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Resolution of central sleep apnoea following implantation of a left ventricular assist device
Letters to the Editor
317
Resolution of central sleep apnoea following implantation of a left ventricular assist device A. Vazir a,c,d,⁎, P.C. Hastings d , M.J. Morrell d , J. Pepper b , M.Y. Henein e , S. Westaby f , P.A. Poole-Wilson a , M.R. Cowie c , A.K. Simonds d a
Department of Cardiac Medicine, Royal Brompton Hospital, National Heart and Lung Institute, Imperial College London, UK Department of Cardiac Surgery, Royal Brompton Hospital, National Heart and Lung Institute, Imperial College London, UK c Health Services Research unit, Royal Brompton Hospital, National Heart and Lung Institute, Imperial College London, UK Academic & Clinical Unit of Sleep and Breathing, Royal Brompton Hospital, National Heart and Lung Institute, Imperial College London, UK e Umea Heart Centre, Umea University, Sweden f Department of Cardiac Surgery, Oxford Heart Centre, John Radcliffe Hospital, Oxford, UK b
d
Received 13 April 2008; accepted 28 June 2008 Available online 26 August 2008
Abstract Central sleep apnoea (CSA) occurs in up to 40% of patients with chronic heart failure (CHF). It is thought to be a consequence of CHF and is associated with an accelerated decline in cardiac function, and increased morbidity and mortality. The optimal treatment of CSA remains unclear. Resolution of CSA has been reported after cardiac transplantation. We report the first case of resolution of CSA 10 months following implantation of a permanent Jarvik™ 2000 left ventricular assist device (LVAD). The correction of CSA after implantation of the LVAD was associated with improvements in symptoms, exercise capacity, renal function, and increased arterial carbon dioxide levels at rest during wakefulness and also reduction in brain natriuretic peptide. © 2008 Published by Elsevier Ireland Ltd. Keywords: Heart failure; Central sleep apnoea; Left ventricular assist device
Central sleep apnoea (CSA) occurs in up to 40% of patients with chronic heart failure (CHF) [1]. It is thought to be a consequence of CHF and is associated with an accelerated decline in cardiac function, and increased morbidity and mortality [2]. The optimal treatment of CSA remains unclear in light of results of the CANPAP study [3]. Resolution of CSA has been reported after cardiac transplantation. However a previous case report of three patients with severe heart failure with moderate to severe CSA who underwent implantation of left ventricular assist device (LVAD) for bridge to transplantation or destination therapy showed persistence of CSA in the acute period post LVAD implantation, 7 to 80 days, despite improvements in haemodynamic and end organ function [4]. We report the first case of resolution of CSA following implantation of a permanent Jarvik™ 2000-LVAD.
Abbreviations: REM, Rapid eye movement sleep; NREM, Non-rapid eye movement sleep; peak VO2, Peak oxygen uptake; VE/VCO2 slope, Slope of ventilation over carbon dioxide production during exercise. ⁎ Corresponding author. Health services unit, Royal Brompton Hospital, Sydney Street, London SW3 9RP, UK. Tel.: +44 7780686629; fax: +44 20 76038099. E-mail address: [email protected] (A. Vazir).
1. Case report A 62-year-old man with a 37-year history of idiopathic dilated cardiomyopathy presented with a 12-month deterioration in congestive heart failure. Previous problems with sick sinus disease had been treated by implantation of a DDDR pacemaker, and episodes of ventricular tachycardia had been treated with radiofrequency ablation. He complained of intractable dependent oedema and fatigue, with breathlessness on minimal exertion (NYHA Class III), despite optimal pharmacological therapy. The left ventricle was dilated and globally hypokinetic (end-diastolic diameter on transthoracic echocardiography 69 mm, contracting down to 60 mm at end-systole, with a calculated left ventricular ejection fraction of 27%). The left atrium was dilated (diameter of 56 mm), as was the right heart. Right and left heart catheterization demonstrated normal coronaries and severely impaired left and right ventricular systolic function, with raised right ventricular and pulmonary artery pressures of 41/6/8 and 40/19/31 mm Hg, respectively. Cardiac index was calculated to be 1.61 l/min using the indirect Fick principle. The results of cardiopulmonary exercise test, venous and arterial blood tests are summarized in Table 1. The patient's partner had noticed
318
Letters to the Editor
Table 1 Cardiac and sleep characteristics of the patient’s pre and post insertion of left ventricular assist device. Variables
Pre LVAD
Post LVAD
NYHA Minnesota scores Epworth sleepiness score
III 71 9
II 24 5
Oedema Diuretic use
2+ Frusemide 20 mg Bendrofluazide 2.5 mg
0 Frusemide 20 mg PRN
Cardiopulmonary exercise test Actual peak VO2 (ml/kg/min) Percent predicted peak VO2 (%) VE/VCO2 slope
9 24 57
12 31 66
Shuttle walk distance (m)
300
360
Serum Creatinine (µmol/l) Urea (mmol/l) Brain natriuretic peptide (pmol/l)
170 14.4 203
132 11.6 25
Arterialised blood sample PaCO2 (kPa) PaO2 (kPa) HCO3 (mmol/l) Base excess
3.75 14.3 22.2 0.6
4.28 13.7 21.9 −1.2
34.4
3.6
294 72.3 23.9 46.2 23.9 5.9
474 92.2 15.7 38.6 23.3 22.3
Polysomnography Apnoea–hypopnoea index (events/hour of sleep) Sleep architecture Total sleep time (min) Sleep efficiency (%) Stage 1 sleep (%) Stage 2 sleep (%) Stage 3 and 4 sleep (%) Stage REM sleep (%)
patient no longer had apnoeic attacks during his sleep. He remained dependent on his LVAD, temporarily switching off the device resulted in rapid increased jugular venous pressure and dyspnoea at rest. The results of cardiac reassessment are summarized in Table 1. Repeat polysomnography showed resolution of CSA (Fig. 1(b)), with an AHI of 3.6 events per hour of sleep, and improved sleep quality with an increase in rapid eye movement sleep and stage 2 and 3 non-rapid eye movement sleep (Table 1). There was also an increase in the patient's arterial partial pressure of carbon dioxide (PaCO2). 2. Discussion
apnoeas during his sleep, but the patient denied daytime sleepiness. Overnight polysomnography (consisting of electroencephalography, electro-oculography, electrocardiography and measurements of breathing during sleep) revealed central sleep apnoea with and apnoea–hypopnoea index (AHI) of 34 events per hour of sleep (Fig. 1(a)). The patient was unsuitable for cardiac transplantation due to a persistently low creatinine clearance (33 ml/min). A Jarvik™ 2000 LVAD was implanted via a left lateral thoracotomy. Immediately following the operation, his DDDR pacemaker malfunctioned and this was replaced by another DDDR system. He was discharged home a month later. Ten months after the LVAD implantation, the patient was in NYHA Class II. He reported improved quality of life, with increased energy level and exercise tolerance. His Minnesota Living with Heart Failure Score had improved from 71 down to 24. The patient's partner reported that the
Central sleep apnoea (CSA) is a consequence of destabilization of the respiratory control system. The pathophysiology of CSA is not fully understood. Central apnoeas result when PaCO2 falls below the apnoeic threshold — the point at which respiratory effort is no longer initiated. So that fluctuation of PaCO2 above and below the apnoeic threshold in the presence of enhanced chemosensitivity to CO2 [5], reduced CO2 reserve [6], hypocapnia (resulting from hyperventilation in response to stimulation of the pulmonary stretch receptors (J-receptors), which are sensitive to pulmonary congestion) and prolonged circulation time [7], leads to cycles of central apnoea separated by periods of hyperpnoea. The Jarvik™ 2000 is a continuous axial-flow pump [8]. It pumps blood out of the left ventricle into the descending aorta and via a conduit. The native left ventricle also contributes to the cardiac output. The increased blood flow throughout both systole and diastole improves perfusion and function of the end organs. In this patient, the Jarvik™ 2000 device produced an increase in cardiac output, symptom relief and increased exercise tolerance. The observed increase in PaCO2 during wakefulness, and probably during sleep, is likely to have resulted in stabilization of his breathing during sleep. The increased PaCO2 may be explained by reduced respiratory drive from the J-receptors due to reduced pulmonary congestion and possibly by increased CO2 reserve in part due to resetting of the CO2 chemosensitivity subsequent to improved circulatory haemodynamics. Unfortunately the patient declined assessment of CO2 chemosensitivity. In summary we have presented a case of severe CHF with CSA, in which there was correction of CSA associated with improved symptoms of CHF following implantation of an LVAD. Acknowledgement AV and PH are supported by a British Heart Foundation project grant and MJM by the Wellcome trust. JP was the lead surgeon. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology [9].
Letters to the Editor
319
Fig. 1. (a) An original record showing the presence of central sleep apnoea, with complete cessation of airflow in association with complete cessation of both abdominal and thoracic cage movement, followed by desaturation lagging approximately 30 s after the end of the apnoea. (b) An original record showing a regular breathing pattern during sleep post LVAD insertion.
References [1] Vazir A, Hastings PC, Dayer M, et al. A high prevalence of sleep disordered breathing in men with mild symptomatic chronic heart failure due to left ventricular systolic dysfunction. Eur J Heart Fail 2006. [2] Hanly PJ, Zuberi-Khokhar NS. Increased mortality associated with Cheyne–Stokes respiration in patients with congestive heart failure. Am J Respir Crit Care Med 1996;153(1):272–6. [3] Bradley TD, Logan AG, Kimoff RJ, et al. Continuous positive airway pressure for central sleep apnea and heart failure. N Engl J Med 2005;353(19):2025–33. [4] Padeletti M, Henriquez A, Mancini DM, Basner RC. Persistence of Cheyne–Stokes breathing after left ventricular assist device implantation in patients with acutely decompensated end-stage heart failure. J Heart Lung Transplant 2007;26(7):742–4.
0167-5273/$ - see front matter © 2008 Published by Elsevier Ireland Ltd. doi:10.1016/j.ijcard.2008.06.072
[5] Javaheri S. A mechanism of central sleep apnea in patients with heart failure. N Engl J Med 1999;341(13):949–54. [6] Xie A, Skatrud JB, Puleo DS, Rahko PS, Dempsey JA. Apnea– hypopnea threshold for CO2 in patients with congestive heart failure. Am J Respir Crit Care Med 2002;165(9):1245–50. [7] Francis DP, Willson K, Davies LC, Coats AJ, Piepoli M. Quantitative general theory for periodic breathing in chronic heart failure and its clinical implications. Circulation 2000;102(18):2214–21. [8] Westaby S, Banning AP, Saito S, et al. Circulatory support for long-term treatment of heart failure: experience with an intraventricular continuous flow pump. Circulation 2002;105(22):2588–91. [9] Coats AJ. Ethical authorship and publishing. Int J Cardiol 2009;131: 149–50.
317
Resolution of central sleep apnoea following implantation of a left ventricular assist device A. Vazir a,c,d,⁎, P.C. Hastings d , M.J. Morrell d , J. Pepper b , M.Y. Henein e , S. Westaby f , P.A. Poole-Wilson a , M.R. Cowie c , A.K. Simonds d a
Department of Cardiac Medicine, Royal Brompton Hospital, National Heart and Lung Institute, Imperial College London, UK Department of Cardiac Surgery, Royal Brompton Hospital, National Heart and Lung Institute, Imperial College London, UK c Health Services Research unit, Royal Brompton Hospital, National Heart and Lung Institute, Imperial College London, UK Academic & Clinical Unit of Sleep and Breathing, Royal Brompton Hospital, National Heart and Lung Institute, Imperial College London, UK e Umea Heart Centre, Umea University, Sweden f Department of Cardiac Surgery, Oxford Heart Centre, John Radcliffe Hospital, Oxford, UK b
d
Received 13 April 2008; accepted 28 June 2008 Available online 26 August 2008
Abstract Central sleep apnoea (CSA) occurs in up to 40% of patients with chronic heart failure (CHF). It is thought to be a consequence of CHF and is associated with an accelerated decline in cardiac function, and increased morbidity and mortality. The optimal treatment of CSA remains unclear. Resolution of CSA has been reported after cardiac transplantation. We report the first case of resolution of CSA 10 months following implantation of a permanent Jarvik™ 2000 left ventricular assist device (LVAD). The correction of CSA after implantation of the LVAD was associated with improvements in symptoms, exercise capacity, renal function, and increased arterial carbon dioxide levels at rest during wakefulness and also reduction in brain natriuretic peptide. © 2008 Published by Elsevier Ireland Ltd. Keywords: Heart failure; Central sleep apnoea; Left ventricular assist device
Central sleep apnoea (CSA) occurs in up to 40% of patients with chronic heart failure (CHF) [1]. It is thought to be a consequence of CHF and is associated with an accelerated decline in cardiac function, and increased morbidity and mortality [2]. The optimal treatment of CSA remains unclear in light of results of the CANPAP study [3]. Resolution of CSA has been reported after cardiac transplantation. However a previous case report of three patients with severe heart failure with moderate to severe CSA who underwent implantation of left ventricular assist device (LVAD) for bridge to transplantation or destination therapy showed persistence of CSA in the acute period post LVAD implantation, 7 to 80 days, despite improvements in haemodynamic and end organ function [4]. We report the first case of resolution of CSA following implantation of a permanent Jarvik™ 2000-LVAD.
Abbreviations: REM, Rapid eye movement sleep; NREM, Non-rapid eye movement sleep; peak VO2, Peak oxygen uptake; VE/VCO2 slope, Slope of ventilation over carbon dioxide production during exercise. ⁎ Corresponding author. Health services unit, Royal Brompton Hospital, Sydney Street, London SW3 9RP, UK. Tel.: +44 7780686629; fax: +44 20 76038099. E-mail address: [email protected] (A. Vazir).
1. Case report A 62-year-old man with a 37-year history of idiopathic dilated cardiomyopathy presented with a 12-month deterioration in congestive heart failure. Previous problems with sick sinus disease had been treated by implantation of a DDDR pacemaker, and episodes of ventricular tachycardia had been treated with radiofrequency ablation. He complained of intractable dependent oedema and fatigue, with breathlessness on minimal exertion (NYHA Class III), despite optimal pharmacological therapy. The left ventricle was dilated and globally hypokinetic (end-diastolic diameter on transthoracic echocardiography 69 mm, contracting down to 60 mm at end-systole, with a calculated left ventricular ejection fraction of 27%). The left atrium was dilated (diameter of 56 mm), as was the right heart. Right and left heart catheterization demonstrated normal coronaries and severely impaired left and right ventricular systolic function, with raised right ventricular and pulmonary artery pressures of 41/6/8 and 40/19/31 mm Hg, respectively. Cardiac index was calculated to be 1.61 l/min using the indirect Fick principle. The results of cardiopulmonary exercise test, venous and arterial blood tests are summarized in Table 1. The patient's partner had noticed
318
Letters to the Editor
Table 1 Cardiac and sleep characteristics of the patient’s pre and post insertion of left ventricular assist device. Variables
Pre LVAD
Post LVAD
NYHA Minnesota scores Epworth sleepiness score
III 71 9
II 24 5
Oedema Diuretic use
2+ Frusemide 20 mg Bendrofluazide 2.5 mg
0 Frusemide 20 mg PRN
Cardiopulmonary exercise test Actual peak VO2 (ml/kg/min) Percent predicted peak VO2 (%) VE/VCO2 slope
9 24 57
12 31 66
Shuttle walk distance (m)
300
360
Serum Creatinine (µmol/l) Urea (mmol/l) Brain natriuretic peptide (pmol/l)
170 14.4 203
132 11.6 25
Arterialised blood sample PaCO2 (kPa) PaO2 (kPa) HCO3 (mmol/l) Base excess
3.75 14.3 22.2 0.6
4.28 13.7 21.9 −1.2
34.4
3.6
294 72.3 23.9 46.2 23.9 5.9
474 92.2 15.7 38.6 23.3 22.3
Polysomnography Apnoea–hypopnoea index (events/hour of sleep) Sleep architecture Total sleep time (min) Sleep efficiency (%) Stage 1 sleep (%) Stage 2 sleep (%) Stage 3 and 4 sleep (%) Stage REM sleep (%)
patient no longer had apnoeic attacks during his sleep. He remained dependent on his LVAD, temporarily switching off the device resulted in rapid increased jugular venous pressure and dyspnoea at rest. The results of cardiac reassessment are summarized in Table 1. Repeat polysomnography showed resolution of CSA (Fig. 1(b)), with an AHI of 3.6 events per hour of sleep, and improved sleep quality with an increase in rapid eye movement sleep and stage 2 and 3 non-rapid eye movement sleep (Table 1). There was also an increase in the patient's arterial partial pressure of carbon dioxide (PaCO2). 2. Discussion
apnoeas during his sleep, but the patient denied daytime sleepiness. Overnight polysomnography (consisting of electroencephalography, electro-oculography, electrocardiography and measurements of breathing during sleep) revealed central sleep apnoea with and apnoea–hypopnoea index (AHI) of 34 events per hour of sleep (Fig. 1(a)). The patient was unsuitable for cardiac transplantation due to a persistently low creatinine clearance (33 ml/min). A Jarvik™ 2000 LVAD was implanted via a left lateral thoracotomy. Immediately following the operation, his DDDR pacemaker malfunctioned and this was replaced by another DDDR system. He was discharged home a month later. Ten months after the LVAD implantation, the patient was in NYHA Class II. He reported improved quality of life, with increased energy level and exercise tolerance. His Minnesota Living with Heart Failure Score had improved from 71 down to 24. The patient's partner reported that the
Central sleep apnoea (CSA) is a consequence of destabilization of the respiratory control system. The pathophysiology of CSA is not fully understood. Central apnoeas result when PaCO2 falls below the apnoeic threshold — the point at which respiratory effort is no longer initiated. So that fluctuation of PaCO2 above and below the apnoeic threshold in the presence of enhanced chemosensitivity to CO2 [5], reduced CO2 reserve [6], hypocapnia (resulting from hyperventilation in response to stimulation of the pulmonary stretch receptors (J-receptors), which are sensitive to pulmonary congestion) and prolonged circulation time [7], leads to cycles of central apnoea separated by periods of hyperpnoea. The Jarvik™ 2000 is a continuous axial-flow pump [8]. It pumps blood out of the left ventricle into the descending aorta and via a conduit. The native left ventricle also contributes to the cardiac output. The increased blood flow throughout both systole and diastole improves perfusion and function of the end organs. In this patient, the Jarvik™ 2000 device produced an increase in cardiac output, symptom relief and increased exercise tolerance. The observed increase in PaCO2 during wakefulness, and probably during sleep, is likely to have resulted in stabilization of his breathing during sleep. The increased PaCO2 may be explained by reduced respiratory drive from the J-receptors due to reduced pulmonary congestion and possibly by increased CO2 reserve in part due to resetting of the CO2 chemosensitivity subsequent to improved circulatory haemodynamics. Unfortunately the patient declined assessment of CO2 chemosensitivity. In summary we have presented a case of severe CHF with CSA, in which there was correction of CSA associated with improved symptoms of CHF following implantation of an LVAD. Acknowledgement AV and PH are supported by a British Heart Foundation project grant and MJM by the Wellcome trust. JP was the lead surgeon. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology [9].
Letters to the Editor
319
Fig. 1. (a) An original record showing the presence of central sleep apnoea, with complete cessation of airflow in association with complete cessation of both abdominal and thoracic cage movement, followed by desaturation lagging approximately 30 s after the end of the apnoea. (b) An original record showing a regular breathing pattern during sleep post LVAD insertion.
References [1] Vazir A, Hastings PC, Dayer M, et al. A high prevalence of sleep disordered breathing in men with mild symptomatic chronic heart failure due to left ventricular systolic dysfunction. Eur J Heart Fail 2006. [2] Hanly PJ, Zuberi-Khokhar NS. Increased mortality associated with Cheyne–Stokes respiration in patients with congestive heart failure. Am J Respir Crit Care Med 1996;153(1):272–6. [3] Bradley TD, Logan AG, Kimoff RJ, et al. Continuous positive airway pressure for central sleep apnea and heart failure. N Engl J Med 2005;353(19):2025–33. [4] Padeletti M, Henriquez A, Mancini DM, Basner RC. Persistence of Cheyne–Stokes breathing after left ventricular assist device implantation in patients with acutely decompensated end-stage heart failure. J Heart Lung Transplant 2007;26(7):742–4.
0167-5273/$ - see front matter © 2008 Published by Elsevier Ireland Ltd. doi:10.1016/j.ijcard.2008.06.072
[5] Javaheri S. A mechanism of central sleep apnea in patients with heart failure. N Engl J Med 1999;341(13):949–54. [6] Xie A, Skatrud JB, Puleo DS, Rahko PS, Dempsey JA. Apnea– hypopnea threshold for CO2 in patients with congestive heart failure. Am J Respir Crit Care Med 2002;165(9):1245–50. [7] Francis DP, Willson K, Davies LC, Coats AJ, Piepoli M. Quantitative general theory for periodic breathing in chronic heart failure and its clinical implications. Circulation 2000;102(18):2214–21. [8] Westaby S, Banning AP, Saito S, et al. Circulatory support for long-term treatment of heart failure: experience with an intraventricular continuous flow pump. Circulation 2002;105(22):2588–91. [9] Coats AJ. Ethical authorship and publishing. Int J Cardiol 2009;131: 149–50.