EDITORIAL
European Journal of Heart Failure (2012) 14, 1083–1084 doi:10.1093/eurjhf/hfs129
Risk of deterioration of cardiac function by frequent ventricular ectopy in patients without structural heart disease Hein J. Wellens* Cardiovascular Research Institute Maastricht, 21 Henric Van Veldekeplein, 6211 TG Maastricht, The Netherlands Online publish-ahead-of-print 8 August 2012
This editorial refers to ‘Prediction and mechanism of frequent ventricular premature contractions related to haemodynamic deterioration’, by K. Kuroki et al., published in this issue on pages 1112– 1120. We have known for many years that frequent (incessantly) occurring episodes of supraventricular and ventricular tachycardias may lead to severe cardiac dysfunction and heart failure in ‘normal’ hearts. This led to the introduction of the name tachycardiainduced cardiomyopathy. That diagnosis requires significant improvement in cardiac fuction following normalization of heart rate by pharmacological rate or rhythm control or cure of the arrhythmia by catheter ablation. Almost two decades ago, Zhu et al. reported on the use of radiofrequency catheter ablation for the management of people with symptomatic ventricular ectopic activity in the absence of structural heart disease.1 The question was then raised about the appropriateness of such an invasive procedure in people whose ventricular premature beats were considered to be benign because no heart disease was present.2 At that time this was based upon lack of knowledge that in the normal heart frequent ventricular premature beats could lead to lasting impairment of cardiac function. However, in 2005 Takemoto et al.3 and Sekiguchi et al.4 showed haemodynamic improvement in patients with frequent monomorphic ventricular premature beats and diminished cardiac function after catheter ablation of the ectopic rhythm. Currently, the presence of frequent symptomatic, predominantly monomorphic ventricular premature beats (VPBs) that are drug resistant or drug intolerant, or if the patient does not want longterm drug therapy, is considered, according to the American College of Cardiology/American Heart Association/European Society of Cardiology (ACC/AHA/ESC) guidelines, a class II A, level of evidence C, indication for catheter ablation.5
Obviously, in decision making about catheter ablation, a key issue is the recognition of patients likely to develop cardiac dysfunction secondary to frequent VPBs. Baman et al.,6 using Holter data in a large group of patients, indicated that a VPB burden (defined as the percentage of total beats that were VPBs) of .24% was independently associated with VPB-induced cardiomyopathy. As indicated in Table 1, a VPB may have both negative and positive haemodynamic consequences. There will be a shorter ventricular filling time related to the prematurity of the VPB. Reduced ventricular filling will also be the case when the VPB occurs earlier than the atrial contraction because of the absence of an atrial contribution to ventricular filling. During a VPB there will be asynchrony of ventricular contraction, the amount of asynchrony being dependent upon the site of origin of the VPB, e.g. more asynchrony (with a wider QRS!) in a biventricular contraction when the VPB has its origin in the free wall of the ventricle as compared with a VPB (with a narrower QRS) arising close to the interventricular septum. Last, but not least, there will be asynchrony in atrial and ventricular contraction during the VPB. When the ventricle contracts before atrial contraction there will be atrioventricular (AV) valve incompetence, and when the atrium contracts against closed AV valves there will be an increase in pulmonary capillary wedge and caval venous pressures and an increase in atrial size. Eventually this may lead to the development of biventricular dysfunction and facilitate the occurrence of atrial fibrillation. A good haemodynamic effect of a VPB is post-pause VPB potentiation, resulting in a more forceful contraction of a better filled ventricle of the subsequent conducted sinus beat. Keeping these different aspects in mind, Kuroki et al.7 looked at the haemodynamic effects of very frequent VPBs in 31 patients, before and after successful catheter ablation of the arrhythmia. These were patients with frequent predominantly monomorphic
The opinions expressed in this article are not necessarily those of the Editors of the European Journal of Heart Failure or of the European Society of Cardiology.
* Corresponding author. Tel: +31 3215440, Fax: +31 3261903, Email:
[email protected] Published on behalf of the European Society of Cardiology. All rights reserved. & The Author 2012. For permissions please email:
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Table 1 Negative and positive haemodynamic effects of a ventricular premature beat Negative Shorter ventricular filling time Absent atrial contribution to ventricular filling Asynchronous ventricular contraction AV valve incompetence when VPB starts before atrial contraction Atrial contraction against closed AV valves resulting in an increase in pulmonary capillary wedge and caval venous pressures and atrial size Positive Post-premature beat potentiation of next conducted sinus beat AV, arteriovenous; VPB, ventricular premature beat.
Editorial
(which may be not so benign, as shown in the study of Kuroki et al.) have their origin in the outflow tract of the right ventricle, but they may be caused by structural cardiac disease such as arrhythmogenic right ventricular cardiomyopathy. I was surprised that in 15 of the 31 VPB patients discussed by Kuroki et al.7 the arrhythmia came from sites other than the right ventricular outflow tract. In my experience, it is unusual to have frequent monomorphic VPBs from other sites without underlying cardiac disease. A very careful investigation is always required to make sure that that is not the case. In conclusion, the observations by Kuroki et al. are of interest, especially because of their finding that the inexpensive ECG is useful to identify patients with very frequent VPBs likely to benefit from catheter ablation. Further validation in a larger group of patients will be helpful. Conflict of interest: none declared.
VPBs with a fixed coupling interval. The important finding was that 19 of them showed marked augmentation of pulmonary capillary wedge pressure (PCWP) by the VPBs, defined as a peak PCWP of .15 mmHg. In those patients, increased values were also found for mean PCWP, right atrial pressure, left ventricular enddiastolic pressure, and the plasma brain natriuretic peptide level. Those values improved immediately and in the long term after successful catheter ablation at the site of origin of the VPB. Most importantly,when they examined the electrocardiogram (ECG), they found a shorter VPB coupling interval (,500 ms) and a VPB– P interval of , 300 ms in the group with marked PCWP augmentation. Those observations could be confirmed by pacing studies in which the intervals of ventricular and atrial pacing were varied. Their message was that the ECG could be an inexpensive way to identify those likely to have or develop haemodynamic deterioration by the VPBs. To use those ECG intervals for risk classification of the patient, it is important to realize that clinically in these patients the length of the VPB coupling interval stays fixed but that the VPB– P interval will vary according to the sinus rate, or the presence or absence of ventriculoatrial conduction. No information is given on how long these patients suffered from these frequently occurring monomorphic VPBs, the percentage of their VPB burden, or the effect of pharmacological attempts to suppress ventricular ectopic activity. One always has to make sure that frequent VPBs are not caused by underlying heart disease. Most of the so-called ‘benign’ VPBs
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