Risk Assessment and Management of PVC.pdf

Risk Assessment and Management of PVC

1. Risk Assessment and Management
of Premature Ventricular Complexes
SAKHAN SOLIDA, MD, MPH, FAsCC, FAPSC
Cardiovascular Department, Preah Kossamak Hospital
Lecturer, University of Health Sciences
Lecturer, Health Science Institute of RCAF

2. No conflict of interest
2

3. OBJECTIVES
1.To deliver an overview of PVCs encompassing their various etiologies and the
associated risk of developing serious arrhythmias and adverse cardiac events.
2.To delineate the systematic approach for evaluating PVCs, including clinical
assessment, and other diagnostic tests.
3.To explore the current guidelines and recommendations for the optimal
management of PVCs.
3

4. ❖ PVC : Premature occurrence of an abnormal QRS
complex.
▪QRS ≥120 ms,
▪Broad T-wave & in the opposite direction of the
major QRS deflection,
▪No preceding P-wave. (European Heart Journal 2022)
❖ Unifocal or monomorphic PVCs
❖ Multifocal, multiform, or polymorphic PVCs
❖ VT / VF
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I. Overview of premature ventricular complexes

5. 5
I. Overview of PVCs (Cont)
❖ Prevalence of PVCs range widely (1 and 40%). (Kennedy HL et al. 1985 ; Cheriyath et al. 2011; Yang J rt al 2014)
▪7.8% exhibited a PVC during a 48-second (1962, US Air Force personnel). (Hiss RG et al. 1962)
▪1.8% on conventional 10-second ECGs from 14 000 participants without heart failure. (ARIC study).
(Nguyen KT et al. 2017)
▪12% of individuals without coronary disease monitored for 1 hour (Framingham Heart Study).
(Bikkina M et al. 1992)
▪24-hour Holter monitoring, healthy adults aged 25 to 41 years in Lichtenstein found at least one PVC
in 69% of participants; and the 95th percentile was 193 PVCs. (Von Rotz M et al. 2017)

6. Fig 1. Potential mechanism of PVCs
Mayo Clin Proc. 2023 6
I. Overview of PVCs (Cont)
❖Potential mechanisms
▪Automaticity
➢Parasystole
➢Secondary to embryologic development
▪Triggered activity
➢Increased intracellular calcium load
causing early or delayed
afterdepolarizations
▪Reentry
➢Within the bundle branches or scar

7. Fig 2. Multivariate adjusted predictors of PVC frequency.
Kerola T et al. 2018
7

8. II. Potential complications of PVCs
Fig 3. Poorly perfused premature ventricular complexes (PVC)
Mayo Clin Proc. 2023
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9. II. Potential complications of PVCs (Cont)
Fig 4. Premature ventricular complexes converted into VT 9

10. II. Potential complications of PVCs (Cont)
❖ Abrupt syncope or sudden arrhythmic death (trigger polymorphic VT or VF).
(Singh P. et al. 2018)
❖ PVCs may cause a decrease in LVEF (Heart failure).
(Dukes JW. et al. 2015; Baman TS. et al. 2010 ; Latchamsetty R. et al. 2015)
❖ Diagnosis of Tachycardia-induced cardiomyopathy (TIC) is generally considered.
▪Absence of underlying SHD
▪Longer Hx of PVCs
▪Burden > 10 %
▪Interpolated or epicardial origin PVCs (wide QRS duration)
▪Lack of diurnal variation of PVC frequency
▪Elimination of PVCs often leads to improvement of cardiomyopathy
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11. III. Evaluation of PVCs
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12. III. Evaluation of PVCs (Cont)
❖ In the absence of SHD or ion channelopathies, PVCs are referred to idiopathic, and considered
as harmless. (Muser D. et al. 2021; L. Calo’ et al. 2024; R. Scorza et al. Europace 2023)
❖ Maybe indicate an underlying SHD and associated with an increased risk of SCD.
(Kennedy HL et al. 1985; Maggioni AP et al. 1993; Bikkina M. et al. J Am Coll Cardiol 1993)
12

13. III. Evaluation of PVCs (Cont)
❖ Symptoms :
➢Palpitation, Pre-syncope, Dyspnea and Fatigue.
➢Abrupt syncope or sudden arrhythmic death attributable to PVC-induced VF.
❖ Family history :
➢Hereditary disorders / SCD.
➢A positive family history >> heighten suspicion for ARVD & other inherited cardiomyopathies.
❖ Personal & Physiological history :
➢Potential cause / mechanism of PVCs
❖ Careful physical examination :
➢Evidence of a PVC
➢PVC frequency
➢Physical signs of reduced systolic function, a dilated left ventricle, and volume overload.
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14. Fig 5. Workup algorithm for PVC
L. Calo’ et al. 2024
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15. III. Evaluation of PVCs (Cont)
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❖12-lead EKG :
➢Evidence of PVC & Frequency
➢Location of origin
➢Channelopathies.

16. 16
STEP 1
Fig 6. Localization of PVCs based on V1 morphology

17. 17
STEP 2
Fig 7. Localization of PVCs based on lead II, II and aVF morphology

18. 18
STEP 3
Fig 8. Localization of PVCs according to axis and precordial transition

19. 19
Fig 9. Schematic representation of the main sites of origin of idiopathic PVC and their EKG features.
Muser D. et al. Diagnostic 2021

20. 20
Fig 10. Example 12-lead ECGs from common
locations of premature ventricular complexes.
Marcus GM. et al. 2020

21. 21
Fig 11. A. EKG demonstrating a short-coupled premature ventricular complex. B. Measurement of the PVC coupling interval
should be taken at the end of the preceding QRS and the start of the PVC. C. Telemetry strip showing polymorphic ventricular
tachycardia triggered by a close-coupled PVC in the same patient.
Mayo Clin Proc. 2023

22. 22
III. Evaluation of PVCs (Cont)
Table 1 : EKG criteria of ARVC
EKG characteristic P-value
QRS axis > 90
o
0.048
Intrinsicoid deflection > 80ms 0.037
QS morphology in lead V1 0.003
Lead I / QRS duration ≥ 120ms 0.005
QRS notching (multiple leads) 0.014
V5 transition or later 0.002
Novak J. et al. 2017; Hoffmayer KS. et al. 2012
Fig 12. EKG suggestive of ARVC

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III. Evaluation of PVCs (Cont)
❖ Lab test
➢Electrolyte imbalance
➢Metabolism disorders
➢Thyroid function
❖Echocardiography
➢Eliminate SHD.
➢Suspect ARVC (RV wall motion abnormalities + disproportionate RVOT dilation)
➢Reduced LVEF
➢Ischemic heart disease

24. 24
III. Evaluation of PVCs (Cont)
❖Response to exercise
➢Disappear at the peak of exercise, and reappear during recovery usually suggest benign behavior
for PVCs.
➢Worsening of VA with increasing workload ➔ underlying cardiomyopathy or ion channel disease ➔
predict the risk of malignant arrhythmias during sports activity.
➢Abrupt start + high intensity / Abrupt stop ➔ unmasking exercise induced arrhythmia (CPVT…)

25. 25
Cipriani A. et al. Heart Rhythm 2018
Fig 13. Non elite, competitive athletes performed CMR for VA

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III. Evaluation of PVCs (Cont)
❖Holter monitoring :
➢Arrhythmic burden in term of frequency, morphology, relation to exercise, and complexity.
➢PVCs couplets with short RR interval or (R/T phenomenon) can caused by myocardial electrical
instability and may predispose to complex VA.
➢Polymorphic morphologies and the presence of couplets, triplets and runs of NSVT was significantly
higher in the group with SHD.

27. 27
III. Evaluation of PVCs (Cont)
❖ Substrate and CMR
➢Crucial to identify the presence of an underlying arrhythmogenic substate.
➢CAD patient, LVEF ≤ 40% and NSVT
➢Various structural cardiomyopathies can be associated with PVCs, both genetic and acquired.
➢Non-ischemic LV scar (NILVS) : Presence of LGE in the sub-epicardial/mid-myocardial layers of the
LV ➔ replacement type myocardial fibrosis, in the absence of significant CAD.
❖Cardiac positron emission tomography (PET Scan)
➢Infiltrative and inflammatory process.
➢LGE-cardiac MRI + PET ➔ increase diagnostic accuracy, in cases of a high suspicion of myocarditis.

28. 28Muser D et al. J Am Coll Cardiol EP 2019Fig 14. Apparently Idiopathic PVCs Risk Stratification

29. Fig 15. Independent predictors of abnormal CMRCipriani A. et al. Heart Rhythm 2018 29

30. Fig 16. Forest plot showing the results of the principle studies investigating the prognostic role of CMR abnormalities in
patients with frequent PVC
Muser D. et al. Diagnostic 2021
30

31. III. Evaluation of PVCs (Cont)
❖ Electrophysiology studies
➢Risk stratification of SCD
➢Mechanism and localization of PVCs.
➢EAM aid in successful ablation despite infrequent PVCs.
❖Coronary Angiography
➢Positive non-invasive tests or symptoms consistent with ischemia or when ablation is indicated to
evaluate the proximity to coronary arteries during CA.
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32. 32
Table 2 : Indications and limitations of imaging test with PVCs
Muser D. et al. Diagnostic 2021
35
32

33. III. Evaluation of PVCs (Cont)
❖Genetic testing
➢Comprehensive clinical phenotyping when the probability of an inherited cardiac disorder is reasonably
high and it can provide prognostic information or be useful for family screening.
➢Features that suggest possible CPVT.
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34. IV. Management of PVCs
Table 3 : Recommendations for treatment of reversible conditions of VAs
(European Heart Journal 2022)
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35. IV. Management of PVCs (Cont)
35
SYMPTOMS? SHD?
BURDEN?

36. IV. Management of PVCs(Cont)
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❑MEDICAL TREATMENT
➢First-line therapy in patients in whom CA is more complex and leads to a higher risk of procedure
complications.
➢ BB or non-dihydropyridine CCB : limited effectiveness & indicated in symptomatic patients
with idiopathic PVCs. (Priori, S. et al. Eur. Heart J. 2015)
➢Amiodarone & Class IC drugs (Flecainide and Propafenone) may reduce PVC burden > 70% of
patients, but Flecainide should be cautiously used. (CAST N.Engl.J.Med)
➢Mexiletine is rarely used as its effectiveness is inferior to either AAD or CA. (Cappuci A. et al.)
❑REASSURANCE
➢PVC without SHD, or inherited arrhythmogenic disorders, who are no symptomatic or mildly
symptomatic. (Pedersen, C.T. et al. Heart Rhythm 2014)

37. IV. Management of PVCs (Cont)
37
➢ CA is recommended as first-line treatment for symptomatic idiopathic VT/PVCs from the RVOT or
the left fascicles.
➢ Symptomatic patient who do not tolerate or do not prefer long-term AAD. (Cronin EM et al. Heart Rhythm 2019)
➢ Success rate > 90% in monomorphic RVOT-PVCs. (Cronin EM et al. Heart Rhythm 2019)
➢ Very challenging in the presence of polymorphic PVCs or epicardial or papillary muscle.
(Marcus GM. et al. 2020)
➢ CA of PVCs (Burden > 22%) improved the efficacy of CRT, LVEF and NYHA functional class.
(Lakkireddy et al. 2012)
❑CATHETER ABALTION

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Table 4 : Idiopathic VA prevalence, procedure success and risk of
complications according to the site of origin as report in larger series.
Muser D. et al. Diagnostic 2021

39. 39
Fig 17. Change in ejection fraction among a series of patients with frequent premature ventricular complexes and
reduced left ventricular systolic function after catheter ablation
Baman TS. et al. 2010

40. 40
❖ The PVC burden threshold at which AAD and/or CA should be considered is variably defined :
▪ > 10% (threshold after which most cases of PVC-CMP occur).
▪ > 16-24% (statistically discriminatory cut-off value for PVC-CMP).
▪ or > 6% (threshold indicating a potential benefit of CA).
Sassone, B. et al. 2019 ; Bogun, F. et al. 2007 ; Dukes, J.W. et al. 2015

41. 41
Fig 18. Algorithm for the management of patients
with idiopathic PVCs/VA and non-apparent SHD.
(European Heart Journal 2022)

42. 42
(European Heart Journal 2022)
Fig 19. Algorithm for the management of patients with
idiopathic PVCs induced/aggravated cardiomyopathy.

43. 43
Table 5 : Summary of the recommendations for the treatment of patients with frequent
idiopathic PVCs/VA pr PVC-induced cardiomyopathy
(European Heart Journal 2022)

44. 44
Fig 20. CA vs AADs for treatment of PVCs-State of Current Evidence
De Silva K. et al. 2023

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Table 6 : Outcomes of AADs vs CA for PVCs
De Silva K, et al. 2023

46. 46
Table 7 : Outcomes of AADs vs CA for PVCs (Continued)
De Silva K. et al. 2023

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❖ Spectrum of clinical implications of PVC, varying from completely benign to development of
cardiomyopathy, HF, and an increased risk for SCD.
❖ Appropriate diagnostic testing, prognostic considerations and management are necessary
when faced with PVCs.
❖ Available published evidence, CA is superior to AAD in reducing the burden or frequency of
PVCs.
❖ Limited evidence comparing AADs and CA for non-RVOT PVCs.
❖ Several upcoming trials will offer important insights for management of PVCs.
Conclusion