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Effects of cardiac resynchronization therapy on left ventricular mechanical dyssynchrony induced by right ventricular pacing in a patient with heart failure and preserved ejection fraction
International Journal of Cardiology 177 (2014) 1069–1072
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Effects of cardiac resynchronization therapy on left ventricular mechanical dyssynchrony induced by right ventricular pacing in a patient with heart failure and preserved ejection fraction Tetsushiro Takeuchi a, Kaoru Dohi a,⁎, Naoto Kumagai a, Shiro Nakamori a, Naoki Fujimoto b, Ryuji Okamoto a, Eitaro Fujii a, Tetsuya Kitamura c, Norikazu Yamada a, Mashio Nakamura d, Masayuki Hamada c, Masaaki Ito a a
Department of Cardiology and Nephrology, Mie University Graduate School of Medicine, Tsu, Japan Department of Molecular and Laboratory Medicine, Mie University Graduate School of Medicine, Tsu, Japan c Department of Cardiology, Suzuka General Hospital, Suzuka, Japan d Department of Clinical Cardiovascular Research, Mie University Graduate School of Medicine, Tsu, Japan b
a r t i c l e
i n f o
Article history: Received 9 October 2014 Accepted 20 October 2014 Available online 5 November 2014 Keywords: Mechanical dyssynchrony Mitral regurgitation Left ventricular apical hypertrophy Echocardiography Pressure–volume loop
We report a case of refractory heart failure (HF) secondary to right ventricular (RV) pacing-induced mechanical dyssynchrony in an 84year-old Japanese man with preserved left ventricular (LV) ejection fraction (EF). He was admitted to our hospital for the evaluation and treatment of HF. He had undergone permanent pacemaker implantation with RV apical pacing for atrial fibrillation and bradycardia 6 years ago. He has been receiving optimal medical therapy including beta-blocker, renin–angiotensin–aldosterone inhibitors, and diuretics. However, he was hospitalized twice for worsening HF. He also had multiple episodes of non-sustained ventricular tachycardia in the last 3 months in a local hospital. On admission, he had a New York Heart Association (NYHA) functional class IV HF symptom. Physical examination showed jugular venous dilatation and peripheral edema. Cardiac auscultation showed a grade 4/6 holosystolic murmur at the apex. The electrocardiogram showed ventricular pacemaker rhythm with a QRS duration of 170 ms (Fig. 1A). The echocardiography revealed a distinct LV apical hypertrophy (Fig. 1B), preserved LVEF with 60%, and severe mitral regurgitation (MR) with MR volume and fraction of 68.4 ml and 60%, due to incomplete coaptation of the mitral leaflets (Fig. 2A and ⁎ Corresponding author at: Department of Cardiology and Nephrology, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu 514-8507, Japan. E-mail address: [email protected] (K. Dohi).
http://dx.doi.org/10.1016/j.ijcard.2014.10.083 0167-5273/© 2014 Elsevier Ireland Ltd. All rights reserved.
B). A two-dimensional speckle-tracking radial strain imaging in the mid-LV short-axis view showed LV mechanical dyssynchrony with septal-to-free delay of 164 ms (Fig. 2C). Coronary angiography revealed only mild coronary artery disease. Hence, we clinically assumed that LV mechanical dyssynchrony secondary to chronic RV apical pacing induces severe MR and refractory HF despite preserved LVEF. To assess the acute effects of biventricular pacing on LV function and MR, we performed pressure–volume loop analysis simultaneously with echocardiography examination. A conductance catheter was placed in the LV, and temporary pacing leads were positioned in the RV apex adjacent to the permanent pacemaker lead and the lateral branch of the coronary sinus. During biventricular pacing, LV stroke work (SW) increased from 3229 to 4641 mm Hg·ml, LV dp/dt increased from 901 to 1146 mm Hg/s, and LV end diastolic pressure decreased from 13.3 to 9.8 mm Hg, respectively (Fig. 3), with a marked reduction in MR assessed using echocardiography, as compared with RV apical pacing. Finally, the patient underwent an upgrade to cardiac resynchronization therapy (CRT) combined with defibrillation (CRT-D) with the lateral LV lead placement, which resulted in the narrowing of the QRS complex to 140 ms. After 1 week of CRT-D implantation, the patient's symptom improved and echocardiography showed a significant reduction in MR (MR volume of 43 ml and fraction of 49%, Fig. 4A and B) and a significant improvement of LV dyssynchrony to only 15 ms (Fig. 4C). The postoperative course was uneventful; the patient was in NYHA class II symptoms and echocardiography showed further reduction in MR (MR volume of 20 ml and fraction of 38%, Fig. 5A and B) at a 3 month follow-up. RV apical pacing induces abnormal electrical and mechanical activation patterns which can lead to worsening of MR [1]. Indeed, the patient in the present case had septal-to-lateral mechanical delay, which is typical for echocardiographic feature of left bundle branch block (LBBB) in patients with reduced EF [2]. Although the patient had several potential factors or conditions that contribute to refractory HF including LV apical hypertrophy and permanent atrial fibrillation, we clinically assumed that LV mechanical dyssynchrony secondary to chronic RV apical pacing induces severe MR and refractory HF despite preserved EF. There are only several case reports which demonstrated successful biventricular pacing in patients with preserved EF and RV apical pacing-induced MR [3,4]. As the guidelines for the treatment of HF do not recommend CRT
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Fig. 1. The electrocardiogram showed ventricular pacing rhythm and left bundle branch block configuration with a QRS duration of 170 ms (A). The echocardiography revealed distinct left ventricular apical hypertrophy (B).
Fig. 2. Color Doppler echocardiography imaging in the parasternal long axis view (A) and the apical four-chamber view (B) showed severe mitral regurgitation. A two-dimensional speckle-tracking radial strain imaging in the mid-LV short-axis view showed left ventricular mechanical dyssynchrony with septal-to-free delay of 164 ms during right ventricular apical pacing (C). Red and green arrows indicate the segments representing the earliest and latest peak systolic strain (upper panel) and corresponding time–strain curves (lower panel) in the 6 segments.
T. Takeuchi et al. / International Journal of Cardiology 177 (2014) 1069–1072
1071
Fig. 3. Comparison of left ventricular pressure–volume loops during right ventricular apical pacing (A) and biventricular pacing (B).
in HF with preserved EF, we tested the effects of biventricular pacing using pressure–volume loop analysis [5] simultaneously with echocardiography examination, and confirmed that it augmented LV function and reduced MR. Consistent with the result from this pre-test, CRT-D successfully normalized LV mechanical synchrony and reduced MR, resulting in improvement of HF symptoms. Long-term follow-up of his clinical cause is important to clarify if chronic biventricular pacing further reduces MR and improves HF symptoms [6]. This case report reinforces the need to deeply and periodically investigate the adverse
effects of RV apical pacing on LV mechanical synchrony as well as MR in all patients with refractory HF despite preserved EF. Echocardiography and pressure–volume analysis help identify patients who will have the greatest benefit from CRT implantation.
Disclosures None.
Fig. 4. Color flow Doppler echocardiography imaging in the parasternal long axis view (A) and the apical four-chamber view (B) showed moderate reduction of mitral regurgitation after cardiac resynchronization therapy (CRT). Speckle tracking radial strain imaging showed restoration of left ventricular synchrony after CRT (C).
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Fig. 5. Color flow Doppler echocardiography imaging in the parasternal long axis view (A) and the apical four-chamber view (B) showed significant reduction of mitral regurgitation at a 3 month follow-up.
References [1] A. Finn, P. Marta, P. Alberto, et al., Chronic right ventricular apical pacing: adverse effects and current therapeutic strategies to minimize them, Int. J. Cardiol. 173 (2014) 351–360. [2] M.S. Suffoletto, K. Dohi, M. Cannesson, et al., Novel speckle-tracking radial strain from routine black-and-white echocardiographic images to quantify dyssynchrony and predict response to cardiac resynchronization therapy, Circulation 113 (2006) 960–968. [3] James M. Irwin, Matthew U. Glover, S. Serge Barold, Treatment of pacemaker induced severe mitral regurgitation with biventricular pacing in two patients with a normal left ventricular ejection fraction, PACE 26 (2003) 2333–2335.
[4] G. Maxime de, B. Pierre, C. Jacques, Regression of mitral regurgitation after cardiac resynchronization therapy in an adult with preserved left ventricular function and right ventricular pacing, Europace 9 (2007) 768–769. [5] P. Martin, K. Viktor, H. Dalibor, et al., Cardiac resynchronization therapy for the causal treatment of heart failure with preserved ejection fraction: insight from a pressure– volume loop analysis, Eur. J. Heart Fail. 12 (2010) 634–636. [6] Martin G. St, John Sutton, Ted Plappert, et al., Effect of cardiac resynchronization therapy on left ventricular size and function in chronic heart failure, Circulation 107 (2003) 1985–1990.
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Effects of cardiac resynchronization therapy on left ventricular mechanical dyssynchrony induced by right ventricular pacing in a patient with heart failure and preserved ejection fraction Tetsushiro Takeuchi a, Kaoru Dohi a,⁎, Naoto Kumagai a, Shiro Nakamori a, Naoki Fujimoto b, Ryuji Okamoto a, Eitaro Fujii a, Tetsuya Kitamura c, Norikazu Yamada a, Mashio Nakamura d, Masayuki Hamada c, Masaaki Ito a a
Department of Cardiology and Nephrology, Mie University Graduate School of Medicine, Tsu, Japan Department of Molecular and Laboratory Medicine, Mie University Graduate School of Medicine, Tsu, Japan c Department of Cardiology, Suzuka General Hospital, Suzuka, Japan d Department of Clinical Cardiovascular Research, Mie University Graduate School of Medicine, Tsu, Japan b
a r t i c l e
i n f o
Article history: Received 9 October 2014 Accepted 20 October 2014 Available online 5 November 2014 Keywords: Mechanical dyssynchrony Mitral regurgitation Left ventricular apical hypertrophy Echocardiography Pressure–volume loop
We report a case of refractory heart failure (HF) secondary to right ventricular (RV) pacing-induced mechanical dyssynchrony in an 84year-old Japanese man with preserved left ventricular (LV) ejection fraction (EF). He was admitted to our hospital for the evaluation and treatment of HF. He had undergone permanent pacemaker implantation with RV apical pacing for atrial fibrillation and bradycardia 6 years ago. He has been receiving optimal medical therapy including beta-blocker, renin–angiotensin–aldosterone inhibitors, and diuretics. However, he was hospitalized twice for worsening HF. He also had multiple episodes of non-sustained ventricular tachycardia in the last 3 months in a local hospital. On admission, he had a New York Heart Association (NYHA) functional class IV HF symptom. Physical examination showed jugular venous dilatation and peripheral edema. Cardiac auscultation showed a grade 4/6 holosystolic murmur at the apex. The electrocardiogram showed ventricular pacemaker rhythm with a QRS duration of 170 ms (Fig. 1A). The echocardiography revealed a distinct LV apical hypertrophy (Fig. 1B), preserved LVEF with 60%, and severe mitral regurgitation (MR) with MR volume and fraction of 68.4 ml and 60%, due to incomplete coaptation of the mitral leaflets (Fig. 2A and ⁎ Corresponding author at: Department of Cardiology and Nephrology, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu 514-8507, Japan. E-mail address: [email protected] (K. Dohi).
http://dx.doi.org/10.1016/j.ijcard.2014.10.083 0167-5273/© 2014 Elsevier Ireland Ltd. All rights reserved.
B). A two-dimensional speckle-tracking radial strain imaging in the mid-LV short-axis view showed LV mechanical dyssynchrony with septal-to-free delay of 164 ms (Fig. 2C). Coronary angiography revealed only mild coronary artery disease. Hence, we clinically assumed that LV mechanical dyssynchrony secondary to chronic RV apical pacing induces severe MR and refractory HF despite preserved LVEF. To assess the acute effects of biventricular pacing on LV function and MR, we performed pressure–volume loop analysis simultaneously with echocardiography examination. A conductance catheter was placed in the LV, and temporary pacing leads were positioned in the RV apex adjacent to the permanent pacemaker lead and the lateral branch of the coronary sinus. During biventricular pacing, LV stroke work (SW) increased from 3229 to 4641 mm Hg·ml, LV dp/dt increased from 901 to 1146 mm Hg/s, and LV end diastolic pressure decreased from 13.3 to 9.8 mm Hg, respectively (Fig. 3), with a marked reduction in MR assessed using echocardiography, as compared with RV apical pacing. Finally, the patient underwent an upgrade to cardiac resynchronization therapy (CRT) combined with defibrillation (CRT-D) with the lateral LV lead placement, which resulted in the narrowing of the QRS complex to 140 ms. After 1 week of CRT-D implantation, the patient's symptom improved and echocardiography showed a significant reduction in MR (MR volume of 43 ml and fraction of 49%, Fig. 4A and B) and a significant improvement of LV dyssynchrony to only 15 ms (Fig. 4C). The postoperative course was uneventful; the patient was in NYHA class II symptoms and echocardiography showed further reduction in MR (MR volume of 20 ml and fraction of 38%, Fig. 5A and B) at a 3 month follow-up. RV apical pacing induces abnormal electrical and mechanical activation patterns which can lead to worsening of MR [1]. Indeed, the patient in the present case had septal-to-lateral mechanical delay, which is typical for echocardiographic feature of left bundle branch block (LBBB) in patients with reduced EF [2]. Although the patient had several potential factors or conditions that contribute to refractory HF including LV apical hypertrophy and permanent atrial fibrillation, we clinically assumed that LV mechanical dyssynchrony secondary to chronic RV apical pacing induces severe MR and refractory HF despite preserved EF. There are only several case reports which demonstrated successful biventricular pacing in patients with preserved EF and RV apical pacing-induced MR [3,4]. As the guidelines for the treatment of HF do not recommend CRT
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T. Takeuchi et al. / International Journal of Cardiology 177 (2014) 1069–1072
Fig. 1. The electrocardiogram showed ventricular pacing rhythm and left bundle branch block configuration with a QRS duration of 170 ms (A). The echocardiography revealed distinct left ventricular apical hypertrophy (B).
Fig. 2. Color Doppler echocardiography imaging in the parasternal long axis view (A) and the apical four-chamber view (B) showed severe mitral regurgitation. A two-dimensional speckle-tracking radial strain imaging in the mid-LV short-axis view showed left ventricular mechanical dyssynchrony with septal-to-free delay of 164 ms during right ventricular apical pacing (C). Red and green arrows indicate the segments representing the earliest and latest peak systolic strain (upper panel) and corresponding time–strain curves (lower panel) in the 6 segments.
T. Takeuchi et al. / International Journal of Cardiology 177 (2014) 1069–1072
1071
Fig. 3. Comparison of left ventricular pressure–volume loops during right ventricular apical pacing (A) and biventricular pacing (B).
in HF with preserved EF, we tested the effects of biventricular pacing using pressure–volume loop analysis [5] simultaneously with echocardiography examination, and confirmed that it augmented LV function and reduced MR. Consistent with the result from this pre-test, CRT-D successfully normalized LV mechanical synchrony and reduced MR, resulting in improvement of HF symptoms. Long-term follow-up of his clinical cause is important to clarify if chronic biventricular pacing further reduces MR and improves HF symptoms [6]. This case report reinforces the need to deeply and periodically investigate the adverse
effects of RV apical pacing on LV mechanical synchrony as well as MR in all patients with refractory HF despite preserved EF. Echocardiography and pressure–volume analysis help identify patients who will have the greatest benefit from CRT implantation.
Disclosures None.
Fig. 4. Color flow Doppler echocardiography imaging in the parasternal long axis view (A) and the apical four-chamber view (B) showed moderate reduction of mitral regurgitation after cardiac resynchronization therapy (CRT). Speckle tracking radial strain imaging showed restoration of left ventricular synchrony after CRT (C).
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T. Takeuchi et al. / International Journal of Cardiology 177 (2014) 1069–1072
Fig. 5. Color flow Doppler echocardiography imaging in the parasternal long axis view (A) and the apical four-chamber view (B) showed significant reduction of mitral regurgitation at a 3 month follow-up.
References [1] A. Finn, P. Marta, P. Alberto, et al., Chronic right ventricular apical pacing: adverse effects and current therapeutic strategies to minimize them, Int. J. Cardiol. 173 (2014) 351–360. [2] M.S. Suffoletto, K. Dohi, M. Cannesson, et al., Novel speckle-tracking radial strain from routine black-and-white echocardiographic images to quantify dyssynchrony and predict response to cardiac resynchronization therapy, Circulation 113 (2006) 960–968. [3] James M. Irwin, Matthew U. Glover, S. Serge Barold, Treatment of pacemaker induced severe mitral regurgitation with biventricular pacing in two patients with a normal left ventricular ejection fraction, PACE 26 (2003) 2333–2335.
[4] G. Maxime de, B. Pierre, C. Jacques, Regression of mitral regurgitation after cardiac resynchronization therapy in an adult with preserved left ventricular function and right ventricular pacing, Europace 9 (2007) 768–769. [5] P. Martin, K. Viktor, H. Dalibor, et al., Cardiac resynchronization therapy for the causal treatment of heart failure with preserved ejection fraction: insight from a pressure– volume loop analysis, Eur. J. Heart Fail. 12 (2010) 634–636. [6] Martin G. St, John Sutton, Ted Plappert, et al., Effect of cardiac resynchronization therapy on left ventricular size and function in chronic heart failure, Circulation 107 (2003) 1985–1990.