Ventricular tachycardia medical therapy: Difference between revisions
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* Chronic [[Beta blocker]]s therapy in [[heart failure]] reduced [[EF]] was associated with reduced [[SCD]], [[ventricular arrhythmia]] and all cause [[mortality]]. | * Chronic [[Beta blocker]]s 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]].<ref name="pmid10023943">{{cite journal |vauthors= |title=The Cardiac Insufficiency Bisoprolol Study II (CIBIS-II): a randomised trial |journal=Lancet |volume=353 |issue=9146 |pages=9–13 |date=January 1999 |pmid=10023943 |doi= |url=}}</ref><ref name="pmid11356434">{{cite journal |vauthors=Dargie HJ |title=Effect of carvedilol on outcome after myocardial infarction in patients with left-ventricular dysfunction: the CAPRICORN randomised trial |journal=Lancet |volume=357 |issue=9266 |pages=1385–90 |date=May 2001 |pmid=11356434 |doi=10.1016/s0140-6736(00)04560-8 |url=}}</ref><ref name="pmid10714728">{{cite journal |vauthors=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 |title=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 |journal=JAMA |volume=283 |issue=10 |pages=1295–302 |date=March 2000 |pmid=10714728 |doi=10.1001/jama.283.10.1295 |url=}}</ref> | *[[Bisoprolol]], [[carvedilol]], sustained-release [[metoprolol]] succinate decrease [[mortality]] in [[patients]] with [[heart failure]] reduced [[EF]].<ref name="pmid10023943">{{cite journal |vauthors= |title=The Cardiac Insufficiency Bisoprolol Study II (CIBIS-II): a randomised trial |journal=Lancet |volume=353 |issue=9146 |pages=9–13 |date=January 1999 |pmid=10023943 |doi= |url=}}</ref><ref name="pmid11356434">{{cite journal |vauthors=Dargie HJ |title=Effect of carvedilol on outcome after myocardial infarction in patients with left-ventricular dysfunction: the CAPRICORN randomised trial |journal=Lancet |volume=357 |issue=9266 |pages=1385–90 |date=May 2001 |pmid=11356434 |doi=10.1016/s0140-6736(00)04560-8 |url=}}</ref><ref name="pmid10714728">{{cite journal |vauthors=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 |title=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 |journal=JAMA |volume=283 |issue=10 |pages=1295–302 |date=March 2000 |pmid=10714728 |doi=10.1001/jama.283.10.1295 |url=}}</ref> | ||
* [[ACEI]] and [[mineralocorticoid-receptor antagonists]] ([[spironolactone]], [[eplerenone]]) reduce [[mortality]] and [[SCD]]. | * [[ACEI]] and [[mineralocorticoid-receptor antagonists]] ([[spironolactone]], [[eplerenone]]) reduce [[mortality]] and [[SCD]]. <ref name="pmid2057035">{{cite journal |vauthors=Cohn JN, Johnson G, Ziesche S, Cobb F, Francis G, Tristani F, Smith R, Dunkman WB, Loeb H, Wong M |title=A comparison of enalapril with hydralazine-isosorbide dinitrate in the treatment of chronic congestive heart failure |journal=N Engl J Med |volume=325 |issue=5 |pages=303–10 |date=August 1991 |pmid=2057035 |doi=10.1056/NEJM199108013250502 |url=}}</ref> | ||
* [[angiotensin receptor-neprilysin inhibitor]] ([[sacubitril]]/[[valsartan]]) reduces [[mortality]] and [[SCD]]. | * [[angiotensin receptor-neprilysin inhibitor]] ([[sacubitril]]/[[valsartan]]) reduces [[mortality]] and [[SCD]]. | ||
Revision as of 15:27, 4 May 2021
Ventricular tachycardia Microchapters |
Differentiating Ventricular Tachycardia from other Disorders |
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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: 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 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:[32]
- 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.
- 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. [36]
- angiotensin receptor-neprilysin inhibitor (sacubitril/valsartan) reduces mortality and SCD.
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
2006 ACC/AHA/ESC Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death (DO NOT EDIT) [37]Management of Cardiac Arrest (DO NOT EDIT) [37]
Ventricular Tachycardia Associated With Low Troponin Myocardial Infarction (DO NOT EDIT) [37]
Sustained Monomorphic Ventricular Tachycardia (DO NOT EDIT) [37]
Repetitive Monomorphic Ventricular Tachycardia (DO NOT EDIT) [37]
Polymorphic Ventricular Tachycardia (DO NOT EDIT) [37]
Torsades de Pointes (DO NOT EDIT) [37]
Incessant Ventricular Tachycardia (DO NOT EDIT) [37]
Idiopathic Ventricular Tachycardia (DO NOT EDIT) [37]
Other Drug-Induced Toxicity (DO NOT EDIT) [37]
References
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