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European Journal of Heart Failure 2006 8(8):869-873; doi:10.1016/j.ejheart.2006.02.011
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© 2006 European Society of Cardiology

‘Frequent’ ventricular bigeminy – A reversible cause of dilated cardiomyopathy. How frequent is ‘frequent’?

N. Shanmugama,*, T.P. Chuaa and D. Warda,b

a Royal Surrey County Hospital Guildford, United Kingdom
b St George's Hospital London

* Corresponding author. E-mail address: nesan_s{at}hotmail.com


   Abstract
Top
 Abstract
1. Introduction
 2. Case report
 Box 1. Ablation procedure
 3. Discussion
 4. Conclusion
 References
 
An interesting development in the field of heart failure has been the link between frequent premature ventricular contractions and cardiomyopathy. We report a patient whose frequent ventricular bigeminy resulted in left ventricular impairment that resolved after the use of non-contact mapping during radiofrequency ablation. A review of the literature regarding possible mechanisms is discussed. For the practicing clinician, the question of ‘frequent’ should be taken in context of symptoms and LV function. A single 24-h Holter monitor may not truly reflect the ectopic load. We recommend that if there is associated LV dysfunction and a causal link to frequent PVCs then suppression with radiofrequency ablation is a safe and effective treatment strategy.

Key Words: Dilated cardiomyopathy • Radiofrequency ablation • Ventricular ectopy • Premature ventricular contractions

Received October 2, 2005; Revised January 30, 2006; Accepted February 9, 2006


   1. Introduction
Top
 Abstract
 1. Introduction
2. Case report
 Box 1. Ablation procedure
 3. Discussion
 4. Conclusion
 References
 
Radiofrequency ablation (RFA) has been successfully employed in combating tachycardia-induced cardiomyopathy [1-3]. However, an interesting development in the field of heart failure has been the role of RFA in the suppression of frequent premature ventricular contractions (PVC)-induced cardiomyopathy [4-7]. All published cases to date have reported ‘frequent’ PVC as greater than 20,000 in 24h. A recent retrospective study showed that RFA suppression of ‘frequent’ PVCs, defined as greater than 20% of the total number of heart beats per 24h, produced clinical benefits in patients with heart failure without structural heart disease [8]. We report a patient whose frequent ventricular bigeminy resulted in left ventricular impairment that resolved after RFA.


   2. Case report
Top
 Abstract
 1. Introduction
 2. Case report
Box 1. Ablation procedure
 3. Discussion
 4. Conclusion
 References
 
A 46-year-old lady was found on preoperative assessment to have ectopic beats. Her 12 lead electrocardiogram (ECG) demonstrated frequent ventricular bigeminy, with uniform left bundle branch block (LBBB) and inferior axis (Fig. 1) suggestive of right ventricular outflow tract (RVOT) ectopic focus.


Figure 1
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  		Fig. 1 12 lead ECG showing ventricular bigeminy. The ectopic beats show right axis deviation, LBBB type morphology, late transition V3-V4, negativity in lead I, notching of the QRS in the inferior leads. These features are more consistent with an anterior free wall origin according to the Dixit algorithm [10].

 
On direct questioning, it was noted that she was increasingly lethargic over the last 3years with associated New York Heart Association class II symptoms and left sided "crushing" chest pain associated with mental anxiety, but not physical exertion. She was a former smoker, with a smoking history of 10packyears. There was no significant past medical history or family history of note. Her alcohol intake was negligible and she was on no medication. There were no signs of overt heart failure.

Laboratory investigations were normal. A single 24-h Holter recording demonstrated 3674 PVCs in 24h, of which 42% were in the form of bigeminy. There was no evidence of greater than 5 consecutive premature ventricular complexes. Two-dimensional echocardiography revealed mildly increased left ventricular (LV) chamber dimensions. The LV end-diastolic and systolic dimensions were 56mm and 43mm, respectively. The apico-anteroseptal wall appeared hypokinetic; corresponding fractional shortening was 22% and ejection fraction 40%. A treadmill exercise test showed no evidence of myocardial ischaemia. The number of ventricular bigeminy decreased with the loading of exercise and increased again after the test. Subsequent cardiac catheterisation demonstrated normal angiographic coronary anatomy. The LV angiogram showed global mild LV systolic impairment.

In view of the frequent ventricular bigeminy, associated symptoms and echocardiographic evidence of mildly impaired dilated left ventricle, (and absence of any other reversible aetiology for a dilated cardiomyopathy (DCM)), the patient was referred for electrophysiological studies and RFA.


   Box 1. Ablation procedure
Top
 Abstract
 1. Introduction
 2. Case report
 Box 1. Ablation procedure
3. Discussion
 4. Conclusion
 References
 

The right femoral vein was punctured. A reference electrode was screwed into the right anterior atrium. A 4mm standard curve EPT ablation catheter was positioned in the right ventricle. Finally, a multi-electrode array (MEA) (Endocardial Solutions, Inc. St Paul, Minnesota, USA) was positioned in the right ventricular outflow tract to allow non-contact mapping [9].

The ECGs performed on admission and in the Catheterisation Laboratory, before any catheters were positioned in the heart, showed ventricular bigeminy of identical morphology to that demonstrated on numerous previous ECGs. Analysis of the ECG had suggested a right anterior free wall position according to the Dixit algorithm [10]. However, the MEA demonstrated otherwise (Fig. 2). Soon after positioning the MEA, there was frequent non-clinical ectopy. However, this settled down within about 10min and she resumed clinical ectopy in a bigeminal pattern. The MEA showed early posteroseptal activation. The virtual electrodes showed slow early activation 50ms pre-QRS and the bipolar mapping electrode showed 20ms pre-QRS. Pace mapping at this site gave a 12/12 lead match. Radiofrequency delivery x5 resulted in sustained ventricular tachycardia during the last three deliveries. The QRS morphology was identical to that of the spontaneous ectopics. During the last delivery ectopy subsided. During a 20-min waiting period following ablation, no clinical ventricular ectopics were seen and there were only very infrequent non-clinical ectopics. After all the hardware had been removed from the heart, further observation period revealed no ectopics whatsoever.

 


Figure 2
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  		Fig. 2 Still image from the non-contact activation sequence of the right ventricular outflow tract by the emerging ectopic focus. The horizontal yellow line shows the line of propagation from the posterior origin. The red asterisk represents the point of instantaneous maximum voltage negativity. The red circles indicate where radiofrequency energy was delivered (three of five lesions shown). The virtual electrogram in trace "9" close to the origin and before the apparent exit site shows an early QS deflection in advance of all other electrograms and the surface ECG.

 
Two subsequent 24-h Holter recordings performed 4 and 8weeks after RFA showed no evidence of PVCs. A repeat two-dimensional echocardiographic study 6weeks following RFA showed normalisation of LV dimensions with LV end-diastolic and systolic dimensions reading 49mm and 35mm, respectively. The fractional shortening was now 30% and ejection fraction 51%. The patient's symptoms had also resolved.


   3. Discussion
Top
 Abstract
 1. Introduction
 2. Case report
 Box 1. Ablation procedure
 3. Discussion
4. Conclusion
 References
 
Premature ventricular contractions (PVC) in the presence of a structurally normal heart are commonly encountered in clinical practice [11], their long-term prognosis has often been considered benign [12]. Interestingly there is a school of thought that PVCs can cause deterioration of the left ventricular function analogous to tachycardia-induced cardiomyopathy.

The improvement of left ventricular function after suppression of PVCs has been reported in patients with a presumed DCM [4-7,13]. Duffee et al. [13] were the first to coin the term ‘PVC-induced cardiomyopathy’. They showed that chemical suppression with sotalol and amiodarone improved symptomatic LV dysfunction. Subsequent reports demonstrated the successful resolution of DCM with the use of RFA [4-7]. Apart from Satish et al. [7] who described a PVC focus from the LV with right bundle branch morphology, all other cases have originated from the RVOT with inferior axis and LBBB morphology.

It is also now well documented that RFA is a safe and effective procedure in patients with symptomatic frequent ventricular ectopic beats [14,15], tachycardia induced cardiomyopathy [1-3], and now PVC-induced cardiomyopathy [8]. Takemoto et al. [8] reported a high acute success rate of 93% and a very low recurrence rate of 3% in 40patients undergoing RFA for RVOT PVCs. With regard to the method of ablation, the MEA was chosen because it provides accurate localisation of the ectopic focus [9]. In fact, in this case, the ECG was misleading suggesting an origin almost diametrically opposite the actual site shown by the MEA. The use of a multi-electrode array may cause non-clinical ectopics and hence suppression of clinical PVCs which certainly can be misleading. However, in this case, they were infrequent and did not interfere with the main object of the procedure. Despite the lack of firm data on the use of non-contact mapping, we believe that the use of non-contact mapping may enhance the success rate of right ventricular outflow ectopic ablation.

The hypothesis behind PVC-induced cardiomyopathy is based on the observation that a significant improvement in LV function occurs after suppression of the ectopic focus, therefore suggesting that the cardiomyopathy actually resulted from the frequent PVCs. The study by Takemoto et al. [8] further reinforces this cause and effect hypothesis. They carried out a 10-year retrospective study of 40patients with RVOT PVCs. In patients who experienced more than 20% PVCs per 24h, i.e. approximately 20,000 beats per day, there was a significant correlation with increased LV dimensions and dysfunction, and significant improvement in LV function following RFA.

The group labelled less than 10% PVCs in the Takemoto et al. [8] study, certainly did not show any significant pathological LV dilatation or dysfunction and therefore no obvious comparable improvement following RFA [8]. Interestingly, however our case demonstrates that there was an improvement in LV dimensions and function following RFA in a patient who only had 4% PVCs on 24-h Holter monitoring. It should be recognised however that a single 24-h recording may not reflect the true ectopic load. Due to such variability and hence limitation of using a single 24-h Holter, where there is a strong suspicion that frequent PVCs may be the cause of LV dysfunction, then several 24-h Holter recordings may be necessary.

Possible mechanisms have been postulated for the development of this reversible cardiomyopathy. Frequent PVCs with LBBB morphology may be potentially harmful for the myocardium analogous to the asynchronous contraction in long term right ventricular apical pacing. This has been shown to result in remodelling and subsequent LV diastolic and systolic dysfunction in previously normal hearts [16]. Histopathological findings have been shown both in animal studies [17] and in patients [18]. Interestingly patients upgraded from RV pacing to biventricular devices have improved LV synchrony and LV systolic function [19]. The asynchrony of LV wall motion caused by LBBB is known to be an independent prognostic indicator in patients with DCM [20]. Stroke volume is decreased as a consequence of prolonged duration of mitral regurgitation flow and diastolic dysfunction. LBBB also causes a reversal of the normal squeezing effect (from apical to basal portions) of LV contraction resulting in reduced cardiac function [4]. The mechanisms underlying tachycardia-induced cardiomyopathy may also give us clues to the pathogenesis e.g. depletion of myocardial energy stores [21], abnormalities in subendocardial to subepicardial flow ratios and impaired coronary flow leading to myocardial ischaemia [22,23], abnormalities in calcium handling [24] and reduced beta-adrenergic responsiveness [25], and down-regulation [26] and free radical oxidative stress injury [27].


   4. Conclusion
Top
 Abstract
 1. Introduction
 2. Case report
 Box 1. Ablation procedure
 3. Discussion
 4. Conclusion
References
 
This case highlights the importance of recognizing that frequent PVCs are a potential reversible cause of cardiomyopathy. The timely recognition and treatment of patients, in the subclinical stage of DCM, with frequent PVCs, as highlighted in this case report, can prevent progression to significant heart failure. The question of ‘how frequent is frequent’ is particularly important for the clinician in everyday practice. We would recommend that the importance of ‘frequent’ is taken in the context of symptoms and LV function. If there is associated LV dysfunction and a causal link to frequent PVCs then suppression with RFA is a safe and effective treatment strategy in this subgroup of patients. The use of non-contact mapping may enhance the success rate of ablation by providing more accurate localisation of the focus than ECG algorithms, which in this case were misleading.


   References
Top
 Abstract
 1. Introduction
 2. Case report
 Box 1. Ablation procedure
 3. Discussion
 4. Conclusion
 References
 

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