Ventricular tachycardia future or investigational therapies: Difference between revisions
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'''Future of medical management of ventricular tachycardia in structural heart disease''' <ref name="pmid24636548">{{cite journal| author=Peck KY, Lim YZ, Hopper I, Krum H| title=Medical therapy versus implantable cardioverter -defibrillator in preventing sudden cardiac death in patients with left ventricular systolic dysfunction and heart failure: a meta-analysis of > 35,000 patients. | journal=Int J Cardiol | year= 2014 | volume= 173 | issue= 2 | pages= 197-203 | pmid=24636548 | doi=10.1016/j.ijcard.2014.02.014 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24636548 }}</ref> | '''Future of medical management of ventricular tachycardia in structural heart disease''' <ref name="pmid24636548">{{cite journal| author=Peck KY, Lim YZ, Hopper I, Krum H| title=Medical therapy versus implantable cardioverter -defibrillator in preventing sudden cardiac death in patients with left ventricular systolic dysfunction and heart failure: a meta-analysis of > 35,000 patients. | journal=Int J Cardiol | year= 2014 | volume= 173 | issue= 2 | pages= 197-203 | pmid=24636548 | doi=10.1016/j.ijcard.2014.02.014 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24636548 }}</ref><ref name="pmid16403928">{{cite journal| author=Connolly SJ, Dorian P, Roberts RS, Gent M, Bailin S, Fain ES | display-authors=etal| title=Comparison of beta-blockers, amiodarone plus beta-blockers, or sotalol for prevention of shocks from implantable cardioverter defibrillators: the OPTIC Study: a randomized trial. | journal=JAMA | year= 2006 | volume= 295 | issue= 2 | pages= 165-71 | pmid=16403928 | doi=10.1001/jama.295.2.165 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16403928 }}</ref> | ||
It has been challenging to develop efficacious anti-arrhythmic drugs for VAs with a limited adverse-effect profile. | It has been challenging to develop efficacious anti-arrhythmic drugs for VAs with a limited adverse-effect profile. | ||
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* Nifekalant, a pure potassium channel blocker that has been approved for use in Japan for VT since 1999, has not been shown to be superior to amiodarone in treating out-of-hospital cardiac arrest or shock-resistant sustained VT/VF | * Nifekalant, a pure potassium channel blocker that has been approved for use in Japan for VT since 1999, has not been shown to be superior to amiodarone in treating out-of-hospital cardiac arrest or shock-resistant sustained VT/VF | ||
* Azimilide (another class III agent) which is not approved in the US has been shown to reduce VAs and appropriate ICD shocks in patients with cardiomyopathies (SHIELD trial) | * Azimilide (another class III agent) which is not approved in the US has been shown to reduce VAs and appropriate ICD shocks in patients with cardiomyopathies (SHIELD trial) | ||
Revision as of 14:47, 13 March 2020
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Ventricular tachycardia Microchapters |
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Differentiating Ventricular Tachycardia from other Disorders |
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Overview
In recent years, the results of pharmacologic therapy for preventing VAs are disappointing. Therapy limitations are due to variable efficacy, pro-arrhythmic effects, patient compliance, and adverse effects from long-term therapy. in patients with ICDs, adjuvant suppressive therapy as amiodarone and sotalol have been shown to reduce the rate of recurrent VT when compared with beta-blockers or placebo. Pharmacologic therapy (amiodarone or sotalol) with or without adjunctive catheter ablation are recommended by the current guidelines to prevent VT/VF recurrence and reducing ICD shocks
Future or investigational studies
In recent years, the results of pharmacologic therapy for preventing VAs are disappointing. Therapy limitations are due to variable efficacy, pro-arrhythmic effects, patient compliance, and adverse effects from long-term therapy. in patients with ICDs, adjuvant suppressive therapy as amiodarone and sotalol have been shown to reduce the rate of recurrent VT when compared with beta-blockers or placebo. Pharmacologic therapy (amiodarone or sotalol) with or without adjunctive catheter ablation are recommended by the current guidelines to prevent VT/VF recurrence and reducing ICD shocks[1]
The goals of management of VAs include:
- Symptom relief (including syncope, worsening heart failure, and ischemic chest pain),
- Improving quality of life, * Reducing implantable cardioverter defibrillator (ICD) shocks,
- Preventing deterioration of left ventricular function
- Reducing risk of arrhythmic death
- Improving overall survival7–10. Treatment of underlying medical conditions, the cardiac disorders, the presence of heart failure, the cause for the arrhythmias, consequences of the VAs, and the risks and benefits of the therapeutic pharmacological or invasive strategy[2]
Recent research and clinical advances allowed to tailor the approach to VA management on the basis of the underlying etiology with higher efficacy. These advances have been focused on:
- The development of diagnostic modalities and imaging tools to identify the arrhythmogenic substrate responsible for VT (focal or scar)
- Genetic screening for markers of channelopathies, and
- Superior mapping and ablation technologies[2][3]
Non-invasive imaging and diagnostic modalities
Over the past 100 years, cardiologists rely on the following to diagnose VT:
- ECG
- Monitoring strategies
- Limited intracardiac electrodes
As the mechanism of VT has become better understood and defined, the following non-invasive imaging modalities have become an integral part of the diagnostic and management strategy: [4][5]
- Echocardiography
- Cardiac computed tomography (CT)
- Cardiac magnetic resonance imaging (MRI) (CMR)
- Nuclear studies
Based on the 2015 European Society of Cardiology Guidelines, If echocardiography fails to provide accurate assessment of ventricular function or underlying structural changes that may be arrhythmogenic (scar size, distribution, and transmurality), perform CMR or CT (extended a class IIa recommendation)
The information derived from these tests are important to:
- Identify structural heart disease
- Assess left and right ventricular function
- Risk-stratify those at highest risk of inducible VT/VF on the basis of scar size in order to select the patients who would benefit most from an ICD
- Serves as a guide for planning ablation procedures
Inherited cardiomyopathies and channelopathies[6][7][8][9]
- Up to half of the families of sudden cardiac arrest victims below 50 years of age are carriers of hereditary cardiomyopathies or cardiac genetic channelopathies
- It is recommended to evaluate patients and first-degree relatives with sudden cardiac arrest caused by inherited cardiovascular disease (diagnosed or suspected) in a dedicated clinic with appropriately trained staff (class I, 2015 Expert Consensus Statement from the Heart Rhythm Society)
- Early identification of a channelopathy or inherited cardiomyopathy can now be done at appropriate centers at a low cost by performing an extended molecular gene panels
- This allows risk stratification of sudden cardiac death and introduction of appropriately timed therapy (lifestyle changes, pharmacologic therapy versus ICD implantation or catheter ablation or both)
- Identification of a potential arrhythmic substrate located in the epicardial right ventricular outflow tract (RVOT) that may trigger VT/VF in some patients with Brugada syndrome has been identified and is considered an example of an important breakthrough in treating genetic arrhythmia syndromes
- Epicardial 3D EAM has shown abnormal low voltage and fractionated late potentials clustered exclusively in the anterior RVOT epicardium.
- Ablation at these sites rendered VT/VF non-inducible in 78% and normalization of the Brugada ECG pattern (coved ST-elevations in V1 and V2) in 89%.
- BRAVE Study is a multicenter randomized study (ablation in Brugada Syndrome for the Prevention of VF episodes) is being planned to assess long-term outcomes of catheter ablation in patients with Brugada syndrome
Future of medical management of ventricular tachycardia in structural heart disease [10][11]
It has been challenging to develop efficacious anti-arrhythmic drugs for VAs with a limited adverse-effect profile.
- Intravenous amiodarone and sodium channel blockers (lidocaine and procainamide) remain the preferred drug regimen in the acute setting
- Intravenous sotalol has been shown to terminate sustained VT acutely with a higher efficacy versus lidocaine
- Neither amiodarone nor lidocaine has been shown to improve survival or neurologic outcomes in patients with pulseless VT/VF and out-of-hospital cardiac arrest
- intravenous procainamide has been shown to be more efficacious in tachycardia termination and was associated with fewer major cardiovascular events than amiodarone in the acute treatment of hemodynamically tolerated acute treatment of VT
- The effect was consistently observed even in those with structural heart disease as well as when adjusted for age and sex.
- Catheter ablation has been shown to be more efficacious in terms of morbidity primary outcome than escalation of anti-arrhythmic drug therapy (amiodarone or mexiletine or both) but no significant difference in terms of mortatlity
- Meta-analysis studies have shown that there is no significant difference between between anti-arrhythmic drugs versus catheter ablation for preventing recurrent VT in patients with ICDs in terms of risk reduction of VT as well as all-cause mortality
- After successful VT ablation, amiodarone may be safely reduced or discontinued to avoid potential long-term adverse effects and reduce mortality, without an increase risk in VT recurrence
- Nifekalant, a pure potassium channel blocker that has been approved for use in Japan for VT since 1999, has not been shown to be superior to amiodarone in treating out-of-hospital cardiac arrest or shock-resistant sustained VT/VF
- Azimilide (another class III agent) which is not approved in the US has been shown to reduce VAs and appropriate ICD shocks in patients with cardiomyopathies (SHIELD trial)
Future for implantable device therapy
Future of Invasive mapping and catheter ablation
References
- ↑ Batul SA, Olshansky B, Fisher JD, Gopinathannair R (2017). "Recent advances in the management of ventricular tachyarrhythmias". F1000Res. 6: 1027. doi:10.12688/f1000research.11202.1. PMC 5497814. PMID 28721212.
- ↑ 2.0 2.1 Priori SG, Blomström-Lundqvist C, Mazzanti A, Blom N, Borggrefe M, Camm J; et al. (2015). "2015 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: The Task Force for the Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death of the European Society of Cardiology (ESC). Endorsed by: Association for European Paediatric and Congenital Cardiology (AEPC)". Eur Heart J. 36 (41): 2793–2867. doi:10.1093/eurheartj/ehv316. PMID 26320108.
- ↑ Priori SG, Wilde AA, Horie M, Cho Y, Behr ER, Berul C; et al. (2013). "HRS/EHRA/APHRS expert consensus statement on the diagnosis and management of patients with inherited primary arrhythmia syndromes: document endorsed by HRS, EHRA, and APHRS in May 2013 and by ACCF, AHA, PACES, and AEPC in June 2013". Heart Rhythm. 10 (12): 1932–63. doi:10.1016/j.hrthm.2013.05.014. PMID 24011539.
- ↑ Zeidan-Shwiri T, Yang Y, Lashevsky I, Kadmon E, Kagal D, Dick A; et al. (2015). "Magnetic resonance estimates of the extent and heterogeneity of scar tissue in ICD patients with ischemic cardiomyopathy predict ventricular arrhythmia". Heart Rhythm. 12 (4): 802–8. doi:10.1016/j.hrthm.2015.01.007. PMC 5774997. PMID 25583153.
- ↑ Esposito A, Palmisano A, Antunes S, Maccabelli G, Colantoni C, Rancoita PMV; et al. (2016). "Cardiac CT With Delayed Enhancement in the Characterization of Ventricular Tachycardia Structural Substrate: Relationship Between CT-Segmented Scar and Electro-Anatomic Mapping". JACC Cardiovasc Imaging. 9 (7): 822–832. doi:10.1016/j.jcmg.2015.10.024. PMID 26897692.
- ↑ Fernández-Falgueras A, Sarquella-Brugada G, Brugada J, Brugada R, Campuzano O (2017). "Cardiac Channelopathies and Sudden Death: Recent Clinical and Genetic Advances". Biology (Basel). 6 (1). doi:10.3390/biology6010007. PMC 5372000. PMID 28146053.
- ↑ Nademanee K, Hocini M, Haïssaguerre M (2017). "Epicardial substrate ablation for Brugada syndrome". Heart Rhythm. 14 (3): 457–461. doi:10.1016/j.hrthm.2016.12.001. PMID 27979714.
- ↑ Zhang P, Tung R, Zhang Z, Sheng X, Liu Q, Jiang R; et al. (2016). "Characterization of the epicardial substrate for catheter ablation of Brugada syndrome". Heart Rhythm. 13 (11): 2151–2158. doi:10.1016/j.hrthm.2016.07.025. PMID 27453126.
- ↑ Ostby SA, Bos JM, Owen HJ, Wackel PL, Cannon BC, Ackerman MJ (2016). "Competitive Sports Participation in Patients With Catecholaminergic Polymorphic Ventricular Tachycardia: A Single Center's Early Experience". JACC Clin Electrophysiol. 2 (3): 253–262. doi:10.1016/j.jacep.2016.01.020. PMID 29766881.
- ↑ Peck KY, Lim YZ, Hopper I, Krum H (2014). "Medical therapy versus implantable cardioverter -defibrillator in preventing sudden cardiac death in patients with left ventricular systolic dysfunction and heart failure: a meta-analysis of > 35,000 patients". Int J Cardiol. 173 (2): 197–203. doi:10.1016/j.ijcard.2014.02.014. PMID 24636548.
- ↑ Connolly SJ, Dorian P, Roberts RS, Gent M, Bailin S, Fain ES; et al. (2006). "Comparison of beta-blockers, amiodarone plus beta-blockers, or sotalol for prevention of shocks from implantable cardioverter defibrillators: the OPTIC Study: a randomized trial". JAMA. 295 (2): 165–71. doi:10.1001/jama.295.2.165. PMID 16403928.