This document discusses premature ventricular complexes (PVCs) and catheter ablation for treating PVCs. It defines PVCs as early ventricular depolarizations that do not necessarily lead to contractions. Common causes of PVCs include electrolyte abnormalities, ischemia, and cardiomyopathies. The prevalence of PVCs increases with age and longer monitoring. Frequent PVCs can impair left ventricular function and cause a PVC-induced cardiomyopathy. Catheter ablation is an effective treatment for eliminating PVCs when medications are ineffective or not tolerated.

1. PREMATURE VENTRICULAR COMPLEX AND
CATHETER ABLATION
AJAY PRATAP SINGH
DEPARTMENT OF CARDIOLOGY
DR. RAM MANOHAR LOHIA HOSPITAL, NEW DELHI.

2. DEFINITION
• Premature Ventricular Complex: It is an early ventricular depolarization with or without mechanical
contraction.
• 2019 HRS guidelines catheter ablation of ventricular arrythmia recommends avoiding the use of the terms
“ventricular premature depolarization” and “premature ventricular contraction” to standardize the literature
and acknowledge that early electrical activity does not necessarily lead to mechanical contraction
• Assessment and treatment of VPCs is challenging and complex and is highly dependent on the clinical
context. The prognostic significance of VPCs is variable and, again, best interpreted in the context of the
underlying cardiac condition.
Cronin EM, Bogun FM, Maury P, et al. 2019 HRS/EHRA/APHRS/LAHRS expert consensus statement on catheter ablation of ventricular arrhythmias. Heart Rhythm.
2020;17(1):e2-e154. doi:10.1016/j.hrthm.2019.03.002

3. PATHOPHYSIOLOGY
Three common mechanisms exist for VPCs, (1) automaticity, (2) reentry, and (3) triggered activity
• Automaticity: This is the development of a new site of depolarization in non-nodal ventricular tissue, which
can lead to a VPC. Automaticity is most probable with electrolyte abnormalities or acute ischemia and is
enhanced by catecholamines. These conditions tend to lower the diastolic transmembrane voltage, resulting in
premature depolarization.
• Reentry Circuit: Reentry typically occurs when slow-conducting tissue (eg, infarcted myocardium) is present
adjacent to normal tissue. Most common mechanism for PVC’s in patients with SHD.
• Triggered activity: After depolarizations triggered by a preceding impulse can lead to premature activation if
the threshold is reached, and this can cause a VPC. Afterdepolarization can occur either during (early) or after
(late) completion of repolarization.

4. ETIOLOGY
CARDIAC CAUSES
• Acute myocardial infarction
• Valvular heart disease, especially mitral valve prolapse
• Cardiomyopathy (eg, ischemic, dilated, hypertrophic,
infiltrative)
• Myocardial stretch
• Cardiac contusion
• Bradycardia
• Tachycardia (high-catecholamine state)
NON-CARDIAC CAUSES
• Electrolyte disturbances (hypokalemia, hypomagnesemia, or
hypercalcemia)
• Medications (eg, digoxin, tricyclic antidepressants,
aminophylline, amitriptyline, pseudoephedrine, fluoxetine)
• Other drugs (eg, cocaine, amphetamines, caffeine, alcohol)
• Anesthetics
• Surgery
• Infection
• Stress

5. PREVELANCE
• The prevalence of VPCs is directly related to the study population, the detection method, and the duration of
observation.
• In one of the first large population-based assessments performed in 1962, a study of 122 043 US Air Force
personnel showed that 7.8 per 1000 exhibited a PVC during a 48-second ECG, with an increasing prevalence
with age. [1]
• The Framingham heart study (with 1-h ambulatory ECG) suggested that the prevalence rate of 1 or more
VPCs per hour was 32% in women and 33% in men without coronary artery disease (CAD). Among patients
with CAD, the prevalence rate of 1 or more VPCs was 58% in men and 49% in women. [2]
• In the ARIC study, a 2-minute ECG detected PVCs in 5.5% of the population.[3]
[1]Hiss RG, Lamb LE. Electrocardiographic findings in 122,043 individuals. Circulation. 1962; 25:947–961. doi: 10.1161/01.cir.25.6.947
[2] Bikkina M, Larson MG, Levy D. Prognostic implications of asymptomatic ventricular arrhythmias: the Framingham Heart Study.Ann Intern Med. 1992; 117:990–
996. doi: 10.7326/0003-4819-117-12-99
[3] Agarwal SK, Simpson RJ, Rautaharju P, Alonso A, Shahar E, Massing M, Saba S, Heiss G. Relation of ventricular premature complexes to heart failure (from the
Atherosclerosis Risk In Communities [ARIC] Study).Am J Cardiol. 2012; 109:105–109. doi: 10.1016/j.amjcard.2011.08.009

6. • Studies using 24-hour ambulatory monitoring showed a VPC prevalence rate of 41% in healthy teenage boys
aged 14-16 years, 50-60% in healthy young adults, and 84% in healthy elderly persons aged 73-82 years.
• Incidence of PVC will likely become more of a common phenomenon as longer monitoring devices are used.
The direct-to-consumer wearables with ECG capabilities, such as the Apple Watch and the Alivecor Kardia
device, will only produce more strips revealing these early ventricular beats for clinicians to consider.
• The common use of wearable patch ECG monitoring, Heckbert et al recently described their findings after fitting
1122 MESA (Multi-Ethnic Study of Atherosclerosis) participants with Zio patches (iRhythm Technologies),
observing at least 1 PVC in 99.5% of those elderly (mean age of 75 years) individuals. They describe a median
PVCcount of 1.9/hour
Heckbert SR, Austin TR, Jensen PN, Floyd JS, Psaty BM, Soliman EZ, Kronmal RA. Yield and consistency of arrhythmia detection with patch electrocardiographic
monitoring: the Multi-Ethnic Study of Atherosclerosis.J Electrocardiol. 2018; 51:997–1002. doi: 10.1016/j.jelectrocard.2018.07.027

7. CLASSIFICATION OF PVC
Lown classification

8. PREDICTORS OF PVC
Marcus GM. Evaluation and Management of Premature Ventricular Complexes. Circulation. 2020;141(17):1404-1418. doi:10.1161/CIRCULATIONAHA.119.042434
UNAVOIDABLE RISK FACTOR AVOIDABLE RISK FACTOR
advancing age and
a taller height.
higher blood pressure, less physical
activity, and smoking.

9. PRESENTATION
• Patients with PVCs typically come to clinical attention for 1 of 2 reasons: symptoms or an incidental finding on
medical examination.
• Symptoms may include palpitations (which may manifest as chest discomfort, a sensation of an intermittently
strong heartbeat, or a sensation of skipped or irregular heartbeats), presyncope, dyspnea, and fatigue. The
symptom is often not attributable to the PVC itself, but rather the sensation of the particularly strong heartbeat
that occurs because of the prolonged ventricular filling time after that PVC, resulting in an enhanced stroke
volume along the Frank- Starling curve and potentiated calcium release.
• VPCs rarely cause true hemodynamic compromise, except when they occur frequently in a patient with severely
depressed left ventricular function or when they are associated with an underlying bradycardia.

10. • Patients may rarely present with abrupt syncope or sudden arrhythmic death attributable to PVC-induced ventricular
fibrillation. [1]
• Although there are no established guidelines to identify patients with PVC at the highest risk of PVC triggered
ventricular fibrillation, the clinical pearl is to consider PVCs as potentially playing a causal role when ventricular
fibrillation is observed.
• A family history is important to elucidate any possible inherited disorders that may be associated with PVCs and a risk
for sudden death.
• Examination: VPCs frequently are associated with variable or decreased intensity of heart sounds, Bounding jugular
pulse (cannon a wave) from a loss of atrioventricular (AV) synchrony may be present.
[1] Singh P, Noheria A. ablation approaches for ventricular fibrillation.Curr Treat Options Cardiovasc Med. 2018; 20:21. doi: 10.1007/s11936-018-0612-4

11. Agarwal SK, Simpson RJ Jr, Rautaharju P, et al. Relation of ventricular premature complexes to heart failure (from the Atherosclerosis Risk In Communities [ARIC]
Study). Am J Cardiol. 2012;109(1):105-109. doi:10.1016/j.amjcard.2011.08.009

12. Ataklte F, Erqou S, Laukkanen J, Kaptoge S. Meta-analysis of ventricular premature complexes and their relation to cardiac mortality in general populations. Am J
Cardiol. 2013;112(8):1263-1270. doi:10.1016/j.amjcard.2013.05.065

13. Ataklte F, Erqou S, Laukkanen J, Kaptoge S. Meta-analysis of ventricular premature complexes and their relation to cardiac mortality in general populations. Am J
Cardiol. 2013;112(8):1263-1270. doi:10.1016/j.amjcard.2013.05.065

14. Agarwal V, Vittinghoff E, Whitman IR, Dewland TA, Dukes JW, Marcus GM. Relation Between Ventricular Premature Complexes and Incident Heart Failure. Am J
Cardiol. 2017;119(8):1238-1242. doi:10.1016/j.amjcard.2016.12.029

16. PVC INDUCED CARDIOMYOPATHY
• Frequent PVCs (usually defined as >10–15% of the total number of beats per 24 h) can impair LV function
(PVC-induced cardiomyopathy).[1]
• However, it is well recognized that not all patients with frequent PVCs will develop LV dysfunction.
Factors associated with the development of LV dysfunction include[2]
1. longer PVC QRS duration,
2. epicardial PVCs,
3. retrograde atrial activation of PVCs,
4. interpolation of PVC
[1]Al-Khatib SM, Stevenson WG, Ackerman MJ, Bryant WJ, Callans DJ, Curtis AB et al. AHA/ACC/HRS guideline for management of patients with ventricular arrhythmias and the prevention of
sudden cardiac death: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Circulation
2017;138:e272–391.
[2] Arnar DO, Mairesse GH, Boriani G, et al. Management of asymptomatic arrhythmias: a European Heart Rhythm Association (EHRA) consensus document, endorsed by the Heart Failure
Association (HFA), Heart Rhythm Society (HRS), Asia Pacific Heart Rhythm Society (APHRS), Cardiac Arrhythmia Society of Southern Africa (CASSA), and Latin America Heart Rhythm
Society (LAHRS) [published online ahead of print, 2019 Mar 18]. Europace. 2019;euz046. doi:10.1093/europace/euz046

17. Arnar DO, Mairesse GH, Boriani G, et al. Management of asymptomatic arrhythmias: a European Heart Rhythm Association (EHRA) consensus document, endorsed
by the Heart Failure Association (HFA), Heart Rhythm Society (HRS), Asia Pacific Heart Rhythm Society (APHRS), Cardiac Arrhythmia Society of Southern Africa
(CASSA), and Latin America Heart Rhythm Society (LAHRS) [published online ahead of print, 2019 Mar 18]. Europace. 2019;euz046. doi:10.1093/europace/euz046

18. Arnar DO, Mairesse GH, Boriani G, et al. Management of asymptomatic arrhythmias: a European Heart Rhythm Association (EHRA) consensus document, endorsed
by the Heart Failure Association (HFA), Heart Rhythm Society (HRS), Asia Pacific Heart Rhythm Society (APHRS), Cardiac Arrhythmia Society of Southern Africa
(CASSA), and Latin America Heart Rhythm Society (LAHRS) [published online ahead of print, 2019 Mar 18]. Europace. 2019;euz046. doi:10.1093/europace/euz046

19. Arnar DO, Mairesse GH, Boriani G, et al. Management of asymptomatic arrhythmias: a European Heart Rhythm Association (EHRA) consensus document, endorsed by the Heart
Failure Association (HFA), Heart Rhythm Society (HRS), Asia Pacific Heart Rhythm Society (APHRS), Cardiac Arrhythmia Society of Southern Africa (CASSA), and Latin America
Heart Rhythm Society (LAHRS) [published online ahead of print, 2019 Mar 18]. Europace. 2019;euz046. doi:10.1093/europace/euz046

20. ELECTROCARDIGRAPHY
• The diagnosis of VPCs is typically established by electrocardiography. The presence of a VPC on a 12-lead ECG provides
essential information about the site-of origin of the VPC. Accordingly, an ECG should be performed to look for
pathophysiologic cardiac abnormalities as well as documenting the presence of VPCs and potentially providing information
about their specific mechanism and frequency.
1-QRS duration of more than 120 msec.
2-Bizarre morphology that does not resemble usual aberration (ie, typical RBBB/typical LBBB).
3-T wave in the opposite direction from the main QRS vector.
4-A fully compensatory pause (ie, the PP interval surrounding the VPC is twice the sinus PP interval); less
frequently, the VPC is interpolated and does not alter the baseline sinus interval (ie, the PP interval surrounding the
VPC is equal to the sinus PP interval)

21. LOCALIZATION OF VPC
• PVC usually origin from
• Right Ventricle outflow tact (70%–80%)
• Non RVOT (10%–15%)(three papillary muscles, moderator
band and tricuspid annulus)
• Left ventricle outflow tract (15%–25%)
• Left ventricle papillary muscles(AL & PM)
• Epicardial (AIV/GCV junction or LV summit) (≈12%)
1. Free wall
2. Right PSC
3. Left PSC
4. Posterior septum
5. Para HISian
6. Right coronary cusp
7. LCC/RCC
8. Left coronary cusp
9. AMC
10. LV summit
11. Mitral annulus (AL)

22. Anderson RD, Kumar S, Parameswaran R, et al. Differentiating Right- and Left-Sided Outflow Tract Ventricular Arrhythmias: Classical ECG Signatures and Prediction
Algorithms. Circ Arrhythm Electrophysiol. 2019;12(6):e007392. doi:10.1161/CIRCEP.119.007392

23. Anderson RD, Kumar S, Parameswaran R, et al. Differentiating Right- and Left-Sided Outflow Tract Ventricular Arrhythmias: Classical ECG Signatures and Prediction
Algorithms. Circ Arrhythm Electrophysiol. 2019;12(6):e007392. doi:10.1161/CIRCEP.119.007392

24. Anderson RD, Kumar S, Parameswaran R, et al. Differentiating Right- and Left-Sided Outflow Tract Ventricular Arrhythmias: Classical ECG Signatures and Prediction
Algorithms. Circ Arrhythm Electrophysiol. 2019;12(6):e007392. doi:10.1161/CIRCEP.119.007392

25. Anderson RD, Kumar S, Parameswaran R, et al. Differentiating Right- and Left-Sided Outflow Tract Ventricular Arrhythmias: Classical ECG Signatures and Prediction
Algorithms. Circ Arrhythm Electrophysiol. 2019;12(6):e007392. doi:10.1161/CIRCEP.119.007392

26. Anderson RD, Kumar S, Parameswaran R, et al. Differentiating Right- and Left-Sided Outflow Tract Ventricular Arrhythmias: Classical ECG Signatures and Prediction
Algorithms. Circ Arrhythm Electrophysiol. 2019;12(6):e007392. doi:10.1161/CIRCEP.119.007392

27. Noheria A, Deshmukh A, Asirvatham SJ. Ablating Premature Ventricular
Complexes: Justification, Techniques, and Outcomes. Methodist Debakey
Cardiovasc J. 2015;11(2):109-120. doi:10.14797/mdcj-11-2-109

29. Cronin EM, Bogun FM, Maury P, et al. 2019 HRS/EHRA/APHRS/LAHRS expert consensus statement on catheter ablation of ventricular arrhythmias [published
correction appears in Europace. 2019 Aug 1;21(8):1144] [published correction appears in J Arrhythm. 2020 Jan 12;36(1):214]. Europace. 2019;21(8):1143-1144.
doi:10.1093/europace/euz132

30. • FIRST EVIDENCE OF
PVC FOLLOW UP.

31. • Successful PVC suppression could
result in an increased risk for death
as in CAST (Cardiac Arrhythmia
Suppression Trial), the notion that
PVCs were causal, or at least should
be considered a reasonable target of
suppression for the purposes of
improving prognosis, was
abandoned.

32. In 1995, this trial showed that PVC
suppression may have mortality benefit
and increases LVEF in long term.

33. • Subsequently, starting in the early 2000s, case reports of successful catheter ablation of PVCs resulting in
improvements in and even complete resolution of systolic dysfunction were published.[1]
• Soon case series of improvements in LVEF after catheter ablation among patients with a high burden of PVCs
and reduced left ventricular systolic function, providing evidence that PVCs could play a causal role in heart
failure
[1] Chugh SS, Shen WK, Luria DM, Smith HC. First evidence of premature ventricular complex-induced cardiomyopathy: a potentially reversible cause of heart
failure. J Cardiovasc Electrophysiol. 2000;11(3):328-329. doi:10.1111/j.1540-8167.2000.tb01802.x

34. Sekiguchi Y, Aonuma K, Yamauchi Y, et al. Chronic hemodynamic effects after
radiofrequency catheter ablation of frequent monomorphic ventricular premature
beats. J Cardiovasc Electrophysiol. 2005;16(10):1057-1063. doi:10.1111/j.1540-
8167.2005.40786.x
Bogun F, Crawford T, Reich S, et al. Radiofrequency ablation of frequent,
idiopathic premature ventricular complexes: comparison with a control group
without intervention. Heart Rhythm. 2007;4(7):863-867.
doi:10.1016/j.hrthm.2007.03.003

35. MANAGEMENT
• Reassurance is the most useful tool for the patient with PVCs, additional management beyond reassurance
should be pursued, 3 key pieces of information are needed: (1) information regarding symptoms, (2) the
burden of the PVCs (typically reported in PVCs as a percentage of all beats), and (3) the presence or absence
of structural heart disease.
• Lifestyles changes to avoid smoking , caffeinated drinks consumption (evidence is mixed for its benefit
currently a RCT CRAVE trial is ongoing on for the same)
• If a patient has bothersome symptoms despite reassurance or a reduced LVEF, either medical treatment or
catheter ablation are reasonable first options.
Marcus GM. Evaluation and Management of Premature Ventricular AComplexes. Circulation. 2020;141(17):1404-1418.
doi:10.1161/CIRCULATIONAHA.119.042434

36. MEDICAL MANAGEMENT
• Either β-blockers or nondihydropyridine calcium channel blockers (diltiazem or verapamil) are considered first-
line medicines for PVCs.
• Randomized controlled clinical trials demonstrate that β-blockers result in a clinically meaningful reduction in
symptomatic outflow tract PVCs by 12% to 24% [1] and CCB especially for fascicular VT [2]
• For the patient in need of treatment who strongly prefers to avoid catheter ablation, for whom catheter ablation
has failed, or who may not be a good ablation candidate (because of frailty or multifocal PVCs), additional
antiarrhythmic drugs to consider include flecainide, propafenone, sotalol, and amiodarone.
• Flecainide and propafenone are generally considered contraindicated in the presence of coronary disease, severe
left ventricular hypertrophy, or heart failure.
• Sotalol can suppress PVCs in most patients but with careful observation for QT prolongation and is a particularly
reasonable choice in the presence of CAD and amiodarone is reserved for older patients.
[1]Krittayaphong R, Bhuripanyo K, Punlee K, Kangkagate C, Chaithiraphan S. Effect of atenolol on symptomatic ventricular arrhythmia without structural heart
disease: a randomized placebo-controlled study.Am Heart J. 2002; 144:e10. doi: 10.1067/mhj.2002.125516
[2] Belhassen B, Horowitz LN. Use of intravenous verapamil for ventricular tachycardia.Am J Cardiol. 1984; 54:1131–1133. doi: 10.1016/s0002-9149(84)80158-7

37. • Frequent symptomatic
VPBs from the >6000
VPBs per 24 hours on
Holter monitoring.
• METOPROLOL
(12.5-25mg)
PROPAFENONE
(100 mg BD)

42. Cronin EM, Bogun FM, Maury P, et al. 2019
HRS/EHRA/APHRS/LAHRS expert
consensus statement on catheter ablation of
ventricular arrhythmias [published
correction appears in Europace. 2019 Aug
1;21(8):1144] [published correction appears
in J Arrhythm. 2020 Jan
12;36(1):214]. Europace. 2019;21(8):1143-
1144. doi:10.1093/europace/euz132

43. CATHETER ABLATION: CHANGE IN GUIDELINES
European Heart Rhythm Association; Heart Rhythm Society, Zipes DP, et al. ACC/AHA/ESC
2006 guidelines for management of patients with ventricular arrhythmias and the prevention of
sudden cardiac death: a report of the American College of Cardiology/American Heart Association
Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing
Committee to Develop Guidelines for Management of Patients With Ventricular Arrhythmias and
the Prevention of Sudden Cardiac Death). J Am Coll Cardiol. 2006;48(5):e247-e346.
doi:10.1016/j.jacc.2006.07.010
Cronin EM, Bogun FM, Maury P, et al. 2019
HRS/EHRA/APHRS/LAHRS expert consensus
statement on catheter ablation of ventricular arrhythmias
[published correction appears in Europace. 2019 Aug
1;21(8):1144] [published correction appears in J
Arrhythm. 2020 Jan 12;36(1):214]. Europace.
2019;21(8):1143-1144. doi:10.1093/europace/euz132

44. • In BrS, VF-triggering premature
ventricular complexes (PVCs)
are almost identical, site
specific, and predominantly
originate from the right
ventricular outflow tract
(RVOT)
Talib AK, Nogami A. Catheter Ablation for
Brugada Syndrome. Korean Circ J.
2020;50(4):289-301.
doi:10.4070/kcj.2019.0344

45. • PVCs are evident, the origin is
usually from one of the three
regions of fibro-fatty replacement
in the “triangle of dysplasia” (i.e.,
right ventricular outflow tract,
apex, and infundibulum).

46. • isthmus 1 bordered by tricuspid annulus and right
ventricular outflow tract patch/right ventricular
incision
• isthmus 2 by right ventricular incision and
pulmonary valve
• isthmus 3 by pulmonary valve and ventricular
septal defect patch
• isthmus 4 by ventricular septal defect patch and
tricuspid annulus
Cronin EM, Bogun FM, Maury P, et al. 2019 HRS/EHRA/APHRS/LAHRS expert consensus statement on catheter ablation of ventricular arrhythmias [published correction appears
in Europace. 2019 Aug 1;21(8):1144] [published correction appears in J Arrhythm. 2020 Jan 12;36(1):214]. Europace. 2019;21(8):1143-1144. doi:10.1093/europace/euz132

47. PACES/HRS expert consensus
statement on the recognition
and management of arrhythmias
in adult congenital heart
disease. Can J Cardiol.
2014;30(10):e1-e63.
doi:10.1016/j.cjca.2014.09.002

48. Recent studies have shown that PVC burden is an
independent predictor of VT in HCM patients apart
from already defined risk factors

49. PROCEDURAL PLANNING FOR CA
• A proper preprocedural risk stratification is crucial to minimize the risk of adverse periprocedural outcomes
such as acute hemodynamic decompensation (AHD), which can have devastating consequences
• A score between 9-14 has a 6% risk of
acute hemodynamic collapse and score
≥15 has a risk increased to 24% during
procedure.
Santangeli P, Muser D, Zado ES, et al. Acute hemodynamic decompensation during catheter ablation of scar-related ventricular tachycardia: incidence, predictors, and
impact on mortality. Circ Arrhythm Electrophysiol. 2015;8(1):68-75. doi:10.1161/CIRCEP.114.002155

50. PRE-PROCEDURE PREPARATION
• AADs, except for amiodarone, should possibly be discontinued for at least 5 half-lives prior to the ablation
procedure.
• Oral anticoagulants are generally discontinued prior to the ablation to achieve an international normalized
ratio within 1.5 at the time of the study
• Direct oral anticoagulants should be withheld for 24–48 hours before the procedure, depending on anticipated
access, and bridging with heparin can be used for patients with mechanical heart valves or other features that
place them at high risk of thrombosis.

52. • Unfractionated heparin is commonly administered after sheath insertion as an initial bolus (empirical dose
5000– 10,000 IU or 50–100 IU/kg) followed by intermittent bolus and/or continuous infusion to maintain a
target activated clotting time (ACT) longer than 250–350 seconds.
• Prophylactic antibiotics are NOT generally indicated for sterile procedures such as VA ablation. However,
patients with ICDs undergoing ablation, in which catheters might be in direct contact with the intravascular
leads, could present a special circumstance.

53. ELECTROPHYSIOLOGICAL TESTING
• PROGRAMMED ELECTRICAL STIULATION (PES) is a key component of the PVC ablation procedure,
allowing for mapping of induced arrhythmias. In addition, a baseline assessment of arrhythmia induction can
be useful by comparison for the eventual assessment of procedural outcome.
• For induction of PVC: in 2019 HRS guidelines 100% of experts stimulated from the RV apex, 66% from the
RVOT and 59% from the LV if LV access has already been obtained.
• In drugs isoproterenol was used frequently (93%), followed by epinephrine (21%), phenylephrine (14%),
atropine (11%), and calcium (7%). In addition, some members of the committee at least considered
dobutamine and caffeine.

54. Mapping and Imaging Techniques: Catheters
• Multielectrode mapping catheters, offer several advantages, particularly in respect to mapping density,
resolution, and speed. The ability to record electrograms from multiple sites at each beat increases the number
of data points and can shorten the duration of mapping.
• Multielectrode catheters allow pacing from multiple electrodes positioned in and around areas of scar. In
addition pacing from one site while recording from surrounding sites allows investigation of propagation in
multiple directions that can identify anisotropy and areas prone to slow conduction and/or block.
The Pentaray catheter (Biosense
Webster,Diamond Bar,CA)
Livewire™ Electrophysiology Catheter Dual-Purpose Duo-
Decapolar (20 electrodes)

55. • Common limitations of multielectrode mapping catheters include mechanical trauma with frequent ectopy,
transient injury of the superficial conduction bundles, limited maneuverability, lack of tissue contact
information, and the potential for thrombus formation with the need for careful anticoagulation.

56. ACTIVATION MAPPING
1. Activation mapping is performed by recording of local electrograms from multiple sites during a PVC.
2. For focal PVCs, the earliest site of activation identifies the SOO and is the target of ablation.
3. At this site, the local bipolar electrogram precedes the QRS onset, and the unipolar signal filter setting
demonstrates a QS configuration , consistent with a centrifugal spread of activation away from the SOO.
4. In scar-related re-entry circuit, the QRS activation occurs when the impulse reaches the exit from the scar to
activate the contractile myocardium, In “exit sites,” electrograms can be fractionated and immediately
precede the onset of the QRS complex. Ablation at exit sites can terminate the tachycardia.

57. ENTRAINMENT MAPPING
1. Entrainment involves the continuous resetting of a reentry circuit during pacing at sites that are either within
or outside the reentry circuit. This technique is used to identify critical sites of the arrhythmia circuit,
through the analysis of the QRS morphology, the measured intervals, and the recorded electrograms.
2. QRS configuration during entrainment provides information about whether the pacing site is within or
outside the protected zone of the reentry circuit.
3. With the pacing site being located outside the reentry circuit, during entrainment, the stimulated
wavefronts that propagate out from the pacing site collide with the orthodromically propagating wave-front
of the reentry circuit and fuse; QRS complex is due to the fusion of wavefronts propagating directly away
from the pacing site with those emerging from the tachycardia circuit (classic entrainment).
4. During pacing from within or near the reentry circuit, pacing entrains VT without changing the QRS
configuration (concealed entrainment or entrainment with concealed fusion)

58. • Entrainment with concealed fusion indicates that the pacing site is within a protected region of the reentry circuit, and can
be located in the common pathway of the reentry circuit
• If pacing is performed from a site in the circuit, the stimulus-QRS interval should be equal to the electrogram-QRS interval
during VT. On the other hand, if stimulation is performed from a bystander site, the stimulus-QRS interval is longer than
the electrogram-QRS interval during tachycardia. A difference in stimulus-QRS and electrogram-QRS up to 30 ms was
superior to other criteria for distinguishing bystander sites from critical sites in one study.
• The stimulus-QRS interval indicates the conduction time from the pacing site to the VT exit site.
• The stimulus-QRS/VT CL ratio is a reflection of the pacing site location within the critical zone of the reentry circuit.
• The PPI is also an indication of the proximity of the pacing site to the reentry circuit ; the PPI measures the interval from
the pacing stimulus to the following non-stimulated depolarization recorded at the pacing site.
Cronin EM, Bogun FM, Maury P, et al. 2019 HRS/EHRA/APHRS/LAHRS expert consensus statement on catheter ablation of ventricular arrhythmias [published correction appears
in Europace. 2019 Aug 1;21(8):1144] [published correction appears in J Arrhythm. 2020 Jan 12;36(1):214]. Europace. 2019;21(8):1143-1144. doi:10.1093/europace/euz132

60. PACE MAPPING
1. Pace mapping is a technique used to locate the origin of a PVC or VT by stimulating the myocardium to
reproduce the clinical 12-lead morphology in the absence of VT
2. Pace mapping can supplement activation mapping and can be particularly useful when activation mapping is
not possible due to suppression of clinical PVCs
3. The optimal site should exactly match the tachycardia QRS, including individual notches as well as major
deflections
4. Pace mapping indicates the location of the origin of focal VAs; a pacing rate close to the VT/PVC rate
should be used.
5. The stimulus to-surface QRS interval can further provide complementary information.
• SHORT: focus of triggered PVC is surrounded by relatively healthy myocardium
• LONG : arrhythmogenic tissue separated from ventricular myocardium by zones of slow conduction

61. SUBSTRATE MAPPING

62. ABLATION TECHNIQUES
• Unipolar Radiofrequency Catheter Ablation:
• Refined with the addition of temperature sensing and larger tip catheters and further with catheter tip cooling. Irrigation of the ablation
electrode reduces temperature at this interface and allows greater power delivery and thus the creation of larger lesions
• A typical initial power setting for ablation with an open irrigated catheter in the LV is 30 watts and can be adjusted up to 50 watts to
achieve an impedance drop of 10 ohms.
• Contact Force Sensing:
• Lesion size is critically dependent on the contact of the ablating electrode with the tissue; RF applications with a mean contact force
.10 g are more likely to result in electrical unexcitability in scar areas
• Hypotonic External Irrigation:
• Most ablation catheter tips are 3.5–4 mm in length and are typically irrigated with 0.9% sodium chloride solution. The efficiency of
delivering current to myocardial tissue can be increased by using smaller electrode tip sizes and less conductive irrigant, such as 0.45%
sodium chloride
• Needle Ablation:
• A catheter with an extendable/retractable needle at the tip can function as an intramural electrode for the temperature-controlled
delivery of RF energy. Infusion needle ablation has been reported as a means to achieve intramural ablation lesions.

63. • Cryoablation:
• Have advantage of good contact and stability when compared with RF ablation, but focal cryoablation
lesions are smaller and take longer to develop. Larger lesions can be created with larger tip cryoablation
catheters
• Trans-vascular Ethanol Ablation:
• Creating an arterial occlusion and controlled infarction has long been used to create ventricular ablation
lesions; Heart block is a frequent risk when a septal substrate is targeted.
• Stereotactic Radiotherapy:
• The use of stereotactic motion-gated external beam radiation for ablation has been explored in animal
models, and its feasibility has been demonstrated in humans. This method requires the accurate pre-
procedure identification of the culprit arrhythmogenic substrate, using either intracardiac mapping,
imaging, or noninvasive ECGI

64. Surgical Therapy
Sympathetic Modulation
Endpoints of Catheter Ablation

65. POST PROCEDURE CARE
The Multicenter Thermocool Ventricular Tachycardia
Ablation Trial has recommended antiplatelet therapy
with aspirin 325 mg/day or anticoagulation with
warfarin for 3 months after ablation, if ablation has been
performed over an area with >3 cm between ablation
sites
Stevenson WG, Wilber DJ, Natale A, et al. Irrigated radiofrequency catheter
ablation guided by electroanatomic mapping for recurrent ventricular tachycardia
after myocardial infarction: the multicenter thermocool ventricular tachycardia
ablation trial. Circulation. 2008;118(25):2773-2782.
doi:10.1161/CIRCULATIONAHA.108.788604

66. COMPLICATIONS
Pothineni NV, Deshmukh A, Padmanabhan D, et al. Complication rates of ventricular tachycardia
ablation: Comparison of safety outcomes derived from administrative databases and clinical
trials. Int J Cardiol. 2015;201:529-531. doi:10.1016/j.ijcard.2015.08.116

67. FUTURE ADVANCES IN CA
• Advances in Mapping: Outside of catheter mapping, tools have been created to take advantage of coronary vasculature
access to intramyocardial structures. The most common example involves mapping the perforator veins facilitated by the
use of electrically protected wires into septal perforating branches, the use of cold saline , and the use of dual site pace
mapping to identify intramural VA origins.
• Entirely noninvasive electrophysiological mapping has been developed with ECGI. This technology combines body
surface unipolar electrograms obtained from a vest of electrodes with patient-specific heart-torso geometry
• Advances in Ablation: catheter with a needle that can be deployed into ventricular myocardium to both map and ablate.
Allowing more precise intramyocardial mapping, injection of dye to assess location of potential ablation using fluoroscopy,
and deeper ablation lesions than standard catheter ablation.
• Alternative energies have been studied, locally applied pulsed field direct current electroporation, and noninvasive
focused stereotactic radiation. Electroporation using localized direct current is a technology in rapid development with
significant advantages of speed (seconds) and a tissue-selective ablation effect in preclinical models and noninvasive
photon ablation.

68. Bipolar devices focus ablation energy between two closely opposed
electrodes, which maintain relatively high current density
Focused ablation energy causes rapid tissue temperature rise producing
contiguous thermal injury
Disadvantage : difficulty of positioning and maintaining the stability of
two catheters
Electroporation

69. THANK YOU