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Reversible left ventricular dyssynchrony and heart failure induced by right ventricular pacing
Letters to the Editor
117
Reversible left ventricular dyssynchrony and heart failure induced by right ventricular pacing Jeffrey W.H. Fung ⁎, Qing Zhang, Gabriel W.K. Yip, Cheuk M. Yu Division of Cardiology, Department of Medicine and Therapeutics, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong SAR, China Received 17 September 2007; accepted 11 December 2007 Available online 6 February 2008
Abstract Right ventricular (RV) pacing related heart failure is reported in some patients after long term pacing. The exact mechanism is not yet clear but may be related to left ventricular (LV) dyssynchrony induced by RV apical pacing. We report one case with baseline normal LV ejection fraction but complicated by heart failure and ventricular tachycardia after 4 months of pacing for complete heart block together with illustration of LV dyssynchrony demonstrated by tissue Doppler imaging. 2007 Elsevier Ireland Ltd. All rights reserved. © 2008 Keywords: Right ventricular pacing; Left ventricular dyssynchrony; Heart failure Keywords: Right ventricular pacing; Left ventricular dyssynchrony; Heart failure
1. Introduction Cumulative data have shown that right ventricular (RV) apical pacing would cause left ventricular (LV) systolic dysfunction and lead to adverse clinical events in patients with standard indications for pacing [1,2]. The exact mechanism of RV pacing related heart failure is not clear but may be related to LV dyssynchrony induced by RV pacing [2]. In the present report, the reversible nature of the LV dyssynchrony was demonstrated by tissue Doppler imaging (TDI) in a patient after short term RV pacing but complicated by heart failure and ventricular tachycardia. 2. Case report A 69-year gentleman presented with syncope. ECG upon admission showed complete heart block with narrow QRS complex (b120 ms) and the escape ventricular rate was 45 bpm. He had no history of hypertension or heart disease. Echocardiographic examination showed that the LV ejection fraction was 55% with normal chambers sizes. A conventional dual chamber pacemaker was implanted with the RV lead positioned to RV apex. The pacemaker was programmed in a DDDR mode with lower rate of 60 bpm and upper tracking rate of 130 bpm. ECG before discharge showed atrial synchronized ventricular pacing with rate of 70 bpm. He was admitted again 4 months later for heart failure. Echocardiography showed dilated LV with ejection fraction of 30%. He developed sustained monomorphic ventricular tachycardia with rate of
⁎ Corresponding author. Tel.: +852 2683 8525; fax: +852 2683 8534. E-mail address: [email protected] (J.W.H. Fung).
180 bpm and was terminated by cardioversion. Troponin T level was not raised and cardiac catheterization showed normal coronary arteries. TDI was performed during on and off RV pacing. The QRS duration was b120 ms and the escape rate was 40 bpm while RV pacing was turned off. The standard deviation of the time from the onset of QRS complex to peak systolic contraction velocity (Ts-sd) among the 12 LV segments in the 6-mid 6-basal segmental model was calculated [3]. The Ts-sd was 39.7 ms during VVI pacing of 50 bpm and reduced to 14.6 ms during no pacing (Fig. 1). Upgrading to cardiac resynchronization therapy (CRT) with defibrillator was recommended but the procedure was complicated by coronary sinus dissection and was postponed. The device was programmed to back up VVI pacing of 40 bpm which would allow native ventricular escape. Echocardiography showed LV reverse remodeling with reduction of LV end-systolic volume from 124 ml to 105 ml and significant improvement in LV ejection fraction to 45% one month later. He had no symptom of heart failure or syncope afterwards and device interrogation showed that cumulative RV pacing was less than 10%. 3. Discussion This case illustrated the reversible nature of RV pacing induced heart failure and it may be related to the reversible LV dyssynchrony induced by RV pacing as demonstrated by TDI. The Ts-sd cut-off for significant LV intraventricular dyssynchrony that may respond favourably to CRT was 32.6 ms [3]. The Ts-sd was 39.7 ms and 14.6 ms when RV pacing was turned on and off respectively. There seems to be no other cause accounted for the heart failure in this patient except for RV pacing. The reason for rapid development of
118 Letters to the Editor Fig. 1. Tissue Doppler imaging during ON and OFF RV pacing. Upper Panel showing the velocity time curve of individual LV segment during RVapical pacing in apical 4 chamber, apical long and apical 2 chamber view (from left to right respectively). The white arrows indicate the peaks of systolic contraction velocity of the 4 LV segments in different echocardiographic view within the ejection phase between aortic valve opening (AVO) and closure (AVC). Note the different timing to reach peak contraction particularly obvious in the apical 2 and 4 chamber views when compared to RV pacing OFF (lower panel). The standard deviation of time (Ts-sd) from the onset of QRS complex to peak systolic contraction velocity among the 12 LV segments was 39.7 ms. Lower Panel showing the velocity time curve of individual LV segment when RV pacing was programmed OFF. The echocardiographic views were identical to Upper Panel for comparison. The green arrows indicate the peaks of systolic contraction velocity of the LV segments when RV pacing was withheld. Note the intraventricular synchronicity demonstrated with similar timing to reach the peak systolic contraction among the LV segments and the Ts-sd was 14.7 ms. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)
Letters to the Editor
heart failure after short period of pacing is unclear. However, the LV systolic function showed dramatic improvement when RV pacing was avoided and this would further support that the reversible cardiomyopathy was possibly related to RV pacing induced LV dyssynchrony. The best treatment option for this patient remains to be determined. CRT may be superior to RV pacing in patients with impaired LV systolic function and standard pacing indication [4] but whether CRT would be equally effective in patients with preserved LV systolic function is unclear. Ongoing prospective randomized trial may be able to address this clinically important question [5]. It was unfortunate that complication was encountered during the upgrading procedure but it seemed that patient tolerated the back up pacing well with gradual recovery of LV systolic function. Cumulative RV pacing less than 40% was associated with a significantly lower risk of adverse events when compared to those with more than 40% in one study [1]. This case has demonstrated the reversible nature of the heart failure and the importance of minimizing RV pacing in vulnerable patient [6].
0167-5273/$ - see front matter © 2007 2008 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2007.12.018
119
References [1] Sweeney MO, Hellkamp AS. Heart failure during cardiac pacing. Circulation 2006;113:2082–8. [2] Tops LF, Schalij MJ, Holman ER, van Erven L, van der Wall EE, Bax JJ. Right ventricular pacing can induce ventricular dyssynchrony in patients with atrial fibrillation after atrioventricular node ablation. J Am Coll Cardiol 2006;48:1642–8. [3] Yu CM, Chau E, Sanderson JE, et al. Tissue Doppler echocardiographic evidence of reverse remodeling and improved synchronicity by simultaneously delaying regional contraction after biventricular pacing therapy in heart failure. Circulation 2002;105:438–45. [4] Kindermann M, Hennen B, Jung J, Geisel J, Bohm M, Frohlig G. Biventricular versus conventional right ventricular stimulation for patients with standard pacing indication and left ventricular dysfunction: the Homburg Biventricular Pacing Evaluation (HOBIPACE). J Am Coll Cardiol 2006;47:1927–37. [5] Fung JW, Chan JY, Omar R, et al. The Pacing to Avoid Cardiac Enlargement (PACE) Trial: clinical background, rationale, design, and implementation. J Cardiovasc Electrophysiol 2007;18:735–9. [6] Gillis AM, Purerfellner H, Israel CW, et al. Medtronic Enrhythm Clinical Study Investigators. Reducing unnecessary right ventricular pacing with the managed ventricular pacing mode in patients with sinus node disease and AV block. Pacing Clin Electrophysiol 2006;29:697–705.
117
Reversible left ventricular dyssynchrony and heart failure induced by right ventricular pacing Jeffrey W.H. Fung ⁎, Qing Zhang, Gabriel W.K. Yip, Cheuk M. Yu Division of Cardiology, Department of Medicine and Therapeutics, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong SAR, China Received 17 September 2007; accepted 11 December 2007 Available online 6 February 2008
Abstract Right ventricular (RV) pacing related heart failure is reported in some patients after long term pacing. The exact mechanism is not yet clear but may be related to left ventricular (LV) dyssynchrony induced by RV apical pacing. We report one case with baseline normal LV ejection fraction but complicated by heart failure and ventricular tachycardia after 4 months of pacing for complete heart block together with illustration of LV dyssynchrony demonstrated by tissue Doppler imaging. 2007 Elsevier Ireland Ltd. All rights reserved. © 2008 Keywords: Right ventricular pacing; Left ventricular dyssynchrony; Heart failure Keywords: Right ventricular pacing; Left ventricular dyssynchrony; Heart failure
1. Introduction Cumulative data have shown that right ventricular (RV) apical pacing would cause left ventricular (LV) systolic dysfunction and lead to adverse clinical events in patients with standard indications for pacing [1,2]. The exact mechanism of RV pacing related heart failure is not clear but may be related to LV dyssynchrony induced by RV pacing [2]. In the present report, the reversible nature of the LV dyssynchrony was demonstrated by tissue Doppler imaging (TDI) in a patient after short term RV pacing but complicated by heart failure and ventricular tachycardia. 2. Case report A 69-year gentleman presented with syncope. ECG upon admission showed complete heart block with narrow QRS complex (b120 ms) and the escape ventricular rate was 45 bpm. He had no history of hypertension or heart disease. Echocardiographic examination showed that the LV ejection fraction was 55% with normal chambers sizes. A conventional dual chamber pacemaker was implanted with the RV lead positioned to RV apex. The pacemaker was programmed in a DDDR mode with lower rate of 60 bpm and upper tracking rate of 130 bpm. ECG before discharge showed atrial synchronized ventricular pacing with rate of 70 bpm. He was admitted again 4 months later for heart failure. Echocardiography showed dilated LV with ejection fraction of 30%. He developed sustained monomorphic ventricular tachycardia with rate of
⁎ Corresponding author. Tel.: +852 2683 8525; fax: +852 2683 8534. E-mail address: [email protected] (J.W.H. Fung).
180 bpm and was terminated by cardioversion. Troponin T level was not raised and cardiac catheterization showed normal coronary arteries. TDI was performed during on and off RV pacing. The QRS duration was b120 ms and the escape rate was 40 bpm while RV pacing was turned off. The standard deviation of the time from the onset of QRS complex to peak systolic contraction velocity (Ts-sd) among the 12 LV segments in the 6-mid 6-basal segmental model was calculated [3]. The Ts-sd was 39.7 ms during VVI pacing of 50 bpm and reduced to 14.6 ms during no pacing (Fig. 1). Upgrading to cardiac resynchronization therapy (CRT) with defibrillator was recommended but the procedure was complicated by coronary sinus dissection and was postponed. The device was programmed to back up VVI pacing of 40 bpm which would allow native ventricular escape. Echocardiography showed LV reverse remodeling with reduction of LV end-systolic volume from 124 ml to 105 ml and significant improvement in LV ejection fraction to 45% one month later. He had no symptom of heart failure or syncope afterwards and device interrogation showed that cumulative RV pacing was less than 10%. 3. Discussion This case illustrated the reversible nature of RV pacing induced heart failure and it may be related to the reversible LV dyssynchrony induced by RV pacing as demonstrated by TDI. The Ts-sd cut-off for significant LV intraventricular dyssynchrony that may respond favourably to CRT was 32.6 ms [3]. The Ts-sd was 39.7 ms and 14.6 ms when RV pacing was turned on and off respectively. There seems to be no other cause accounted for the heart failure in this patient except for RV pacing. The reason for rapid development of
118 Letters to the Editor Fig. 1. Tissue Doppler imaging during ON and OFF RV pacing. Upper Panel showing the velocity time curve of individual LV segment during RVapical pacing in apical 4 chamber, apical long and apical 2 chamber view (from left to right respectively). The white arrows indicate the peaks of systolic contraction velocity of the 4 LV segments in different echocardiographic view within the ejection phase between aortic valve opening (AVO) and closure (AVC). Note the different timing to reach peak contraction particularly obvious in the apical 2 and 4 chamber views when compared to RV pacing OFF (lower panel). The standard deviation of time (Ts-sd) from the onset of QRS complex to peak systolic contraction velocity among the 12 LV segments was 39.7 ms. Lower Panel showing the velocity time curve of individual LV segment when RV pacing was programmed OFF. The echocardiographic views were identical to Upper Panel for comparison. The green arrows indicate the peaks of systolic contraction velocity of the LV segments when RV pacing was withheld. Note the intraventricular synchronicity demonstrated with similar timing to reach the peak systolic contraction among the LV segments and the Ts-sd was 14.7 ms. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)
Letters to the Editor
heart failure after short period of pacing is unclear. However, the LV systolic function showed dramatic improvement when RV pacing was avoided and this would further support that the reversible cardiomyopathy was possibly related to RV pacing induced LV dyssynchrony. The best treatment option for this patient remains to be determined. CRT may be superior to RV pacing in patients with impaired LV systolic function and standard pacing indication [4] but whether CRT would be equally effective in patients with preserved LV systolic function is unclear. Ongoing prospective randomized trial may be able to address this clinically important question [5]. It was unfortunate that complication was encountered during the upgrading procedure but it seemed that patient tolerated the back up pacing well with gradual recovery of LV systolic function. Cumulative RV pacing less than 40% was associated with a significantly lower risk of adverse events when compared to those with more than 40% in one study [1]. This case has demonstrated the reversible nature of the heart failure and the importance of minimizing RV pacing in vulnerable patient [6].
0167-5273/$ - see front matter © 2007 2008 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2007.12.018
119
References [1] Sweeney MO, Hellkamp AS. Heart failure during cardiac pacing. Circulation 2006;113:2082–8. [2] Tops LF, Schalij MJ, Holman ER, van Erven L, van der Wall EE, Bax JJ. Right ventricular pacing can induce ventricular dyssynchrony in patients with atrial fibrillation after atrioventricular node ablation. J Am Coll Cardiol 2006;48:1642–8. [3] Yu CM, Chau E, Sanderson JE, et al. Tissue Doppler echocardiographic evidence of reverse remodeling and improved synchronicity by simultaneously delaying regional contraction after biventricular pacing therapy in heart failure. Circulation 2002;105:438–45. [4] Kindermann M, Hennen B, Jung J, Geisel J, Bohm M, Frohlig G. Biventricular versus conventional right ventricular stimulation for patients with standard pacing indication and left ventricular dysfunction: the Homburg Biventricular Pacing Evaluation (HOBIPACE). J Am Coll Cardiol 2006;47:1927–37. [5] Fung JW, Chan JY, Omar R, et al. The Pacing to Avoid Cardiac Enlargement (PACE) Trial: clinical background, rationale, design, and implementation. J Cardiovasc Electrophysiol 2007;18:735–9. [6] Gillis AM, Purerfellner H, Israel CW, et al. Medtronic Enrhythm Clinical Study Investigators. Reducing unnecessary right ventricular pacing with the managed ventricular pacing mode in patients with sinus node disease and AV block. Pacing Clin Electrophysiol 2006;29:697–705.