Ventricular Premature Contractions in the Athlete

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Ventricular Premature Contractions in the Athlete
Ventricular Premature Contractions
in the Athlete
Ronn E. Tanel, MD
Pediatric Arrhythmia Service
UCSF Benioff Children’s Hospital
Professor of Clinical Pediatrics
UCSF School of Medicine
Disclosures
None
The Tragic Event
PVCs may be the initial manifestation of clinically
silent arrhythmogenic conditions…
PVCs may be the initial manifestation of clinically
silent arrhythmogenic conditions…
PVCs may be the initial manifestation of clinically
silent arrhythmogenic conditions…
PVCs may be the initial manifestation of clinically
silent arrhythmogenic conditions…
PVCs may be the initial manifestation of clinically
silent arrhythmogenic conditions…
PVCs may be the initial manifestation of clinically
silent arrhythmogenic conditions…
But what do we know about the occurrence of
simple and complex VEA?
 < 5% of healthy teen
boys have more than
50 PVCs/24 h
 < 2% have multiform
PVCs, couplets, or NS
VT in 24 h
Scott, et al. Br Heart J 1980
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26% of healthy boys
PVCs were rare and single
Sometimes multifocal
Sometimes during exercise
Ventricular Premature Contractions
in the Athlete
Assuming …..
Ventricular Premature Contractions
in the Athlete
What is Normal?
Ventricular Premature Contractions
in the Athlete
What is Normal?
Ventricular Premature Contractions
in the Athlete
What is Normal?
Ventricular Premature Contractions
in the Athlete
What is Normal?
What are we willing to tolerate?
Concern?
Concern?
Concern?
Concern?
Concern?
Concern?
VEA Prevalence in the Athlete
Biffi, et al. Cardiol Clin
2007
VEA Prevalence in the Athlete
Biffi, et al. Cardiol Clin
2007
VEA Prevalence in the Athlete
Biffi, et al. Cardiol Clin
2007
The “Athlete’s Heart” Syndrome
“In the process of training, the getting wind , as it is called,
largely a gradual increase in the capability of the heart …. The
large heart of athletes may be due to prolonged use of their
muscles, but no man becomes a great runner or oarsman who
has not naturally a capable if not a large heart”
Osler 1892
- A normal physiologic, adaptive response to intense and repetitive
physical training reversible with deconditioning
- This response has both morphologic and electrophysiologic
changes
- Conflicting data regarding the incidence of VEA
Does “Athlete’s Heart” Syndrome result
in increased VEA?
35 boys age 14-16 y; 35 controls
Viitasalo, et al. Europ Heart J 1984
Hanne-Paparo, et al. Med Sci Sports Exerc 1981
Training-Induced LVH and VEA
Biffi, et al. AJC 2008
- N=175, mean age 23.6 y
- Training-induced LVH does not increase risk for VEA
More VEA trended toward lower LV mass
Increased LV mass correlated with less VEA
- Supports the benign nature of VEA in trained athlete and the
expression of athlete’s heart
Response to Deconditioning
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Biffi, et al. JACC 2004
87 athletes; 44 deconditioned
Holter monitor pre- and postPVCs, couplets, NS VT assessed
No significant change in either
group in pre- vs post
Delise, et al. J Cardiovasc Med 2011
The Evaluation
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Burden
Morphology (uniform vs multiform)
Morphology (RBBB vs LBBB, axis)
Single vs couplets vs NS VT
Response to exercise
Rate of NS VT
Cardiac function
Exercise Stress Test
- 5283 athletes
- Mean age 24.5 y
- Bicycle stress test
- Follow-up 7.4 y
- Spont. Reduction
- No SCA/SCD
Exercise Stress Test
- 5283 athletes
- Mean age 24.5 y
- Bicycle stress test
- Follow-up 7.4 y
- Spont. Reduction
- No SCA/SCD
Suppression of VEA with exercise is so common that it is
difficult to use this criterion diagnostically
Follow-up Studies
N = 120, median age 16 y, median f/up 84 m
 Benign long-term prognosis without structural heart disease
 Continued participation does not change the benign outcome
PVC burden decreases whether active or sedentary
 EF slightly decreases over time in 14.5% sedentary
Athletes with decreased EP had higher PVC burden
Delise, et al. AJC 2013
Ventricular Ectopy in Athletes:
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355 competitive athletes
Palps (n=18) or > 3 PVCs on ECG (n=337)
7% w structural heart disease, most in group A
All Group A athletes excluded
1 Group A athlete died during sport: ARVC
Frequent and complex VEA in athletes with no structural heart disease
should not raise concern for adverse clinical events
Biffi, et al. JACC 2002
AVR in the Athlete
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AVR is almost always benign
Due to increased vagal tone at rest
Immediately resolves with activity
Rarely represents a more malignant VT
Without symptoms, dysfunction, or underlying condition,
intervention is not indicated
Non-sustained VT in the Athlete
- Sporadic in athletes
- Idiopathic
- Low risk for SCD
- RVOT VT most common
- Exclude ARVC
- Medications have limited efficacy
- Catheter ablation can be curative
- Exercise restrictions are generally not indicated
Guidelines and Recommendations
For PVCs in an asymptomatic patient without CHD:
Bethesda Conference #36:
Athlete may participate, but may be restricted for:
- increase in PVCs with exercise
- symptoms with exercise
European Society of Cardiology (ESC):
Athletes may participate, but may be restricted for:
- a family history of SCD
- symptoms with effort
- increase in PVCs with exercise
- frequent couplets with short R-R coupling interval
Guidelines and Recommendations
For NS VT in an asymptomatic patient without CHD:
Bethesda Conference #36:
Athlete may participate if::
- NS VT < 10 beats
- NS VT < 150 bpm
- suppression (or no worsening) with exercise
European Society of Cardiology (ESC):
Athletes may participate if:
- NS VT is “rare”
- is not triggered by exercise
- occurs without a short R-R interval
- there is no family history of sudden death
Conclusions
 PVCs in the athlete are not uncommon, but frequent and
complex forms are less usual and should be evaluated for
possible underlying structural or electrophysiologic
disease
 In the asymptomatic patient with a structurally normal
heart, PVCs, including frequent and complex, are
generally benign and may improve over time
 Medications have not been demonstrated to show
benefit, catheter ablation may be curative in select
cases, and ICD therapy is generally not indicated
Mechanism of VEA in the Athlete
- LVH data suggest that cellular changes are an unlikely cause
of VEA in athletes, as in pathologic LVH, like HCM
- Autonomic nervous system alterations as a mechanism:
- bradycardia-dependent ectopy
- shift of CV autonomic modulation from
parasympathetic toward sympathetic dominance
- enhanced sympathetic tone tends toward ventricular
irritability
- supported by the decreased VEA observed
with deconditioning
Are these concerning?
Are these concerning?
Are these concerning?
Are these concerning?
Ventricular Premature Contractions
in an Athlete:
Frequency of VEA was similar in
athletes and controls
Athletes did not have complex
forms
VEA in athletes occurred
randomly throughout the
recording
Viitasalo, et al. BHJ 1982
Ventricular Premature Contractions
in an Athlete:
A Common Occurrence
Simple ventricular arrhythmias occur among athletes with similar
frequency as in general population
Complex ventricular forms of arrhythmia should always prompt
cardiology evaluation (cardiomyopathy)
Ventricular arrhythmias w/o structural heart disease does not
indicate an increased risk of SCD
Zehender, et al. AHJ 1990

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