Ventricular tachycardia medical therapy
|
Ventricular tachycardia Microchapters |
|
Differentiating Ventricular Tachycardia from other Disorders |
|---|
|
Diagnosis |
|
Treatment |
|
Case Studies |
|
Ventricular tachycardia medical therapy On the Web |
|
to Hospitals Treating Ventricular tachycardia medical therapy |
|
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
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, treating the underlying causes of VT including ischemic heart disease or decompensated heart failure are warranted.
Medical Therapy
Common medications for treatment of VT include:[1]
Antiarrhythmic medications
Sodium channel blocker
- In patients with ischemic heart disease, chronic use of sodium channel blocker increased risk of mortality.
- Some sodium channel blockers with 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.
- Reducion ICD shocks in drug resistant VT, VF[1]
- Reducion VT in the first days after NSTEMI according to MERLIN TIMI-36.[6]
Beta blocker
- First line therapy for the most of ventricular arrhythmia such as PVC, VT because of safety and efficacy[8]
- Supression of ventricular arrhythmia in structurally normal heart.
- Reducing all-cause mortality and SCD in patients with heart failure with reduced EF[9]
- Reducing 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 resuscitation 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 with 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]
Management of patients with Polymorphic Ventricular arrhythmia
| The above algorithm adopted from 2022 ESC Guideline[38] |
|---|
Management of sustained monomorphic ventricular tachycardia
| Recommendations for acute management of sustained VT |
| DC cardiovertion (Class I, Level of Evidence B): |
|
❑ DC cardioversion is recommended as the first-line therapy for hemodynamically not-tolerated sustained monomorphic ventricular tachycardia |
| DC cardiovertion (Class I, Level of Evidence C) : |
|
❑ DC cardioversion is recommended as the first-line treatment for patients presenting with tolerated sustained monomorphic VT when anesthetic/sedation risk is low |
| Supraventricular tachycardia (Class IIa, Level of Evidence C) |
|
❑ In patients presenting with a regular hemodynamically tolerated wide QRS complex tachycardia suspected for supraventricular tachycardia, administration of adenosine or vagal maneuvers should be considered |
| Procainamide (Class IIa, Level of Evidence B) |
|
❑In patients presenting with a hemodynamically tolerated sustained monomorphic VT and presence of structural heart disease, intravenous procainamide should be considered |
| Flecainide, ajmaline, sotalol (Class IIb, Level of Evidence B) |
|
❑In patients presenting with a hemodynamically tolerated sustained monomorphic VT in the absence of significant structural heart disease, flecainide, ajmaline, or sotalol may be considered |
| Verapamil (Class III, Level of Evidence B) |
|
❑Intravenous verapamil is not recommended in wide QRS complex tachycardia of unknown mechanism |
| The above table adopted from 2022 ESC Guideline[38] |
|---|
Management of electrical storm
| Recommendations for management of electrical storm |
| Sedation (Class I, Level of Evidence C): |
|
❑ Mild to moderate sedation is recommended in patients with the electrical storm to reduce psychological distress and reduce sympathetic tone |
| Strucrural heart disease (Class I, Level of Evidence B) : |
|
❑ Antiarrhythmic therapy with beta-blockers (non-selective preferred) in combination with intravenous amiodarone is recommended in patients with structural heart disease and electrical storm unless contraindicated |
| Torsades depointes (Class I, Level of Evidence C) |
|
❑ Intravenous magnesium with supplementation of potassium is recommended in patients with TdP |
| Procainamide (Class IIa, Level of Evidence B) |
|
❑In patients presenting with a hemodynamically tolerated sustained monomorphic VT and presence of structural heart disease, intravenous procainamide should be considered |
| Intubation (Class IIa, Level of Evidence C) |
|
❑Deep sedation/intubation should be considered in patients with an intractable electrical storm non-responsive drug treatment ❑Catheter ablation should be considered in patients with recurrent episodes of VT/VF triggered by a similar PVC, refractory to medical treatment
or coronary revascularization |
| Quinidine (Class IIb, Level of Evidence C) |
|
❑Quinidine may be considered in patients with coronary artery disease and electrical storm due to recurrent VT refractory to other antiarrhythmic drugs |
| Refractory electerical storm (Class IIb, Level of Evidence C) |
|
❑Autonomic modulation may be considered in patients with electrical storm refractory to medical therapy and in whom catheter ablation is
ineffective or not possible |
| The above table adopted from 2022 ESC Guideline[38] |
|---|
Recommendations for treatment with heart failure medication
| Class I |
| "Optimal medical treatment including ACE-I/ARB/ ARNIs, mineralocorticoid receptor antagonist, beta-blockers, and SGLT2 inhibitors is indicated in all heart failure patients with reduced EF' (Level of Evidence A)" |
| The above table adopted from 2022 ESC Guideline[38] |
|---|
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.[39]
- 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%.[40]
- 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.[41]
- 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.[42][43]
- 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. [44]
- In the presence of incessant VT, amiodarone was more effective than lidocaine and improved survival at 24 hours.[45]
- 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.[46]
- 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).[47]
- Administration of vasopressin is no longer recommended in the most recent advanced cardiovascular life support guideline.[48]
- 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.[49]
- 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.[50]
- Prophylactic use of Higher dose amiodarone after MI increase mortality, whereas moderate dose amiodarone was not superior to placebo.[51]
- 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) | |||||||||||||||||||||||||||||||||||||||||||||||||||||||
| 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][52]
- Amiodarone is more effective than sotalol but discontinuation may happen during 12-24 months of use due to adverse effects.[53]
- 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.[54]
- 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.[55]
- 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 can be due to scar-related reentry, but not acute ischemia.
- Antiarrhythmic medications or ablation may be needed to prevent recurrence of VT in scar-related settings.[56]
- Revascularization is recommended in the setting of ischemia for prevention of VF, polymorphic VT. [57]
| 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 |
| 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 |
| The above table adopted from 2017 AHA/ACC/HRS Guideline[2] |
|---|
Message
- Although ICD reduced mortality, painful ICD shocks can affect on the quality of life and increases 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.[53]
- All types of non-ischemic cardiomyopathy can produce scar-related VT especially cardiac sarcoidosis.[58]
- Catheter ablation can be used for treatment of scar related VT in non-ischemic cardiomyopathy.[59]
| 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[2] |
|---|
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.
- ↑ 2.0 2.1 2.2 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.
- ↑ 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.
- ↑ 14.0 14.1 14.2 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.
- ↑ 19.0 19.1 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.
- ↑ Badhwar, Nitish; Scheinman, Melvin M. (2007). "Idiopathic Ventricular Tachycardia: Diagnosis and Management". Current Problems in Cardiology. 32 (1): 7–43. doi:10.1016/j.cpcardiol.2006.10.002. ISSN 0146-2806.
- ↑ 22.0 22.1 Cooper, Howard A.; Dries, Daniel L.; Davis, C. E.; Shen, Yuan Li; Domanski, Michael J. (1999). "Diuretics and Risk of Arrhythmic Death in Patients With Left Ventricular Dysfunction". Circulation. 100 (12): 1311–1315. doi:10.1161/01.CIR.100.12.1311. ISSN 0009-7322.
- ↑ Yan, Gan-Xin; Antzelevitch, Charles (1998). "Cellular Basis for the Normal T Wave and the Electrocardiographic Manifestations of the Long-QT Syndrome". Circulation. 98 (18): 1928–1936. doi:10.1161/01.CIR.98.18.1928. ISSN 0009-7322.
- ↑ Tzivoni, D; Banai, S; Schuger, C; Benhorin, J; Keren, A; Gottlieb, S; Stern, S (1988). "Treatment of torsade de pointes with magnesium sulfate". Circulation. 77 (2): 392–397. doi:10.1161/01.CIR.77.2.392. ISSN 0009-7322.
- ↑ Cohn, Jay N.; Kowey, Peter R.; Whelton, Paul K.; Prisant, L. Michael (2000). "New Guidelines for Potassium Replacement in Clinical Practice". Archives of Internal Medicine. 160 (16): 2429. doi:10.1001/archinte.160.16.2429. ISSN 0003-9926.
- ↑ Goyal, Abhinav; Spertus, John A.; Gosch, Kensey; Venkitachalam, Lakshmi; Jones, Philip G.; Van den Berghe, Greet; Kosiborod, Mikhail (2012). "Serum Potassium Levels and Mortality in Acute Myocardial Infarction". JAMA. 307 (2): 157. doi:10.1001/jama.2011.1967. ISSN 0098-7484.
- ↑ Antman, Elliott M (2002). "Early administration of intravenous magnesium to high-risk patients with acute myocardial infarction in the Magnesium in Coronaries (MAGIC) Trial: a randomised controlled trial". The Lancet. 360 (9341): 1189–1196. doi:10.1016/S0140-6736(02)11278-5. ISSN 0140-6736.
- ↑ Leaf, Alexander; Kang, Jing X.; Xiao, Yong-Fu; Billman, George E. (2003). "Clinical Prevention of Sudden Cardiac Death by n-3 Polyunsaturated Fatty Acids and Mechanism of Prevention of Arrhythmias by n-3 Fish Oils". Circulation. 107 (21): 2646–2652. doi:10.1161/01.CIR.0000069566.78305.33. ISSN 0009-7322.
- ↑ Marchioli, Roberto; Barzi, Federica; Bomba, Elena; Chieffo, Carmine; Di Gregorio, Domenico; Di Mascio, Rocco; Franzosi, Maria Grazia; Geraci, Enrico; Levantesi, Giacomo; Maggioni, Aldo Pietro; Mantini, Loredana; Marfisi, Rosa Maria; Mastrogiuseppe, G.; Mininni, Nicola; Nicolosi, Gian Luigi; Santini, Massimo; Schweiger, Carlo; Tavazzi, Luigi; Tognoni, Gianni; Tucci, Corrado; Valagussa, Franco (2002). "Early Protection Against Sudden Death by n-3 Polyunsaturated Fatty Acids After Myocardial Infarction". Circulation. 105 (16): 1897–1903. doi:10.1161/01.CIR.0000014682.14181.F2. ISSN 0009-7322.
- ↑ "n–3 Fatty Acids and Cardiovascular Outcomes in Patients with Dysglycemia". New England Journal of Medicine. 367 (4): 309–318. 2012. doi:10.1056/NEJMoa1203859. ISSN 0028-4793.
- ↑ LaRosa, John C.; He, Jiang; Vupputuri, Suma (1999). "Effect of Statins on Risk of Coronary Disease". JAMA. 282 (24): 2340. doi:10.1001/jama.282.24.2340. ISSN 0098-7484.
- ↑ Tavazzi L, Maggioni AP, Marchioli R, Barlera S, Franzosi MG, Latini R, Lucci D, Nicolosi GL, Porcu M, Tognoni G (October 2008). "Effect of rosuvastatin in patients with chronic heart failure (the GISSI-HF trial): a randomised, double-blind, placebo-controlled trial". Lancet. 372 (9645): 1231–9. doi:10.1016/S0140-6736(08)61240-4. PMID 18757089.
- ↑ Cohn JN, Johnson G, Ziesche S, Cobb F, Francis G, Tristani F, Smith R, Dunkman WB, Loeb H, Wong M (August 1991). "A comparison of enalapril with hydralazine-isosorbide dinitrate in the treatment of chronic congestive heart failure". N Engl J Med. 325 (5): 303–10. doi:10.1056/NEJM199108013250502. PMID 2057035.
- ↑ "The Cardiac Insufficiency Bisoprolol Study II (CIBIS-II): a randomised trial". Lancet. 353 (9146): 9–13. January 1999. PMID 10023943.
- ↑ Dargie HJ (May 2001). "Effect of carvedilol on outcome after myocardial infarction in patients with left-ventricular dysfunction: the CAPRICORN randomised trial". Lancet. 357 (9266): 1385–90. doi:10.1016/s0140-6736(00)04560-8. PMID 11356434.
- ↑ Hjalmarson A, Goldstein S, Fagerberg B, Wedel H, Waagstein F, Kjekshus J, Wikstrand J, El Allaf D, Vítovec J, Aldershvile J, Halinen M, Dietz R, Neuhaus KL, Jánosi A, Thorgeirsson G, Dunselman PH, Gullestad L, Kuch J, Herlitz J, Rickenbacher P, Ball S, Gottlieb S, Deedwania P (March 2000). "Effects of controlled-release metoprolol on total mortality, hospitalizations, and well-being in patients with heart failure: the Metoprolol CR/XL Randomized Intervention Trial in congestive heart failure (MERIT-HF). MERIT-HF Study Group". JAMA. 283 (10): 1295–302. doi:10.1001/jama.283.10.1295. PMID 10714728.
- ↑ Pitt B, Zannad F, Remme WJ, Cody R, Castaigne A, Perez A, Palensky J, Wittes J (September 1999). "The effect of spironolactone on morbidity and mortality in patients with severe heart failure. Randomized Aldactone Evaluation Study Investigators". N Engl J Med. 341 (10): 709–17. doi:10.1056/NEJM199909023411001. PMID 10471456.
- ↑ 38.0 38.1 38.2 38.3 Zeppenfeld K, Tfelt-Hansen J, de Riva M, Winkel BG, Behr ER, Blom NA, Charron P, Corrado D, Dagres N, de Chillou C, Eckardt L, Friede T, Haugaa KH, Hocini M, Lambiase PD, Marijon E, Merino JL, Peichl P, Priori SG, Reichlin T, Schulz-Menger J, Sticherling C, Tzeis S, Verstrael A, Volterrani M (August 2022). "2022 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death". Eur Heart J. doi:10.1093/eurheartj/ehac262. PMID 36017572 Check
|pmid=value (help). - ↑ Zipes, Douglas P.; Camm, A. John; Borggrefe, Martin; Buxton, Alfred E.; Chaitman, Bernard; Fromer, Martin; Gregoratos, Gabriel; Klein, George; Moss, Arthur J.; Myerburg, Robert J.; Priori, Silvia G.; Quinones, Miguel A.; Roden, Dan M.; Silka, Michael J.; Tracy, Cynthia (2006). "ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death". Circulation. 114 (10). doi:10.1161/CIRCULATIONAHA.106.178233. ISSN 0009-7322.
- ↑ Sasson, Comilla; Rogers, Mary A.M.; Dahl, Jason; Kellermann, Arthur L. (2010). "Predictors of Survival From Out-of-Hospital Cardiac Arrest". Circulation: Cardiovascular Quality and Outcomes. 3 (1): 63–81. doi:10.1161/CIRCOUTCOMES.109.889576. ISSN 1941-7713.
- ↑ Connolly, S (2000). "Meta-analysis of the implantable cardioverter defibrillator secondary prevention trials". European Heart Journal. 21 (24): 2071–2078. doi:10.1053/euhj.2000.2476. ISSN 0195-668X.
- ↑ Spaulding, Christian M.; Joly, Luc-Marie; Rosenberg, Alain; Monchi, Mehran; Weber, Simon N.; Dhainaut, Jean-François A.; Carli, Pierre (1997). "Immediate Coronary Angiography in Survivors of Out-of-Hospital Cardiac Arrest". New England Journal of Medicine. 336 (23): 1629–1633. doi:10.1056/NEJM199706053362302. ISSN 0028-4793.
- ↑ Zanuttini, Davide; Armellini, Ilaria; Nucifora, Gaetano; Carchietti, Elio; Trillò, Giulio; Spedicato, Leonardo; Bernardi, Guglielmo; Proclemer, Alessandro (2012). "Impact of Emergency Coronary Angiography on In-Hospital Outcome of Unconscious Survivors After Out-of-Hospital Cardiac Arrest". The American Journal of Cardiology. 110 (12): 1723–1728. doi:10.1016/j.amjcard.2012.08.006. ISSN 0002-9149.
- ↑ Dumas, Florence; Bougouin, Wulfran; Geri, Guillaume; Lamhaut, Lionel; Rosencher, Julien; Pène, Frédéric; Chiche, Jean-Daniel; Varenne, Olivier; Carli, Pierre; Jouven, Xavier; Mira, Jean-Paul; Spaulding, Christian; Cariou, Alain (2016). "Emergency Percutaneous Coronary Intervention in Post–Cardiac Arrest Patients Without ST-Segment Elevation Pattern". JACC: Cardiovascular Interventions. 9 (10): 1011–1018. doi:10.1016/j.jcin.2016.02.001. ISSN 1936-8798.
- ↑ Somberg, John C; Bailin, Steven J; Haffajee, Charles I; Paladino, Walter P; Kerin, Nicholas Z; Bridges, Duane; Timar, Sandor; Molnar, Janos (2002). "Intravenous lidocaine versus intravenous amiodarone (in a new aqueous formulation) for incessant ventricular tachycardia". The American Journal of Cardiology. 90 (8): 853–859. doi:10.1016/S0002-9149(02)02707-8. ISSN 0002-9149.
- ↑ Gorgels, Anton P.M.; van den Dool, Adri; Hofs, Anton; Mulleneers, Rob; Smeets, Joep L.R.M.; Vos, Marc A.; Wellens, Hein J.J. (1996). "Comparison of procainamide and lidocaine in terminating sustained monomorphic ventricular tachycardia". The American Journal of Cardiology. 78 (1): 43–46. doi:10.1016/S0002-9149(96)00224-X. ISSN 0002-9149.
- ↑ Callaham M, Madsen CD, Barton CW, Saunders CE, Pointer J (November 1992). "A randomized clinical trial of high-dose epinephrine and norepinephrine vs standard-dose epinephrine in prehospital cardiac arrest". JAMA. 268 (19): 2667–72. PMID 1433686.
- ↑ Link, Mark S.; Berkow, Lauren C.; Kudenchuk, Peter J.; Halperin, Henry R.; Hess, Erik P.; Moitra, Vivek K.; Neumar, Robert W.; O’Neil, Brian J.; Paxton, James H.; Silvers, Scott M.; White, Roger D.; Yannopoulos, Demetris; Donnino, Michael W. (2015). "Part 7: Adult Advanced Cardiovascular Life Support". Circulation. 132 (18 suppl 2): S444–S464. doi:10.1161/CIR.0000000000000261. ISSN 0009-7322.
- ↑ Hassan, T B (2002). "A randomised trial to investigate the efficacy of magnesium sulphate for refractory ventricular fibrillation". Emergency Medicine Journal. 19 (1): 57–62. doi:10.1136/emj.19.1.57. ISSN 1472-0205.
- ↑ Teo KK, Yusuf S, Furberg CD (October 1993). "Effects of prophylactic antiarrhythmic drug therapy in acute myocardial infarction. An overview of results from randomized controlled trials". JAMA. 270 (13): 1589–95. PMID 8371471.
- ↑ Elizari, M (2000). "Morbidity and mortality following early administration of amiodarone in acute myocardial infarction". European Heart Journal. 21 (3): 198–205. doi:10.1053/euhj.1999.1687. ISSN 0195-668X.
- ↑ Kettering, Klaus; Mewis, Christian; Dornberger, Volker; Vonthein, Reinhard; Bosch, Ralph F.; Kuhlkamp, Volker (2002). "Efficacy of Metoprolol and Sotalol in the Prevention of Recurrences of Sustained Ventricular Tachyarrhythmias in Patients with an Implantable Cardioverter Defibrillator". Pacing and Clinical Electrophysiology. 25 (11): 1571–1576. doi:10.1046/j.1460-9592.2002.01571.x. ISSN 0147-8389.
- ↑ 53.0 53.1 Connolly, Stuart J. (2006). "Comparison of β-Blockers, Amiodarone Plus β-Blockers, or Sotalol for Prevention of Shocks From Implantable Cardioverter Defibrillators<SUBTITLE>The OPTIC Study: A Randomized Trial</SUBTITLE>". JAMA. 295 (2): 165. doi:10.1001/jama.295.2.165. ISSN 0098-7484.
- ↑ Tung, Roderick; Vaseghi, Marmar; Frankel, David S.; Vergara, Pasquale; Di Biase, Luigi; Nagashima, Koichi; Yu, Ricky; Vangala, Sitaram; Tseng, Chi-Hong; Choi, Eue-Keun; Khurshid, Shaan; Patel, Mehul; Mathuria, Nilesh; Nakahara, Shiro; Tzou, Wendy S.; Sauer, William H.; Vakil, Kairav; Tedrow, Usha; Burkhardt, J. David; Tholakanahalli, Venkatakrishna N.; Saliaris, Anastasios; Dickfeld, Timm; Weiss, J. Peter; Bunch, T. Jared; Reddy, Madhu; Kanmanthareddy, Arun; Callans, David J.; Lakkireddy, Dhanunjaya; Natale, Andrea; Marchlinski, Francis; Stevenson, William G.; Della Bella, Paolo; Shivkumar, Kalyanam (2015). "Freedom from recurrent ventricular tachycardia after catheter ablation is associated with improved survival in patients with structural heart disease: An International VT Ablation Center Collaborative Group study". Heart Rhythm. 12 (9): 1997–2007. doi:10.1016/j.hrthm.2015.05.036. ISSN 1547-5271.
- ↑ Echt, Debra S.; Liebson, Philip R.; Mitchell, L. Brent; Peters, Robert W.; Obias-Manno, Dulce; Barker, Allan H.; Arensberg, Daniel; Baker, Andrea; Friedman, Lawrence; Greene, H. Leon; Huther, Melissa L.; Richardson, David W. (1991). "Mortality and Morbidity in Patients Receiving Encainide, Flecainide, or Placebo". New England Journal of Medicine. 324 (12): 781–788. doi:10.1056/NEJM199103213241201. ISSN 0028-4793.
- ↑ Brugada, Josep; Aguinaga, Luis; Mont, Lluı́s; Betriu, Amadeu; Mulet, Jaume; Sanz, Ginés (2001). "Coronary artery revascularization in patients with sustained ventricular arrhythmias in the chronic phase of a myocardial infarction: effects on the electrophysiologic substrate and outcome". Journal of the American College of Cardiology. 37 (2): 529–533. doi:10.1016/S0735-1097(00)01133-5. ISSN 0735-1097.
- ↑ Berntsen, R. F.; Gunnes, P.; Lie, M.; Rasmussen, K. (1993). "Surgical revascularization in the treatment of ventricular tachycardia and fibrillation exposed by exercise-induced ischaemia". European Heart Journal. 14 (10): 1297–1303. doi:10.1093/eurheartj/14.10.1297. ISSN 0195-668X.
- ↑ Naruse, Yoshihisa; Sekiguchi, Yukio; Nogami, Akihiko; Okada, Hiroyuki; Yamauchi, Yasuteru; Machino, Takeshi; Kuroki, Kenji; Ito, Yoko; Yamasaki, Hiro; Igarashi, Miyako; Tada, Hiroshi; Nitta, Junichi; Xu, Dongzhu; Sato, Akira; Aonuma, Kazutaka (2014). "Systematic Treatment Approach to Ventricular Tachycardia in Cardiac Sarcoidosis". Circulation: Arrhythmia and Electrophysiology. 7 (3): 407–413. doi:10.1161/CIRCEP.113.000734. ISSN 1941-3149.
- ↑ Dinov, Borislav; Fiedler, Lukas; Schönbauer, Robert; Bollmann, Andreas; Rolf, Sascha; Piorkowski, Christopher; Hindricks, Gerhard; Arya, Arash (2014). "Outcomes in Catheter Ablation of Ventricular Tachycardia in Dilated Nonischemic Cardiomyopathy Compared With Ischemic Cardiomyopathy". Circulation. 129 (7): 728–736. doi:10.1161/CIRCULATIONAHA.113.003063. ISSN 0009-7322.