Ventricular tachycardia medical therapy: Difference between revisions
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* [[Procainamide]] is preferred to use in the setting of recurrent stable hemodynamic [[VT]], without evidence of acute[[ MI]], and absence of [[Long QTC]] in the [[ECG]]. | * [[Procainamide]] is preferred to use in the setting of recurrent stable hemodynamic [[VT]], without evidence of acute[[ MI]], and absence of [[Long QTC]] in the [[ECG]]. | ||
* [[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]] 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. | ||
*[[Lidociane]] improved [[survival]] to [[hospital]] discharge in witnessed [[SCA]] due to initial shock-refractory [[VF]] or pulseless [[VT]]. | |||
==References== | ==References== | ||
Revision as of 05:23, 12 May 2021
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Ventricular tachycardia Microchapters |
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Differentiating Ventricular Tachycardia from other Disorders |
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Diagnosis |
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Treatment |
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Case Studies |
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Ventricular tachycardia medical therapy On the Web |
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to Hospitals Treating Ventricular tachycardia medical therapy |
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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: Sara Zand, M.D.[2] Cafer Zorkun, M.D., Ph.D. [3], Avirup Guha, M.B.B.S.[4]
Overview
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.
- Reducing ICD shocks in drug resistant VT, VF[1]
- Reducing 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 arrhythmias.
- 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]
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. [27]
- Among patients with recent MI using fish oil 1 g/d reduced SCD and mortality.[28]
- Another clinical trial showed using n–3 Fatty Acids was not effective in the reduction of the cardiovascular event in high risk patients.[29]
- Statin clearly reduced mortality and SCD associated ischemic heart disease.[30]
- 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.[31]
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, angiotensin-receptor blockers decreasing myocardial oxygen demand, preload, afterload, prevention the formation of angiotensin II, and slowing the process of ventricular remodeling and fibrosis.[32]
- 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.[33][34][35]
- ACEI and mineralocorticoid-receptor antagonists (spironolactone, eplerenone) reduce mortality and SCD in patients with severe heart failure. [36]
Antiarrhythmic medications
| 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 |
Specific recommendation
- 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.
- Factors associated 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%.
- 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.
- The 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.
- 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.
- In the presence of incessant VT, amiodarone was more effective than lidocaine and improved survival at 24 hours.
- Procainamide is preferred to use in the setting of recurrent stable hemodynamic VT, without evidence of acuteMI, and absence of Long QTC in the ECG.
- 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.
- Lidociane improved survival to hospital discharge in witnessed SCA due to initial shock-refractory VF or pulseless VT.
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.
- ↑ Reiter, Michael J.; Reiffel, James A. (1998). "Importance of beta blockade in the therapy of serious ventricular arrhythmias". The American Journal of Cardiology. 82 (4): 9I–19I. doi:10.1016/S0002-9149(98)00468-8. ISSN 0002-9149.
- ↑ "Effect of metoprolol CR/XL in chronic heart failure: Metoprolol CR/XL Randomised Intervention Trial in Congestive Heart Failure (MERIT-HF)". Lancet. 353 (9169): 2001–7. June 1999. PMID 10376614.
- ↑ Kontos, Michael C.; Diercks, Debra B.; Ho, P. Michael; Wang, Tracy Y.; Chen, Anita Y.; Roe, Matthew T. (2011). "Treatment and outcomes in patients with myocardial infarction treated with acute β-blocker therapy: Results from the American College of Cardiology's NCDR®". American Heart Journal. 161 (5): 864–870. doi:10.1016/j.ahj.2011.01.006. ISSN 0002-8703.
- ↑ Hirsowitz, Geoffrey; Podrid, Philip J.; Lampert, Steven; Stein, Joseph; Lown, Bernard (1986). "The role of beta blocking agents as adjunct therapy to membrane stabilizing drugs in malignant ventricular arrhythmia". American Heart Journal. 111 (5): 852–860. doi:10.1016/0002-8703(86)90633-2. ISSN 0002-8703.
- ↑ Bardy, Gust H.; Lee, Kerry L.; Mark, Daniel B.; Poole, Jeanne E.; Packer, Douglas L.; Boineau, Robin; Domanski, Michael; Troutman, Charles; Anderson, Jill; Johnson, George; McNulty, Steven E.; Clapp-Channing, Nancy; Davidson-Ray, Linda D.; Fraulo, Elizabeth S.; Fishbein, Daniel P.; Luceri, Richard M.; Ip, John H. (2005). "Amiodarone or an Implantable Cardioverter–Defibrillator for Congestive Heart Failure". New England Journal of Medicine. 352 (3): 225–237. doi:10.1056/NEJMoa043399. ISSN 0028-4793.
- ↑ Thomas, Kevin L.; Al-Khatib, Sana M.; Lokhnygina, Yuliya; Solomon, Scott D.; Kober, Lars; McMurray, John J.V.; Califf, Robert M.; Velazquez, Eric J. (2008). "Amiodarone use after acute myocardial infarction complicated by heart failure and/or left ventricular dysfunction may be associated with excess mortality". American Heart Journal. 155 (1): 87–93. doi:10.1016/j.ahj.2007.09.010. ISSN 0002-8703.
- ↑ 13.0 13.1 13.2 Claro, Juan Carlos; Candia, Roberto; Rada, Gabriel; Baraona, Fernando; Larrondo, Francisco; Letelier, Luz M (2015). "Amiodarone versus other pharmacological interventions for prevention of sudden cardiac death". Cochrane Database of Systematic Reviews. doi:10.1002/14651858.CD008093.pub2. ISSN 1465-1858.
- ↑ Kudenchuk, Peter J.; Cobb, Leonard A.; Copass, Michael K.; Cummins, Richard O.; Doherty, Alidene M.; Fahrenbruch, Carol E.; Hallstrom, Alfred P.; Murray, William A.; Olsufka, Michele; Walsh, Thomas (1999). "Amiodarone for Resuscitation after Out-of-Hospital Cardiac Arrest Due to Ventricular Fibrillation". New England Journal of Medicine. 341 (12): 871–878. doi:10.1056/NEJM199909163411203. ISSN 0028-4793.
- ↑ Epstein, Andrew E.; Olshansky, Brian; Naccarelli, Gerald V.; Kennedy, John I.; Murphy, Elizabeth J.; Goldschlager, Nora (2016). "Practical Management Guide for Clinicians Who Treat Patients with Amiodarone". The American Journal of Medicine. 129 (5): 468–475. doi:10.1016/j.amjmed.2015.08.039. ISSN 0002-9343.
- ↑ Waldo AL, Camm AJ, deRuyter H, Freidman PL, MacNeil DJ, Pitt B, Pratt CM, Rodda BE, Schwartz PJ (May 1995). "Survival with oral d-sotalol in patients with left ventricular dysfunction after myocardial infarction: rationale, design, and methods (the SWORD trial)". Am J Cardiol. 75 (15): 1023–7. doi:10.1016/s0002-9149(99)80717-6. PMID 7747682.
- ↑ Page, Richard L (2000). "Effects of antiarrhythmic medication on implantable cardioverter-defibrillator function". The American Journal of Cardiology. 85 (12): 1481–1485. doi:10.1016/S0002-9149(00)00799-2. ISSN 0002-9149.
- ↑ Buxton, Alfred E.; Marchlinski, Francis E.; Doherty, John U.; Flores, Belinda; Josephson, Mark E. (1987). "Hazards of intravenous verapamil for sustained ventricular tachycardia". The American Journal of Cardiology. 59 (12): 1107–1110. doi:10.1016/0002-9149(87)90857-5. ISSN 0002-9149.
- ↑ Gill, Jaswinder S.; Ward, David E.; Camm, A. John (1992). "Comparison of Verapamil and Diltiazem in the Suppression of Idiopathic Ventricular Tachycardia". Pacing and Clinical Electrophysiology. 15 (11): 2122–2126. doi:10.1111/j.1540-8159.1992.tb03033.x. ISSN 0147-8389.
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