Erika Maharani

Sardjito General Hospital

Yogyakarta
Treat It or Leave It?
 The Cardiologists’ Worst Nightmare:
Sudden Death From “Benign” Ventricular Arrhythmias
Introduction
 3.5%
40–75% 1.39 incidence of Mostly
In General sustained
Population
Male Only need
compared VT or Reassurance
to female
SCD
 Ventricular Arrhythmias: Clinical Spectrum

• Reassurance
• Ablation

• Asymptomatic • ICD
and Benign • Frequent and
Symptomatic • Sudden
Cardiac Death

Heart Rhythm, Vol 11, No 10, October 2014

 } Structural heart disease
} Ischaemic heart disease
} Inheritable arrhythmogenic
diseases

Screening is important

European Heart Journal (2015) 36, 2793–2867

 • 12 Lead ECG & Specific
Morphology
Structural heart disease ? • Echocardiography
Inherited and acquired cardiomyopathies? • Holter Monitoring, Loop recorder
• Magnetic Resonance Imaging
Myocardial ischemia ?
• Test for myocardial ischaemia
• Electrophysiology study
 No detectable heart disease

Premature Ventricular Contraction

Structural heart disease and
Ventricle Tachycardia
congenital heart diseases
Ventricle Fibrillation
Inherited arrhythmogenic disease
or cardiomyopathy
} Risk factors predicting the development of severe ventricular
arrhythmias:
◦ Multiple myocardial infarctions (MI)
◦ Syncope
◦ Complex and frequent ventricular ectopy including VT
◦ Activation of the sympathetic nervous system
◦ Detection of sites of slow ventricular conduction or ventricular
conduction abnormalities
◦ Left ventricular (LV) dysfunction and presence of ventricular aneurysm

Gatzoulis KA et al. Hellenic J Cardiol 2012; 53: 217-233

PVC and LV Dysfunction
} Several studies have demonstrated an association between frequent PVCs
and a potentially reversible cardiomyopathy

} The number of PVCs/24 h that is associated with impaired LV function has

generally been reported at burdens above 15–25% of the total cardiac

beats, though this may be as low as 10%

} Dyssynchronous ventricular contraction presumably leads to deterioration

in LV systolic function through effects on ventricular remodeling.

Gatzoulis KA et al. Hellenic J Cardiol 2012; 53: 217-233

Kanei et al. A.N.E. 2008;13(1):81–85
 } PVCs originating from the Right Ventricle were associated with a
significantly increased prevalence of reduced LVEF at a PVC burden ≥10%
whereas PVCs originating from the Left Ventricle were associated with
reduced LVEF only at a PVC burden ≥20%

} Fascicular PVCs would be expected to not cause much LV dyssynchrony.

Munoz et al, J Cardiovasc Electrophysiol, Vol. 22, pp. 791-798, July 2011
Bogun et al. J Am Coll Cardiol 2009;53:1138–45
Right Ventricle Left Ventricle

Munoz et al, J Cardiovasc Electrophysiol, Vol. 22, pp. 791-798, July 2011
} PVCs following the preceding QRS complex at a short coupling interval
can result in substantially reduced stroke volumes due to less LV filling
time.

RR’/RR ratio = VPC coupling interval divided by the RR interval during sinus rhythm;
LVEF – left ventricular ejection fraction; CI – cardiac index; PVC – premature ventricular contraction.

Sun Y et al. Int J of Cardiovascular Imaging 19: 295–299, 2003.

Coupling Interval (CI)
} A retrograde contraction of the atrium following a PVC, which may cause
an abnormal ventriculo-atrial contraction, has the potential to include
transient hemodynamic compromise and LV dysfunction.

Comparison of patients with and without left ventricular dysfunction

PVCs, premature ventricular complexes; VT, ventricular tachycardia; CI, confidence interval.

Ban JE. Europace (2013) 15, 735–741

} Nonsustained VT was as an independent predictor of LV dysfunction.

} PVC duration ≥140 ms cause greater LV dyssynchrony

} Reduced LVEF compared to normal LVEF, however, was associated with a

longer PVC duration

} Patients with a reduced LVEF as compared to those with normal LVEF were
more likely to have multiform PVCs

Munoz et al, J Cardiovasc Electrophysiol, Vol. 22, pp. 791-798, July 2011
Bogun et al. J Am Coll Cardiol 2009;53:1138–45
 PVC and Malignant
Ventricle Arrhythmia
 } There is a growing body of evidence that very short coupled PVC’s
may initiate idiopathic VF.

} Haïssaguerre et al reported the initial observation that VPBs arising

from the Purkinje system had an important role in the induction of
idiopathic VF; initiated by a short-coupled PVC.

} Short-coupled PVC from outflow tract could also cause idiopathic VF

Haissaguerre et al. Circulation. 2002;106:962-967

Examples of VF initiation by premature beats later found to originate from the right
(top) or left (bottom) ventricle. The inferior panel is continuous Holter recording.
Viskin S et al. J Cardiovasc Electrophysiol, Vol. 16, pp. 912-916, August 2005
} In the study of Viskin et al., the coupling intervals of the initiating PVC in
those with idiopathic VF, malignant RVOT VT, and benign RVOT VT

was 300 ± 40 ms, 340 ± 30 ms, and 427 ± 76 ms, respectively.

} Knecht et al reviewed 38 patients presenting with idiopathic VF - patients

with triggering PVCs originating from the RVOT showed a CI of
355±23 ms versus 276±22 ms for those PVCs originating from the
Purkinje system.

Viskin S et al. J Cardiovasc Electrophysiol. 2005;16:912–916

Knecht S et al. J Am Coll Cardiol. 2009;54:522–528.
Noda et al. J Am Coll Cardiol 2005;46:1288 –94
} Distinguishing malignant from benign PVCs is essential because proper
management can prevent unexpected cardiac events.
} Dyssynchronous ventricular contraction due to PVC presumably leads to
deterioration in LV systolic function through effects on ventricular
remodeling

} Several differences in ECG characteristics have been reported to

differentiate between malignant and benign forms of PVCs.
Thank You