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Copyright © 2014 International Center for Artificial Organs and Transplantation and Wiley Periodicals, Inc.
Letters to the Editor Successful Explant of a Continuous-Flow Left Ventricular Assist Device After Two Years of Circulatory Support To the Editor, Successful continuous-flow left ventricular assist device (CF-LVAD) explant for left ventricular (LV) recovery is more commonly achieved in younger, nonischemic patients with a short duration of heart failure symptoms (1,2). While signs of recovery most commonly appear within 12 months, some patients show evidence of later LV recovery (3). Vigilance for late recovery is especially relevant in countries such as Australia where stable LVAD patients are not prioritized for cardiac transplant. We describe the case of a 48-year-old man with an idiopathic dilated cardiomyopathy. He had no significant past medical history and presented with 6 months of progressive dyspnea. Echocardiography showed his LV to be severely dilated (end-diastolic diameter 74 mm) and impaired (ejection fraction 10–15%), with trace aortic regurgitation. Despite maximally tolerated medical therapy including inotropes, he remained clinically unstable in NYHA Class 4, INTERMACS 3. A HeartWare CF-LVAD was inserted approximately 1 month after presentation, allowing the patient to discharge home 15 days later. By 3 months post-LVAD insertion, the patient had been listed for cardiac transplant and titrated onto carvedilol 37.5 mg twice daily, candesartan 24 mg daily (due to cough with angiotensin-converting enzyme inhibitor), and spironolactone 25 mg daily, with the LV returning to normal size but remaining severely impaired. By 12 months, LV function had not significantly improved, and symptomatic hypotension and low LVAD flows had necessitated cessation of candesartan and spironolactone and halving of the carvedilol dose. Despite this, signs of improvement were noted at 15 months, and by
18 months systolic function was low normal, with “ramp” echocardiographic studies showing stable LV size with decreasing LVAD speeds. New moderate aortic regurgitation had steadily developed postLVAD despite most echocardiograms showing at least partial opening of the aortic valve (Fig. 1). The patient was then delisted for cardiac transplant, and up-titration of neurohormonal blockers was retrialed and better tolerated over the next 2–3 months. A cardiopulmonary exercise test at 21 months with LVAD speed at 2500 rpm showed a peak VO2 of 18.6 mL/kg/min (52% predicted, respiratory exchange ratio 1.24). Progress was halted 3 weeks later by a cardioembolic stroke in the setting of dual anti-platelet therapy with a subtherapeutic international normalized ratio. The patient made a full neurological recovery, and after intensive exercise rehabilitation, a repeat exercise test at 24 months at the same LVAD speed showed a peak VO2 of 25.6 mL/kg/min (71% predicted, respiratory exchange ratio 1.21). An exercise right heart catheterization with the LVAD speed set to a minimum of 1800 rpm subsequently showed no significant change in LV size or filling pressures at a workload of 75% peak VO2. The patient underwent LVAD explant with patch repair and mechanical aortic valve replacement 770 days post-LVAD insertion. He was discharged from ICU on day 2 and from hospital on day 7. He is now 20 months post-explant and remains NYHA Class I, with only mild LV dysfunction. Late LV recovery can occur after LVAD insertion, though successful explants after 2 years of circulatory support had not previously been reported. This case highlights the need for maintaining vigilance for late improvements in LV function post-CF-LVAD. *Jay Baumwol, FRACP, *Kaitlyn Lam, FRACP, and *†Andrew J. Maiorana, PhD *Advanced Heart Failure and Cardiac Transplant Service, Royal Perth Hospital, and †School of Physiotherapy and Curtin Health Innovation Research Institute, Curtin University Perth, Western Australia, Australia E-mail: [email protected]
doi:10.1111/aor.12286 Presented in part at the 21st Congress of the International Society for Rotary Blood Pumps, held September 26–28, 2013, in Yokohama, Japan. Artificial Organs 2014, 38(9):823–825
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824
LETTERS TO THE EDITOR
FIG. 1. Echocardiographic changes post-LVAD insertion.
REFERENCES 1. Birks EJ, George RS, Hedger M, et al. Reversal of severe heart failure with a continuous-flow left ventricular assist device and pharmacological therapy: a prospective study. Circulation 2011; 123:381–90. 2. Goldstein DJ, Maybaum S, Macgillivray TE, et al. Young patients with nonischemic cardiomyopathy have higher likelihood of left ventricular recovery during left ventricular assist device support. J Cardiac Fail 2012;18:392–5. 3. Matsumiya G, Monta O, Fukushima N, et al. Who would be a candidate for bridge to recovery during prolonged mechanical left ventricular support in idiopathic dilated cardiomyopathy? J Thorac Cardiovasc Surg 2005;130:699–704.
Addition of Monosodium Dihydrogen Phosphate to an Acid Concentrate to Prepare a Phosphate-Enriched, Bicarbonate-Based Hemodialysis Solution To the Editor, Previously we have used proprietary sodium phosphate preparations geared for enteral use to
doi:10.1111/aor.12373 Artif Organs, Vol. 38, No. 9, 2014
produce phosphate-enriched, bicarbonate-based hemodialysis solutions to treat hemodialysis-related hypophosphatemia on a short-term basis (1). However, as the exact composition (including preservatives and other undesirable additives) of these enteral products that are being produced by myriad manufacturers throughout the world are often not fully known, it would seem prudent to abandon the use of these products and create one’s own phosphate-enriched dialysis solution concentrates with fully known ingredients instead. So far we have reported our experience of adding: (i) a combination of disodium monohydrogen phosphate and monosodium dihydrogen phosphate (2) and (ii) disodium monohydrogen phosphate alone (3) into the acid concentrate of a dual-concentrate, bicarbonatebased dialysis solution delivery system to produce phosphate-enriched dialysis solutions. In the present in vitro study, we added 6.28 g of monosodium dihydrogen phosphate (NaH2PO4.H2O; obtained from Sigma, St. Louis, MO, USA) to 1 L of the acid concentrate of a 1:1.225:32.775 (acid concentrate : bicarbonate concentrate : product water) dilution, dual-concentrate, bicarbonatebased dialysis solution delivery system (4). This acid concentrate was obtained from Rockwell Medical (Wixom, MI, USA). After 10 min of vigorous shaking to dissolve the phosphate salt thoroughly, this phosphate-containing acid concentrate, along with a
Copyright © 2014 International Center for Artificial Organs and Transplantation and Wiley Periodicals, Inc.
Letters to the Editor Successful Explant of a Continuous-Flow Left Ventricular Assist Device After Two Years of Circulatory Support To the Editor, Successful continuous-flow left ventricular assist device (CF-LVAD) explant for left ventricular (LV) recovery is more commonly achieved in younger, nonischemic patients with a short duration of heart failure symptoms (1,2). While signs of recovery most commonly appear within 12 months, some patients show evidence of later LV recovery (3). Vigilance for late recovery is especially relevant in countries such as Australia where stable LVAD patients are not prioritized for cardiac transplant. We describe the case of a 48-year-old man with an idiopathic dilated cardiomyopathy. He had no significant past medical history and presented with 6 months of progressive dyspnea. Echocardiography showed his LV to be severely dilated (end-diastolic diameter 74 mm) and impaired (ejection fraction 10–15%), with trace aortic regurgitation. Despite maximally tolerated medical therapy including inotropes, he remained clinically unstable in NYHA Class 4, INTERMACS 3. A HeartWare CF-LVAD was inserted approximately 1 month after presentation, allowing the patient to discharge home 15 days later. By 3 months post-LVAD insertion, the patient had been listed for cardiac transplant and titrated onto carvedilol 37.5 mg twice daily, candesartan 24 mg daily (due to cough with angiotensin-converting enzyme inhibitor), and spironolactone 25 mg daily, with the LV returning to normal size but remaining severely impaired. By 12 months, LV function had not significantly improved, and symptomatic hypotension and low LVAD flows had necessitated cessation of candesartan and spironolactone and halving of the carvedilol dose. Despite this, signs of improvement were noted at 15 months, and by
18 months systolic function was low normal, with “ramp” echocardiographic studies showing stable LV size with decreasing LVAD speeds. New moderate aortic regurgitation had steadily developed postLVAD despite most echocardiograms showing at least partial opening of the aortic valve (Fig. 1). The patient was then delisted for cardiac transplant, and up-titration of neurohormonal blockers was retrialed and better tolerated over the next 2–3 months. A cardiopulmonary exercise test at 21 months with LVAD speed at 2500 rpm showed a peak VO2 of 18.6 mL/kg/min (52% predicted, respiratory exchange ratio 1.24). Progress was halted 3 weeks later by a cardioembolic stroke in the setting of dual anti-platelet therapy with a subtherapeutic international normalized ratio. The patient made a full neurological recovery, and after intensive exercise rehabilitation, a repeat exercise test at 24 months at the same LVAD speed showed a peak VO2 of 25.6 mL/kg/min (71% predicted, respiratory exchange ratio 1.21). An exercise right heart catheterization with the LVAD speed set to a minimum of 1800 rpm subsequently showed no significant change in LV size or filling pressures at a workload of 75% peak VO2. The patient underwent LVAD explant with patch repair and mechanical aortic valve replacement 770 days post-LVAD insertion. He was discharged from ICU on day 2 and from hospital on day 7. He is now 20 months post-explant and remains NYHA Class I, with only mild LV dysfunction. Late LV recovery can occur after LVAD insertion, though successful explants after 2 years of circulatory support had not previously been reported. This case highlights the need for maintaining vigilance for late improvements in LV function post-CF-LVAD. *Jay Baumwol, FRACP, *Kaitlyn Lam, FRACP, and *†Andrew J. Maiorana, PhD *Advanced Heart Failure and Cardiac Transplant Service, Royal Perth Hospital, and †School of Physiotherapy and Curtin Health Innovation Research Institute, Curtin University Perth, Western Australia, Australia E-mail: [email protected]
doi:10.1111/aor.12286 Presented in part at the 21st Congress of the International Society for Rotary Blood Pumps, held September 26–28, 2013, in Yokohama, Japan. Artificial Organs 2014, 38(9):823–825
bs_bs_banner
824
LETTERS TO THE EDITOR
FIG. 1. Echocardiographic changes post-LVAD insertion.
REFERENCES 1. Birks EJ, George RS, Hedger M, et al. Reversal of severe heart failure with a continuous-flow left ventricular assist device and pharmacological therapy: a prospective study. Circulation 2011; 123:381–90. 2. Goldstein DJ, Maybaum S, Macgillivray TE, et al. Young patients with nonischemic cardiomyopathy have higher likelihood of left ventricular recovery during left ventricular assist device support. J Cardiac Fail 2012;18:392–5. 3. Matsumiya G, Monta O, Fukushima N, et al. Who would be a candidate for bridge to recovery during prolonged mechanical left ventricular support in idiopathic dilated cardiomyopathy? J Thorac Cardiovasc Surg 2005;130:699–704.
Addition of Monosodium Dihydrogen Phosphate to an Acid Concentrate to Prepare a Phosphate-Enriched, Bicarbonate-Based Hemodialysis Solution To the Editor, Previously we have used proprietary sodium phosphate preparations geared for enteral use to
doi:10.1111/aor.12373 Artif Organs, Vol. 38, No. 9, 2014
produce phosphate-enriched, bicarbonate-based hemodialysis solutions to treat hemodialysis-related hypophosphatemia on a short-term basis (1). However, as the exact composition (including preservatives and other undesirable additives) of these enteral products that are being produced by myriad manufacturers throughout the world are often not fully known, it would seem prudent to abandon the use of these products and create one’s own phosphate-enriched dialysis solution concentrates with fully known ingredients instead. So far we have reported our experience of adding: (i) a combination of disodium monohydrogen phosphate and monosodium dihydrogen phosphate (2) and (ii) disodium monohydrogen phosphate alone (3) into the acid concentrate of a dual-concentrate, bicarbonatebased dialysis solution delivery system to produce phosphate-enriched dialysis solutions. In the present in vitro study, we added 6.28 g of monosodium dihydrogen phosphate (NaH2PO4.H2O; obtained from Sigma, St. Louis, MO, USA) to 1 L of the acid concentrate of a 1:1.225:32.775 (acid concentrate : bicarbonate concentrate : product water) dilution, dual-concentrate, bicarbonatebased dialysis solution delivery system (4). This acid concentrate was obtained from Rockwell Medical (Wixom, MI, USA). After 10 min of vigorous shaking to dissolve the phosphate salt thoroughly, this phosphate-containing acid concentrate, along with a
