Europace Advance Access originally published online on March 12, 2008
Europace 2008 10(6):769-770; doi:10.1093/europace/eun060
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VENTRICULAR TACHYCARDIA
Reversal of premature ventricular complex-induced cardiomyopathy following successful radiofrequency catheter ablation
Second Department of Cardiology, Evangelismos General Hospital of Athens, 25, 28th Octovriou st, 15235, 10676 Athens, Greece
Manuscript submitted 30 November 2007. Accepted after revision 18 February 2008.
* Corresponding author. Tel: +30 2106843854; fax: +30 2106513317. E-mail address: k.letsas{at}mail.gr
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Abstract |
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Premature ventricular complex (PVC)-induced cardiomyopathy is an underappreciated cause of left-ventricular (LV) dysfunction. The present report describes the case of an elderly man with a very high burden of monomorphic PVCs and LV dysfunction. Elimination of the left ventricular focus following radiofrequency catheter ablation resulted in reversal of cardiomyopathy.
Key Words: Premature ventricular complexes, Left ventricular dysfunction, Cardiomyopathy, Radiofrequency catheter ablation
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Introduction |
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A 74-year-old male with history of palpitations was referred to our hospital for further evaluation. On physical examination, heart sounds were normal, without any murmurs or gallops. Baseline ECG showed sinus rhythm and frequent premature ventricular complexes (PVCs) with a qr pattern in V1, early transition in V2, and an inferior axis (II > III). QTc interval was normal. Transthoracic echocardiography revealed normal-wall motion of both ventricles with an estimated left-ventricular (LV) ejection fraction of 60%. Holter monitoring showed frequent monomorphic PVCs and bigeminy without episodes of ventricular tachycardia. Exercise treadmill test failed to demonstrate any ST-segment or T wave changes suggestive of ischaemia, while the number of monomorphic PVCs was increased. Coronary angiography revealed no significant stenosis. The patient was discharged using a β-blocker. Six months later, he presented to the emergency department complaining of easy fatigue and dyspnoea on exertion. Transthoracic echocardiography revealed global hypokinesis of the LV with an ejection fraction of 40–45%. Holter recordings revealed >50 000 monomorphic PVCs in a 24 h period.
In the setting of no other apparent cause of LV dysfunction, we decided to attempt radiofrequency (RF) catheter ablation of the monomorphic PVCs, using the CARTO electroanatomical mapping system (CARTO, Biosense Webster, Inc., Diamond Bar, CA, USA). Left-ventricular mapping was performed during monomorphic PVCs, using a 4 mm tip deflectable catheter (NAVISTAR, Biosense Webster). The earliest activation site of the PVCs (preceding the onset of the surface QRS by 30 ms) was identified at the septal aspect of the basal LV (Figure 1A). Pace-mapping at this location demonstrated ‘perfect match’ (12 of 12 leads) with the morphology of the PVCs (Figure 1B and C). The first RF energy application (target temperature of 60°C, 30 W, 60 s) abolished all premature beats. Additional RF applications (3 of 60 s and 7 of 30 s) were delivered at this region in order to ensure a long-term success. Holter recordings performed the next 48 h following RF ablation failed to demonstrate any PVCs and β-blocker administration was discontinued. After a 3 month follow-up period, the patient was asymptomatic and transthoracic echocardiography showed a significant improvement of the LV ejection fraction (55%).
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Discussion |
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Premature ventricular complex-induced cardiomyopathy, an underappreciated cause of LV dysfunction, is principally observed in older patients.1
Ventricular dyssynchrony and increased oxygen consumption have been reported as possible underlying mechanisms.2 Reversibility of LV dysfunction has been demonstrated following RF catheter ablation of the PVC focus.1–3 In a recent study including patients with idiopathic, frequent PVCs (>10 h–1), mainly originating from the right ventricular outflow tract (52%), LV ejection fraction was normalized in 82% of patients with PVC-induced cardiomyopathy within 6 months following RF catheter ablation.2 The present report shows that a very high burden of monomorphic PVCs (> 50.000 per 24 h) coming from the LV may lead to symptomatic cardiomyopathy, a condition which is completely reversible within 3 months following RF elimination of the ectopic focus. Physicians should always be aware of this condition when treating subjects with frequent PVCs, particularly those who do not respond to antiarrhythmic therapy (β-blockers and sotalol). Close follow-up with transthoracic echocardiography is recommended. |
References |
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[1] Yarlagadda RK, Iwai S, Stein KM, Markowitz SM, Shah BK, Cheung JW, et al. Reversal of cardiomyopathy in patients with repetitive monomorphic ventricular ectopy originating from the right ventricular outflow tract. Circulation (2005) 112:1092–7.
[2] Bogun F, Crawford T, Reich S, Koelling TM, Armstrong W, Good E, et al. Radiofrequency ablation of frequent, idiopathic premature ventricular complexes: comparison with a control group without intervention. Heart Rhythm (2007) 4:863–7.[CrossRef][Web of Science][Medline]
[3] Readfearn DP, Hill JD, Keal R, Toff WD, Stafford PJ. Left ventricular dysfunction resulting from frequent unifocal ventricular ectopics with resolution following radiofrequency ablation. Europace (2003) 5:247–50.
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