignant VT[10]
- 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[11]
- Use of amiodarone after MI in patients with NYHA 3 symptoms was associated with increased risk of mortality.[12]
- In patients with nonischemic cardiomyopathy (LVEF<40%) using amiodarone reduced the risk of SCD (with low quality of support of article), but there was NO benefit of using amiodarone for secondary prevention.[13]
- Infused amiodarone during cardiopulmonary resucitation prevents recurrent VT, VF.[14]
- Amiodarone decreased risk of SCD and all-cause mortality compared with betablocker or sotalol.[13]
- Chronic use of amiodarone has adverse effect on lung, liver, thyroid, skin, and nervous system.[13]
- 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.[15]
- Although sotalol suppressed ventricular arrhythmia, it was associated with increased risk of mortality in heart failure patients.[16]
- Sotalol may decrease defibrillation threshold and should be avoided in patients with LVEF< 20% due to decompensation of heart failure.[17]
Calcium channel blocker
- Non-dihydropyridines calcium channel blockers have no role in the treatment of most ventricular arrhythmia.
- In patients with prior MI administration of intravenous verapamil for sustained VT has been associated with hemodynamic collapse .[18]
- Verapamil and diltiazem can be used for suppression of some VT originated outflow tract.[19]
- Oral and intravenous verapamil is effective for the treatment of idiopathic interfascicular reentrant left VT in patients with normal structurally heart.[20]
- Calcium channel blockers should be avoided in heart failure reduced EF.
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.[21]
- Duiretic therapy in heart failure patients may lead to hypokalemia or hypomagnesemia.[21]
- Hypokalemia and hypomagnesemia may cause ventricular arrhythmia during acute myocardial infarction .
- Hypokalemia and hypomagnesemia may increase the risk of torsades de pointes in the setting of some medications or long QT syndrome.[22]
- Administration of intravenous magnesium in the setting of torsades de pointes as the first line therapy is recommended.[23]
- Potassium level should be kept 4.5 mmol/L and 5 mmol/L to prevent ventricular arrhythmia or sudden cardiac death.[24]
- 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 [25]
- Early administration of intravenous magnesium in patients with acute STEMI has not effect on short term mortality.[26]
| Arrhythmiac medication, class, dose | Indication | Receotor 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 |
Antiarrhythmic Drug Therapy
- Drugs such as amiodarone, epinephrine and vasopressin may be used in addition to defibrillation to terminate VT while the underlying cause of the VT can be determined.
- Possible causes or contributing factors to VT can be remembered as the six H's and five T's: hypovolemia, hypoxia, hydrogen ion (acidosis), hypo- or hyperglycemia, hypothermia; and toxins, tamponade (cardiac), tension pneumothorax, thrombosis, trauma.
- Long term anti-arrhythmic therapy may be indicated to prevent recurrence of VT.
- Beta-blockers and a number of class III anti-arrhythmics are commonly used. For some of the rare congenital syndromes of VT, other drugs, and sometimes even catheter ablation therapy may be useful.
- The implantation of an ICD is more effective than drug therapy for prevention of sudden cardiac death due to VT and VF, but may be constrained by cost issues, and well as patient comorbidities and patient preference.
Contraindicated medications
Ventricular tachycardia is considered an absolute contraindication to the use of the following medications:
2006 ACC/AHA/ESC Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death (DO NOT EDIT) [27]
Management of Cardiac Arrest (DO NOT EDIT) [27]
| Class I |
| "1. After establishing the presence of definite, suspected, or impending cardiac arrest, the first priority should be activation of a response team capable of identifying the specific mechanism and carrying out prompt intervention. (Level of Evidence: B) " |
| "2. Cardiopulmonary resuscitation (CPR) should be implemented immediately after contacting a response team. (Level of Evidence: A) " |
| "3. In an out-of-hospital setting, if an AED is available, it should be applied immediately and shock therapy administered according to the algorithms contained in the documents on CPR[28][29] developed by the AHA in association with the International Liaison Committee on Resuscitation (ILCOR) and/or the European Resuscitation Council (ERC). (Level of Evidence: C) " |
| "4. For victims with ventricular tachyarrhythmic mechanisms of cardiac arrest, when recurrences occur after a maximally defibrillating shock (generally 360 J for monophasic defibrillators), intravenous amiodarone should be the preferred antiarrhythmic drug for attempting a stable rhythm after further defibrillations. (Level of Evidence: B) " |
| "5. For recurrent ventricular tachyarrhythmias or non-tachyarrhythmic mechanisms of cardiac arrest, it is recommended to follow the algorithms contained in the documents on CPR[28][29] developed by the AHA in association with ILCOR and/or the ERC. (Level of Evidence: C) " |
| "6. Reversible causes and factors contributing to cardiac arrest should be managed during advanced life support, including management of hypoxia, electrolyte disturbances, mechanical factors, and volume depletion. (Level of Evidence: C) " |
| Class IIa |
| " 1. For response times greater than or equal to 5 min, a brief (less than 90 to 180 s) period of CPR is reasonable prior to attempting defibrillation. (Level of Evidence: B ) " |
| Class IIb |
| " 1. A single precordial thump may be considered by health care professional providers when responding to a witnessed cardiac arrest. (Level of Evidence: C) " |
Ventricular Tachycardia Associated With Low Troponin Myocardial Infarction (DO NOT EDIT) [27]
| Class I |
| "1. Patients presenting with sustained VT in whom low level elevations in cardiac biomarkers of myocyte injury/necrosis are documented should be treated similarly to patients who have sustained VT and in whom no biomarker rise is documented. (Level of Evidence: C)" |
Sustained Monomorphic Ventricular Tachycardia (DO NOT EDIT) [27]
| Class I |
| "1. Wide QRS tachycardia should be presumed to be VT if the diagnosis is unclear. (Level of Evidence: C) " |
| "2. Direct current cardioversion with appropriate sedation is recommended at any point in the treatment cascade in patients with suspected sustained monomorphic VT with hemodynamic compromise. (Level of Evidence: C) " |
| Class III |
| "1. Calcium channel blockers such as verapamil and diltiazem should not be used in patients to terminate wide QRS complex tachycardia of unknown origin, especially in patients with a history of myocardial dysfunction. (Level of Evidence: C) " |
| Class IIa |
| " 1. Intravenous procainamide (or ajmaline in some European countries) is reasonable for initial treatment of patients with stable sustained monomorphic VT. (Level of Evidence: B) " |
| " 2. Intravenous amiodarone is reasonable in patients with sustained monomorphic VT that is hemodynamically unstable, refractory to conversion with countershock, or recurrent despite procainamide or other agents. (Level of Evidence: C) " |
| " 3. Transvenous catheter pace termination can be useful to treat patients with sustained monomorphic VT that is refractory to cardioversion or is frequently recurrent despite antiarrhythmic medication. (Level of Evidence: C) " |
| Class IIb |
| " 1. Intravenous lidocaine might be reasonable for the initial treatment of patients with stable sustained monomorphic VT specifically associated with acute myocardial ischemia or infarction. (Level of Evidence: C)" |
Repetitive Monomorphic Ventricular Tachycardia (DO NOT EDIT) [27]
| Class IIa |
| "1.Intravenous amiodarone, beta blockers, and intravenous procainamide (or sotalol or ajmaline in Europe) can be useful for treating repetitive monomorphic VT in the context of coronary disease[30] and idiopathic VT. (Level of Evidence: C)" |
Polymorphic Ventricular Tachycardia (DO NOT EDIT) [27]
| Class I |
| "1. Direct current cardioversion with appropriate sedation as necessary is recommended for patients with sustained polymorphic VT with hemodynamic compromise and is reasonable at any point in the treatment cascade. (Level of Evidence: B) " |
| "2. Intravenous beta blockers are useful for patients with recurrent polymorphic VT, especially if ischemia is suspected or cannot be excluded. (Level of Evidence: B) " |
| "3. Intravenous loading with amiodarone is useful for patients with recurrent polymorphic VT in the absence of abnormal repolarization related to congenital or acquired LQTS. (Level of Evidence: C) " |
| "4. Urgent angiography with a view to revascularization should be considered for patients with polymorphic VT when myocardial ischemia cannot be excluded. (Level of Evidence: C) " |
| Class IIb |
| " 1. Intravenous lidocaine may be reasonable for treatment of polymorphic VT specifically associated with acute myocardial ischemia or infarction. (Level of Evidence: C)" |
Torsades de Pointes (DO NOT EDIT) [27]
| Class I |
| "1.Withdrawal of any offending drugs and correction of electrolyte abnormalities are recommended in patients presenting with torsades de pointes. (Level of Evidence: A) " |
| "2. Acute and long-term pacing is recommended for patients presenting with torsades de pointes due to heart block and symptomatic bradycardia. (Level of Evidence: A)" |
| Class IIa |
| "1. Management with intravenous magnesium sulfate is reasonable for patients who present with LQTS and few episodes of torsades de pointes. Magnesium is not likely to be effective in patients with a normal QT interval. (Level of Evidence: B)" |
| "2. Acute and long-term pacing is reasonable for patients who present with recurrent pause-dependent torsades de pointes. (Level of Evidence: B)" |
| "3. Beta blockade combined with pacing is reasonable acute therapy for patients who present with torsades de pointes and sinus bradycardia. (Level of Evidence: C)" |
| "4. Isoproterenol is reasonable as temporary treatment in acute patients who present with recurrent pause-dependent torsades de pointes who do not have congenital LQTS. (Level of Evidence: B)" |
| Class IIb |
| "1. Potassium repletion to 4.5 to 5 mM/L may be considered for patients who present with torsades de pointes. (Level of Evidence: B)" |
| "2. Intravenous lidocaine or oral mexiletine may be considered in patients who present LQT3 and torsades de pointes. (Level of Evidence: C)" |
Incessant Ventricular Tachycardia (DO NOT EDIT) [27]
| Class I |
| " 1. Revascularization and beta blockade followed by intravenous antiarrythmic drugs such as procainamide or amiodarone are recommended for patients with recurrent or incessant polymorphic VT due to acute myocardial ischemia. (Level of Evidence: C) " |
| Class IIa |
| " 1. Intravenous amiodarone or procainamide followed by VT ablation can be effective in the management of patients with frequently recurring or incessant monomorphic VT. (Level of Evidence: B)" |
| Class IIb |
| " 1. Intravenous amiodarone and intravenous beta blockers separately or together may be reasonable in patients with VT storm. (Level of Evidence: C)" |
| " 2. Overdrive pacing or general anesthesia may be considered for patients with frequently recurring or incessant VT. (Level of Evidence: C)" |
| " 3. Spinal cord modulation may be considered for some patients with frequently recurring or incessant VT. (Level of Evidence: C)" |
Idiopathic Ventricular Tachycardia (DO NOT EDIT) [27]
| Class I |
| "1. Catheter ablation is useful in patients with structurally normal hearts with symptomatic, drug-refractory VT arising from the RV or LV or in those who are drug intolerant or who do not desire long-term drug therapy. (Level of Evidence: C)" |
| Class IIa |
| "1. EP testing is reasonable for diagnostic evaluation in patients with structurally normal hearts with palpitations or suspected outflow tract VT. (Level of Evidence: B)" |
| "2. Drug therapy with beta blockers and/or calcium channel blockers (and/or IC agents in RVOT VT) can be useful in patients with structurally normal hearts with symptomatic VT arising from the RV. (Level of Evidence: C)" |
| "3. ICD implantation can be effective therapy for the termination of sustained VT in patients with normal or near normal ventricular function and no structural heart disease who are receiving chronic optimal medical therapy and who have reasonable expectation of survival for more than 1 y. (Level of Evidence: C)" |
Other Drug-Induced Toxicity (DO NOT EDIT) [27]
| Class I |
| "1. High intermittent doses and cumulative doses exceeding the recommended levels should be avoided in patients receiving anthracyclines such as doxorubicin. (Level of Evidence: B)" |
| "2. All patients receiving 5-fluorouracil therapy should receive close supervision and immediate discontinuation of the infusion if symptoms or signs of myocardial ischemia occur. Further treatment with 5-fluorouracil must be avoided in these individuals. (Level of Evidence: C)" |
| "3. Patients with known cardiac disease should have a full cardiac assessment including echocardiography, which should be undertaken prior to use of anthracyclines such as doxorubicin, and regular long-term follow-up should be considered. (Level of Evidence: C)" |
References
- ↑ 1.0 1.1 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.
- ↑ 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.
- ↑ Mazzanti, Andrea; Maragna, Riccardo; Faragli, Alessandro; Monteforte, Nicola; Bloise, Raffaella; Memmi, Mirella; Novelli, Valeria; Baiardi, Paola; Bagnardi, Vincenzo; Etheridge, Susan P.; Napolitano, Carlo; Priori, Silvia G. (2016). "Gene-Specific Therapy With Mexiletine Reduces Arrhythmic Events in Patients With Long QT Syndrome Type 3". Journal of the American College of Cardiology. 67 (9): 1053–1058. doi:10.1016/j.jacc.2015.12.033. ISSN 0735-1097.
- ↑ Watanabe, Hiroshi; Chopra, Nagesh; Laver, Derek; Hwang, Hyun Seok; Davies, Sean S; Roach, Daniel E; Duff, Henry J; Roden, Dan M; Wilde, Arthur A M; Knollmann, Björn C (2009). "Flecainide prevents catecholaminergic polymorphic ventricular tachycardia in mice and humans". Nature Medicine. 15 (4): 380–383. doi:10.1038/nm.1942. ISSN 1078-8956.
- ↑ Scirica, Benjamin M.; Braunwald, Eugene; Belardinelli, Luiz; Hedgepeth, Chester M.; Spinar, Jindrich; Wang, Whedy; Qin, Jie; Karwatowska-Prokopczuk, Ewa; Verheugt, Freek W.A.; Morrow, David A. (2010). "Relationship Between Nonsustained Ventricular Tachycardia After Non–ST-Elevation Acute Coronary Syndrome and Sudden Cardiac Death". Circulation. 122 (5): 455–462. doi:10.1161/CIRCULATIONAHA.110.937136. ISSN 0009-7322.
- ↑ Zareba, Wojciech; Daubert, James P.; Beck, Christopher A.; Huang, David T.; Alexis, Jeffrey D.; Brown, Mary W.; Pyykkonen, Kathryn; McNitt, Scott; Oakes, David; Feng, Changyong; Aktas, Mehmet K.; Ayala-Parades, Felix; Baranchuk, Adrian; Dubuc, Marc; Haigney, Mark; Mazur, Alexander; McPherson, Craig A.; Mitchell, L. Brent; Natale, Andrea; Piccini, Jonathan P.; Raitt, Merritt; Rashtian, Mayer Y.; Schuger, Claudio; Winters, Stephen; Worley, Seth J.; Ziv, Ohad; Moss, Arthur J.; Zareba, W.; Pyykkonen, K.; Buttaccio, A.; Perkins, E.; DeGrey, D.; Robertson, S.; Moss, A.J.; Brown, M.; Lansing, R.; Oberer, A.; Polonsky, B.; Ross, V.; Papernov, A.; Schleede, S.; Beck, C.; Oakes, D.; Feng, C.; McNitt S, S.; Hall, W.J.; Zareba, W.; Moss, A.; Daubert, J.; Beck, C.; Brown, M.; Huang, D.; Winters, S.; Schuger, C.; Haigney, M.; Piccini, J.; Alexis, J.; Chen, L.; Miller, A.; Richeson, J.F.; Rosero, S.; Huang, D.; Kutyifa, V.; Shah, A.; Lamas, G.; Cohn, F.; Harrell, F.; Piña, I.; Poole, J.; Sullivan, M.; Lathrop, D.; Geller, N.; Boineau, R.; Trondell, J.; Cooper, L.; Itturiaga, E.; Boineau, R.; Gottlieb, C.; Greer, S.; Perzanowski, C.; McPherson, C.; Hedgepeth, C.; Assal, C.; Salam, T.; Woollett, I.; Tomassoni, G.; Ayala-Paredes, F.; Russo, A.; Punnam, S.; Sangrigoli, R.; Sloan, S.; Kutalek, S.; Piccini, J.; Sun, A.; Lustgarten, D.; Monir, G.; Haithcock, D.; Sorrentino, R.; Cannom, D.; Kluger, J.; Schuger, C.; Varanasi, S.; Rashtian, M.; Philippon, F.; Berger, R.; Mazzella, M.; Lessmeier, T.; Silver, J.; Worley, S.; Bernabei, M.; Esberg, D.; Dixon, M.; LeLorier, P.; Greenberg, Y.; Essebag, V.; Venkataraman, G.; Shinn, T.; Dubuc, M.; Winters, S.; Turitto, G.; Henrikson, C.; Mirro, M.; Raitt, M.; Baranchuk, A.; O'Neill, G.; Lockwood, E.; Vloka, M.; Hurwitz, J.; Mead, R.H.; Somasundarum, P.; Aziz, E.; Rashba, E.; Budzikowski, A.; Cox, M.; Natale, A.; Chung, E.; Ziv, O.; McGrew, F.; Tamirisa, K.; Greenspon, A.; Estes, M.; Taylor, S.; Janardhanan, R.; Mitchell, L.B.; Burke, M.; Attari, M.; Mikaelian, B.; Hsu, S.; Conti, J.; Mazur, A.; Shorofsky, S.; Rosenthal, L.; Sakaguchi, S.; Wolfe, D.; Flaker, G.; Saba, S.; Aktas, M.; Mason, P.; Shalaby, A.; Musat, D.; Abraham, R.; Ellenbogen, K.; Fellows, C.; Venkataraman, G.; Kavesh, N.; Thomas, G.; Hemsworth, D.; Williamson, B. (2018). "Ranolazine in High-Risk Patients With Implanted Cardioverter-Defibrillators". Journal of the American College of Cardiology. 72 (6): 636–645. doi:10.1016/j.jacc.2018.04.086. ISSN 0735-1097.
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