Alessandro Zorzi, MD - European Society of Cardiology · Key message: exercised-induced PVBs may be...

Ventricular arrhythmias

Understanding the clinical significance

Alessandro Zorzi, MDDepartment of cardiac, thoracic and

vascular sciences

University of Padova

2nd EACPR Course on Sports Cardiology

Classification of ventricular arrhythmias

VENTRICULAR ECTOPIC BEATS

MONOMORPHIC VENTRICULAR

TACHYCARDIA

POLYMORPHIC VENTRICULAR

TACHYCARDIA/TORSADE DE POINTES

VENTRICULAR FIBRILLATION

Percentiles 5° 15° 30° 50° 70° 85° 95°

PVB/24 hours

0 0 0 1 3 10 220

0

50

100

150

200

250

300

350

400

0 50 100 150 200 250 300

PV

B n

°/d

ie

Recruitment number

Premature ventricular beats count

in amateur athletes (>6 hours/week)

7%

21% 22% 23%

55%

16-25 26-35 36-45 46-55 >55

Exp (B) 95% p

Male gender 1.506 0.606-3.743 0.38

Type of sport

Anaerobic sport 1 0.91

Mix aerobic/anaerobic 1.207 0.492-2.966 0.68

Aerobic sport 1.008 0.361-2.813 0.99

Age 1.046 1.010-1.083 0.01

Years of sports activity 1.015 0.976-1.083 0.46

Determinants of recording of >10 PVB or repetitive ventricular

arrhythmias on 24 hours ECG monitoring

Age classes

Hingorani et al.

N=1273

General population

Our study

N=260

Athletes

p

>0 BPV 43.3% 65.2% <0.001

>50 BPV 11.8% 13.2% 0.684

>100 BPV 9.1% 9.6% 0.878

>1000 BPV 1.8% 3.0% 0.357

>2000 BPV 1.3% 1.2% 1.000

Do athletes have more ventricular

arrhythmias than the general population?

PVBs ARE NOT A FEATURE OF THE ATHLETE’S HEART!!

Biffi et al. J Am Coll Cardiol 2002;40:446 –52

Long-term clinical significance of frequent and

complex ventricular tachyarrhythmias in trained athletes

Impact of physical deconditioning

on ventricular tachyarrhythmias in trained athletes

Biffi et al. J Am Coll Cardiol 2004;44:1053– 8

Assessment of ventricular

ectopic beats in the athlete

• Evaluation of morphology/site of origin

(rather than simply PVB count)

• Response to exercise testing

• Search for underlying structural heart

diseases

LBBB/inferior axis

Early ARVC

Idiopathic

RVOT VA

A B

D E

RV LV

C

LBBB/LAD

RBBB (narrow QRS)

RBBB (wide QRS)

Scand J Med Sci Sports 2016






diseases

24-hour ambulatory ECG monitoring

(including training)

What is the diagnostic power of

exercise-induced ventricular

arrhythmias?

What would

have

happened?

Heart Rhythm 2015;12:78-85

Key message: exercised-induced PVBs may be more frequent in

athletes with structural heart disease but if a substrate is excluded

there is no demonstration that they are malignant

One important exception: CPVT






diseases

INVESTIGATION OF AN UNDERLYING

MYOCARDIAL SUBSTRATE: HOW

DEEP SHOULD WE DIG?

.

PIERMARIO MOROSINI

Professional soccer player

DIED SUDDENLY AT THE AGE of 26

REGULAR MEDICAL EVALUATIONS

No symptoms

Normal ECG

Normal ECHOCARDIOGRAPHY

R.D.R.

Professional soccer player

ARRHYTHMIC SYNCOPE AT THE AGE of 23

REGULAR MEDICAL EVALUATIONS

No symptoms

Abnormal ECG (lateral T-wave inversion)

Normal ECHOCARDIOGRAPHY

D’Amati et al. Int J Cardiol 2016;206:84–86

Br J Sports Med 2015

Arrhythmias with and w/o substrateGroup A

VA and LGE

N=35

Group B

VA and NO LGE

N=38

P

Electrocardiogram

Normal

Low (≤ 0.5 mV) QRS voltages in limb leads

Intraventricular conduction delay

QRS duration 100-120 ms

QRS duration >120 ms

Pathologic Q-waves

T-wave inversion in V1-V3

T-wave inversion in V4-V6 ± 1/aVL

T-wave inversion in 2/aVF/3

22 (63)

7 (20)

3 (9)

0

2 (6)

1 (3)

7 (20)

2 (6)

35 (92)

1 (3)

2 (6)

0

0

0

0

1 (3)

0.004

0.02

0.67

-

0.23

0.48

0.004

0.60

Late potentials at SAECG 6/15 (40) 1/20 (5) 0.03

24-Hour ECG monitoring

Frequent (>500/day) PVB

Couplets and/or triplets

Non-sustained VT (≥4 PVB)

Sustained VT/VF

30 (86)

20 (57)

8 (23)

1 (3)

35 (92)

18 (47)

2 (6)

0

0.47

0.40

0.04

0.48

Response to exercise testing

No/suppression

Isolated PVB

Repetitive PVB

9 (26)

16 (46)

10 (29)

15 (39)

19 (50)

4 (11)

0.21

0.71

0.07

Echocardiogram

Normal

Regional LV wall motion abnormalities

30 (86)

5 (14)

38 (100)

0

0.02

All 27 athletes with venticular arrhythmias and underlying substrate (LV scar with a

stria pattern) showed PVBs with a RBBB pattern

The vast majority of athletes with arrhythmias and no or junctional (benign) late

enhancement showed RVOT PVBs (LBBB/inferior axis)

Clinical workout in young athletes with PVBs

Scand J Med Sci Sports 2016

Note: if RBBB morphology,

polymorphic and exercise-

induced consider genetic

testing for CPVT


VENTRICULAR ECTOPIC BEAT


TACHYCARDIA





TACHYCARDIA

When due to an underlying structural heart disease they are usually

caused by a re-entry mechanism. Two main categories:

Scar-related re-entrant VT: typical of post MI or cardiomyopathies

Bundle-bundle re-entrant mechanism: typical of heart failure

Zorzi et al, Circ Arrhythm Electrophysiol 2016

RE-ENTRANT VT ARE USUALLY ASSOCIATED

WITH A STRUCTURAL HEART DISEASE

FACTORS NEEDED FOR A RE-ENTRANT

SUSTAINED VT TO OCCUR

SUBSTRATE

TRIGGER CONTRIBUTING FACTORS

FACTORS NEEDED FOR A RE-ENTRANT

SUSTAINED VT TO OCCUR

SUBSTRATE

TRIGGER

CONTRIBUTING

FACTORS

- Hypo K+/Mg++

- Hyperthermia

- Adrenergic stimulation

FACTORS THAT INFLUENCE HEMODYNAMIC

TOLLERABILITY OF VENTRICULAR

TACHYCARDIA

Heart rate -> number of turnovers/minute

(increased by adrenergic stimulation during physical exercise)

Degree of

synchronization

(worsened by

adrenergic

stimulation during

physical exercise )

Ventricular systolic

function

THE IMPORTANCE OF PHYSICAL EXERCISE AS A

CAUSE OF TRASFORMATION OF “SIMPLE”

MONOMORPHIC VT INTO VF

ABLATION OF THE CIRCUIT (TARGETS THE CRITICAL

ARRHYTHMIA “ISTMUS”)

DENSE

SCAR

DENSE

SCAR

DENSE

SCAR

INTERVENTIONAL TREATMENT OF RE-

ENTRANT VT

IN PATIENTS WITH STRUCTURALLY NORMAL HEART,

MONOMORPHIC VENTRICULAR TACHYCARDIA ARE

USUALLY FOCAL AND REPRESENT THE REPETITIVE

FORM OF SIMPLE PVBs

Sustained right ventricular outflow tract is benign in terms of sudden death risk but

rarely can be so fast as to cause syncope even in subjects with normal heart.

TREATMENT OF FOCAL PVB/VT

Earliest ventricular

activation during PVB/VT:

site of arrhythmia origin

Focal radiofrequency

ablation and elimination of

the arrhythmogenic focus

Success rate ≈90%




TACHYCARDIA






The substrate of these arrhythmias is usually at a cellular level:

-Cellular toxicity (hypokaliemia, drug toxicity …)

-Genetically determined (it is the classic arrhythmia of long

QT/Brugada syndrome)

-Acute ischemia/reperfusion

MECHANISM OF TORSADE DE POINTES

PHASE 2 RE-ENTRY

When the length of the refractory period is not

homogenous among myocytes, cells that are

already repolarized (-) can be re-activated by

nearby cells that are still depolarized (+).

This mechanism gives rise to a very early

ventricular ectopic beat, called “R on T”

THE EXAMPLE OF LONG QT

Drugs

Electrolytic abnormalities (hypo Ca, hypo Mg,

hypo K+)

Genetically determined long QT

THE EXAMPLE OF BRUGADA SYNDROME




TACHYCARDIA





SUSTAINED

VENTRICULAR

TACHYCARDIA

ADRENERGIC

STIMULATION and/or

CELLULAR ACIDOSIS

IMPULSE CONDUCTION DISTURBANCES

SEVERE MYOCITE

ABNORMALITIES (e.

g. acute myocardial

infarction)

PREMATURE

VENTRICULAR

ECTOPIC BEAT

TORSADE DE

POINTES/

POLYMORPHIC

VENTRICULAR

TACHYCARDIA

TREATMENT OF VENTRICULAR

FIBRILLATION

CONCLUSIONS

The clinical significance of arrhythmias in the athletes depends on

the presence of an underlying heart disease that may be:

1) Structural (e.g. myocardial scar)

2) Cellular (genetically determined ion channel disease)

There is no demonstration that ventricular arrhythmias in the

athletes (even if they are frequent or persist after detraining)

confer an increased risk of sudden death and should prompt

sport disqualification if an underlying heart disease is ruled

out.

However…

The presence of a myocardial substrate (either macroscopic or

cellular/genetic) should be carefully investigated:

echocardiography is often not enough.

Alessandro Zorzi, MD - European Society of Cardiology · Key message: exercised-induced PVBs may be...

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