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Continuous ambulatory peritoneal dialysis as a promising therapy for light chain amyloidosis with congestive heart failure
International Journal of Cardiology 223 (2016) 807–809
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Correspondence
Continuous ambulatory peritoneal dialysis as a promising therapy for light chain amyloidosis with congestive heart failure Julio Núñez a,⁎, Anabel Teruel b, Carmen Quiñones-Torrelo c, Sergio García-Blas a, Arturo Carratalá c, Gema Miñana a, Enrique Santas a, Isidro Torregrosa d, Carlos Solano b, Miguel González d a
Servicio de Cardiología, Hospital Clínico Universitario, Universitat de Valencia, INCLIVA, Valencia, Spain Servicio de Hematología, Hospital Clínico Universitario, Universitat de Valencia, INCLIVA, Valencia, Spain Servicio de Bioquímica Clínica, Hospital Clínico Universitario, Universitat de Valencia, INCLIVA, Valencia, Spain d Servicio de Nefrología, Hospital Clínico Universitario, Universitat de Valencia, INCLIVA, Valencia, Spain b c
a r t i c l e
i n f o
Article history: Received 11 August 2016 Accepted 13 August 2016 Available online 20 August 2016 Keywords: Light-chain amyloidosis Congestive heart failure Continuous ambulatory heart failure
Light chain amyloidosis (AL) is usually a systemic disease associated with different kinds of monoclonal plasma cell dyscrasias [1]. The heart is affected in most of patients, and represents the most important prognostic determinant. Indeed, when heart failure (HF) is present, median survival is less than 12 months [1–3]. Unfortunately, in this setting, most of current treatment strategies failed to demonstrate a proved and consistent benefit [1–3]. We present a 58-year-old patient referred to the Heart Failure Unit of our center after 4 episodes of acute heart failure (AHF). Patient's past medical history was unimpressive, except for being a heavy former smoker (up to 60 packs per year); indeed, there was no history of diabetes or hypertension. The patient was recently diagnosed of AL, confirmed by bone marrow and rectum biopsy (Congo red positive stain and apple-green birefringence under polarized light). Further workout indicated multi-organ involvement: renal (proteinuria: 24hour urine excretion of 1.7 g), neurological (peripheral and autonomic), soft tissue (macroglossia), and congestive HF. Concerning the latter, cardiac magnetic resonance (CMR) showed evidence of cardiac amyloidosis such as: 1) left ventricular hypertrophy (202 g/m2), 2) global systolic dysfunction (left ventricular ejection fraction: 37%), and 3) a diffuse (early and late) gadolinium enhancement through left and right myocardium, papillary muscles and atrial wall (Fig. 1A, Online video 1). Two-dimensional echocardiography also revealed left and right ventricular hypertrophy, restrictive diastolic pattern, and mild
⁎ Corresponding author at: Cardiology Department, Hospital Clínico Universitario, Avda. Blasco Ibáñez 17, 46010 Valencia, Spain.
http://dx.doi.org/10.1016/j.ijcard.2016.08.255 0167-5273/© 2016 Elsevier Ireland Ltd. All rights reserved.
global left systolic dysfunction (Online video 2). At that time, the patient was not considered a candidate for bone marrow transplantation and received treatment with 4 cycles of cyclophosphamide/dexamethasone and cyclophosphamide/dexamethasone/bortezomib, obtaining a partial hematological response, but absence of organ response. At the time of the initial HF-unit assessment (6 months after AL diagnosis), this patient displayed severe functional impairment (NYHA class III/IV), hypotension (80/50 mm Hg), and clear signs of fluid overload (bibasilar crackles, jugular vein ingurgitation, ascites and peripheral edema) (Fig. 1B). Electrocardiogram showed sinus rhythm (68 bpm) and complete right bundle branch block. Laboratory tests showed abnormal serum free light-chains (SFLC) kappa/lambda ratio = 0.06 (normal range: 0.26 to 1.65), high plasma levels of NTpro-brain natriuretic peptide (NT-proBNP = 12,734 pg/mL), highsensitivity troponin T (46.3 pg/mL), and normal renal function (estimated glomerular filtration rate of 95.3 mL/min/m2). According to the Mayo Clinic prognostic index, the patient was classified on stage 4 of the disease [1]. The patient was on treatment with furosemide (120 mg/day), spironolactone (25 mg/day), ivabradine (7.5 mg tid), folic acid, and allopurinol (300 mg/day). Previous hypotensive episodes precluded to initiate angiotensin converting enzyme inhibitors (ACEI), angiotensin receptor blockers (ARB), or betablockers. After a thoroughly clinical evaluation, depletive treatment was intensified by adding chlorthalidone (25–50 mg/day) and initiating ambulatory administration of high doses of intravenous furosemide (120–240 mg per session) for 8 weeks. Despite this treatment intensification, there was a progressive and sustained increase of symptoms and signs of systemic congestion. In this refractory congestive stage, as an ultrafiltration technique proposed to be potentially useful in advanced CHF [4–6], inclusion in a continuous ambulatory peritoneal dialysis (CAPD) program was proposed and, after acceptance and the informed consent obtained, it was initiated in March 2013 (12 months after AL diagnosis). CAPD consisted of 2 to 4 times/day exchange with dialysate solution (1.36%–2.27% of glucose) according to clinical response. Few weeks after CAPD onset, the patient started showing a substantial (and sustained) clinical improvement, reflected on an increase in blood pressure and amelioration of fluid overload, evidenced by a decrease of a) jugular ingurgitation (Fig. 1B), b) weight (Fig. 1C), and c) fluid overload, assessed by bioimpedance (Fig. 1D). Likewise,
808
J. Núñez et al. / International Journal of Cardiology 223 (2016) 807–809
Fig. 1. Evolution of heart failure parameters after CAPD onset. A. Cardiac magnetic resonance in four chambers projection. Cine sequence with left and right ventricular wall hypertrophy, along with pleural and mild pericardial effusion (left). Phase-sensitive inversion recovery sequence with diffuse and transmural late gadolinium enhancement typical of cardiac amyloidosis (right). B. Jugular ingurgitation. C. Weight. D. Hydration status assessed by systemic bioimpedance. E. Functional Capacity and quality of life assessed by 6-minute walking test and Minnesota Living With Heart Failure Questionnaire, respectively. F. NT-pro-brain natriuretic peptide. CAPD: Continuous ambulatory peritoneal dialysis; 6MWT: 6-minute walking test; MLHFQ: Minnesota Living With Heart Failure Questionnaire.
a sustained increase of functional capacity and quality of life was registered (Fig. 1E). NT-proBNP decreased early, although it was followed by a slow increase until reaching initial levels over the following months (Fig. 1F). In addition, a substantial improvement in extra-cardiac organ involvement was also identified. At 10 months since CAPD onset, the SFLC ratio became normal (Fig. 2A), indicating a favorable hematologic response. Neurological symptoms also subsided. Renal response was judged as partial. No additional treatment with chemotherapy was administered until 21 months after initiation of dialysis, when 2 cycles of dexamethasone/bortezomib were administered due to macroglossia; however, the treatment was prematurely stopped because of severe asthenia as adverse event. Repeated immunofixation electrophoresis (IFE) studies for monoclonal amyloid protein evaluation (Fig. 2B and C) showed no detectable levels in plasma and urine. Bone marrow biopsy also showed b5% of amyloid protein. Conversely, immunoglobulin lambda light chain was detected in dialysate (peritoneal efflux) IFE (Fig. 2D). At 40-month follow-up, the patient is still alive and has not been readmitted for AHF or for any other cardiovascular cause. In the last office visit, the patient remained stable with a NYHA class IIb. Serial echocardiography and CMR showed slightly improvement in left ventricular ejection fraction (44% in CMR). Cardiac dysfunction in AL amyloid occurs due to two mechanisms: extracellular infiltration and direct toxic effect of circulating light chains [1]. Despite advances in disease-specific treatment, mortality remains about 50% at 1 year [1,2]. HF in cardiac AL is generally progressive and difficult to treat [1,7]. Conventional HF treatments, such as betablockers, ACEI, and ARB, are generally poor tolerated due to a questionable balance between efficacy and safety [1]. With this case, we are
highlighting the potential utility of CAPD as a therapeutic alternative in patients with advanced congestive HF due to cardiac AL. At the time of CAPD onset, patient's clinical status was poor and short-term prognosis was ominous. Indeed, having advanced refractory congestive HF, stage 4 systemic AL, and absent of chemotherapy response indicate poor life expectancy [3]. After initiating CAPD, there was a significant and sustained improvement in surrogates of HF severity and no HF decompensations occurred in the following 40 months. Several authors have endorsed the utility of CAPD to ameliorate fluid overload in patients with advanced CHF [4–6]. Indeed, our group have shown that CAPD was associated with a significant improvement of functional capacity, quality of life, and reduction of adverse clinical events in patients with advanced HF and concomitant renal dysfunction [4,5], aims achieved with an acceptable safety profile. In parallel to the evidence of cardiac improvement, CAPD also showed a sizable hematological and extra-cardiac organ beneficial effect. Despite we cannot totally clarify the crucial pathophysiological mechanisms underlying these effects, the presence of AL chain in peritoneal dialysate together with non-detectable values in serum and urine after CAPD onset, lead us to postulate this technique may be a useful tool for ultrafiltration of light-chains. A dual effect by providing supportive cardiac care (control of fluid overload providing a slow ultrafiltration) and, perhaps, a diseasemodifying treatment (ultrafiltration of light-chains) makes this technique a promissory alternative for the treatment of cardiac AL. Further studies might be needed in order to reproduce our findings, and to clarify the pathophysiological mechanisms by which peritoneal dialysate exerted this favorable effect on this patient. Supplementary data to this article can be found online at http://dx. doi.org/10.1016/j.ijcard.2016.08.255.
J. Núñez et al. / International Journal of Cardiology 223 (2016) 807–809
809
Fig. 2. Hematological response. A. Red lines represent the reference interval limits and the blue one represents the SFLC ratio evolution. Following CAPD onset serum free light-chains kappa/lambda ratio increased and remained within normal values. B and C. Serum (B) and urine (C) immunofixation electrophoresis images. The lanes are broad and there is a gradual and smooth reduction in the color density toward the edges of the lane with no narrow dense band with sharp borders identified within the lane. Monoclonal protein was not detected. D. Peritoneal dialysate immunofixation electrophoresis image. A narrow band with sharp borders (arrow) can be identified in the lambda light chain lane, which implies the presence of a monoclonal protein. CAPD: Continuous ambulatory peritoneal dialysis; SFLC: serum free light-chains. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)
Conflict of interest The authors have no conflicts of interest to declare. Funding This work was supported in part by grants from Instituto de Salud Carlos III, Red de Investigación Cardiovascular, Programa 7 (RD12/ 0042/0010), FEDER and PIE15/00013. References [1] M. Grogan, A. Dispenzieri, M. Grogan, A. Dispenzieri, Natural history and therapy of AL cardiac amyloidosis, Heart Fail. Rev. 20 (2015) 155–162. [2] S.K. Kumar, M.A. Gertz, M.Q. Lacy, D. Dingli, S.R. Hayman, F.K. Buadi, et al., Recent improvements in survival in primary systemic amyloidosis and the importance of an early mortality risk score, Mayo Clin. Proc. 86 (2011) 12–18.
[3] S. Kumar, A. Dispenzieri, M.Q. Lacy, S.R. Hayman, F.K. Buadi, C. Colby, et al., Revised prognostic staging system for light chain amyloidosis incorporating cardiac biomarkers and serum free light chain measurements, J. Clin. Oncol. 30 (2012) 989–995. [4] J. Núñez, M. González, G. Miñana, R. Garcia-Ramón, J. Sanchis, V. Bodí, et al., Continuous ambulatory peritoneal dialysis as a therapeutic alternative in patients with advanced congestive heart failure, Eur. J. Heart Fail. 14 (2012) 540–548. [5] J. Núñez, M. González, G. Miñana, R. Garcia-Ramón, J. Sanchis, V. Bodí, et al., Continuous ambulatory peritoneal dialysis and clinical outcomes in patients with refractory congestive heart failure, Rev. Esp. Cardiol. (Engl. Ed.) 65 (2012) 986–995. [6] R. Lu, M.J. Muciño-Bermejo, L.C. Ribeiro, E. Tonini, C. Estremadoyro, S. Samoni, et al., Peritoneal dialysis in patients with refractory congestive heart failure: a systematic review, Cardiorenal Med. 5 (2015) (145–56). [7] T. Nakahashi, T. Arita, K. Yamaji, K. Inoue, T. Yokota, Y. Hoshii, et al., Impact of clinical and echocardiographic characteristics on occurrence of cardiac events in cardiac amyloidosis as proven by endomyocardial biopsy, Int. J. Cardiol. 176 (2014) 753–759.
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Correspondence
Continuous ambulatory peritoneal dialysis as a promising therapy for light chain amyloidosis with congestive heart failure Julio Núñez a,⁎, Anabel Teruel b, Carmen Quiñones-Torrelo c, Sergio García-Blas a, Arturo Carratalá c, Gema Miñana a, Enrique Santas a, Isidro Torregrosa d, Carlos Solano b, Miguel González d a
Servicio de Cardiología, Hospital Clínico Universitario, Universitat de Valencia, INCLIVA, Valencia, Spain Servicio de Hematología, Hospital Clínico Universitario, Universitat de Valencia, INCLIVA, Valencia, Spain Servicio de Bioquímica Clínica, Hospital Clínico Universitario, Universitat de Valencia, INCLIVA, Valencia, Spain d Servicio de Nefrología, Hospital Clínico Universitario, Universitat de Valencia, INCLIVA, Valencia, Spain b c
a r t i c l e
i n f o
Article history: Received 11 August 2016 Accepted 13 August 2016 Available online 20 August 2016 Keywords: Light-chain amyloidosis Congestive heart failure Continuous ambulatory heart failure
Light chain amyloidosis (AL) is usually a systemic disease associated with different kinds of monoclonal plasma cell dyscrasias [1]. The heart is affected in most of patients, and represents the most important prognostic determinant. Indeed, when heart failure (HF) is present, median survival is less than 12 months [1–3]. Unfortunately, in this setting, most of current treatment strategies failed to demonstrate a proved and consistent benefit [1–3]. We present a 58-year-old patient referred to the Heart Failure Unit of our center after 4 episodes of acute heart failure (AHF). Patient's past medical history was unimpressive, except for being a heavy former smoker (up to 60 packs per year); indeed, there was no history of diabetes or hypertension. The patient was recently diagnosed of AL, confirmed by bone marrow and rectum biopsy (Congo red positive stain and apple-green birefringence under polarized light). Further workout indicated multi-organ involvement: renal (proteinuria: 24hour urine excretion of 1.7 g), neurological (peripheral and autonomic), soft tissue (macroglossia), and congestive HF. Concerning the latter, cardiac magnetic resonance (CMR) showed evidence of cardiac amyloidosis such as: 1) left ventricular hypertrophy (202 g/m2), 2) global systolic dysfunction (left ventricular ejection fraction: 37%), and 3) a diffuse (early and late) gadolinium enhancement through left and right myocardium, papillary muscles and atrial wall (Fig. 1A, Online video 1). Two-dimensional echocardiography also revealed left and right ventricular hypertrophy, restrictive diastolic pattern, and mild
⁎ Corresponding author at: Cardiology Department, Hospital Clínico Universitario, Avda. Blasco Ibáñez 17, 46010 Valencia, Spain.
http://dx.doi.org/10.1016/j.ijcard.2016.08.255 0167-5273/© 2016 Elsevier Ireland Ltd. All rights reserved.
global left systolic dysfunction (Online video 2). At that time, the patient was not considered a candidate for bone marrow transplantation and received treatment with 4 cycles of cyclophosphamide/dexamethasone and cyclophosphamide/dexamethasone/bortezomib, obtaining a partial hematological response, but absence of organ response. At the time of the initial HF-unit assessment (6 months after AL diagnosis), this patient displayed severe functional impairment (NYHA class III/IV), hypotension (80/50 mm Hg), and clear signs of fluid overload (bibasilar crackles, jugular vein ingurgitation, ascites and peripheral edema) (Fig. 1B). Electrocardiogram showed sinus rhythm (68 bpm) and complete right bundle branch block. Laboratory tests showed abnormal serum free light-chains (SFLC) kappa/lambda ratio = 0.06 (normal range: 0.26 to 1.65), high plasma levels of NTpro-brain natriuretic peptide (NT-proBNP = 12,734 pg/mL), highsensitivity troponin T (46.3 pg/mL), and normal renal function (estimated glomerular filtration rate of 95.3 mL/min/m2). According to the Mayo Clinic prognostic index, the patient was classified on stage 4 of the disease [1]. The patient was on treatment with furosemide (120 mg/day), spironolactone (25 mg/day), ivabradine (7.5 mg tid), folic acid, and allopurinol (300 mg/day). Previous hypotensive episodes precluded to initiate angiotensin converting enzyme inhibitors (ACEI), angiotensin receptor blockers (ARB), or betablockers. After a thoroughly clinical evaluation, depletive treatment was intensified by adding chlorthalidone (25–50 mg/day) and initiating ambulatory administration of high doses of intravenous furosemide (120–240 mg per session) for 8 weeks. Despite this treatment intensification, there was a progressive and sustained increase of symptoms and signs of systemic congestion. In this refractory congestive stage, as an ultrafiltration technique proposed to be potentially useful in advanced CHF [4–6], inclusion in a continuous ambulatory peritoneal dialysis (CAPD) program was proposed and, after acceptance and the informed consent obtained, it was initiated in March 2013 (12 months after AL diagnosis). CAPD consisted of 2 to 4 times/day exchange with dialysate solution (1.36%–2.27% of glucose) according to clinical response. Few weeks after CAPD onset, the patient started showing a substantial (and sustained) clinical improvement, reflected on an increase in blood pressure and amelioration of fluid overload, evidenced by a decrease of a) jugular ingurgitation (Fig. 1B), b) weight (Fig. 1C), and c) fluid overload, assessed by bioimpedance (Fig. 1D). Likewise,
808
J. Núñez et al. / International Journal of Cardiology 223 (2016) 807–809
Fig. 1. Evolution of heart failure parameters after CAPD onset. A. Cardiac magnetic resonance in four chambers projection. Cine sequence with left and right ventricular wall hypertrophy, along with pleural and mild pericardial effusion (left). Phase-sensitive inversion recovery sequence with diffuse and transmural late gadolinium enhancement typical of cardiac amyloidosis (right). B. Jugular ingurgitation. C. Weight. D. Hydration status assessed by systemic bioimpedance. E. Functional Capacity and quality of life assessed by 6-minute walking test and Minnesota Living With Heart Failure Questionnaire, respectively. F. NT-pro-brain natriuretic peptide. CAPD: Continuous ambulatory peritoneal dialysis; 6MWT: 6-minute walking test; MLHFQ: Minnesota Living With Heart Failure Questionnaire.
a sustained increase of functional capacity and quality of life was registered (Fig. 1E). NT-proBNP decreased early, although it was followed by a slow increase until reaching initial levels over the following months (Fig. 1F). In addition, a substantial improvement in extra-cardiac organ involvement was also identified. At 10 months since CAPD onset, the SFLC ratio became normal (Fig. 2A), indicating a favorable hematologic response. Neurological symptoms also subsided. Renal response was judged as partial. No additional treatment with chemotherapy was administered until 21 months after initiation of dialysis, when 2 cycles of dexamethasone/bortezomib were administered due to macroglossia; however, the treatment was prematurely stopped because of severe asthenia as adverse event. Repeated immunofixation electrophoresis (IFE) studies for monoclonal amyloid protein evaluation (Fig. 2B and C) showed no detectable levels in plasma and urine. Bone marrow biopsy also showed b5% of amyloid protein. Conversely, immunoglobulin lambda light chain was detected in dialysate (peritoneal efflux) IFE (Fig. 2D). At 40-month follow-up, the patient is still alive and has not been readmitted for AHF or for any other cardiovascular cause. In the last office visit, the patient remained stable with a NYHA class IIb. Serial echocardiography and CMR showed slightly improvement in left ventricular ejection fraction (44% in CMR). Cardiac dysfunction in AL amyloid occurs due to two mechanisms: extracellular infiltration and direct toxic effect of circulating light chains [1]. Despite advances in disease-specific treatment, mortality remains about 50% at 1 year [1,2]. HF in cardiac AL is generally progressive and difficult to treat [1,7]. Conventional HF treatments, such as betablockers, ACEI, and ARB, are generally poor tolerated due to a questionable balance between efficacy and safety [1]. With this case, we are
highlighting the potential utility of CAPD as a therapeutic alternative in patients with advanced congestive HF due to cardiac AL. At the time of CAPD onset, patient's clinical status was poor and short-term prognosis was ominous. Indeed, having advanced refractory congestive HF, stage 4 systemic AL, and absent of chemotherapy response indicate poor life expectancy [3]. After initiating CAPD, there was a significant and sustained improvement in surrogates of HF severity and no HF decompensations occurred in the following 40 months. Several authors have endorsed the utility of CAPD to ameliorate fluid overload in patients with advanced CHF [4–6]. Indeed, our group have shown that CAPD was associated with a significant improvement of functional capacity, quality of life, and reduction of adverse clinical events in patients with advanced HF and concomitant renal dysfunction [4,5], aims achieved with an acceptable safety profile. In parallel to the evidence of cardiac improvement, CAPD also showed a sizable hematological and extra-cardiac organ beneficial effect. Despite we cannot totally clarify the crucial pathophysiological mechanisms underlying these effects, the presence of AL chain in peritoneal dialysate together with non-detectable values in serum and urine after CAPD onset, lead us to postulate this technique may be a useful tool for ultrafiltration of light-chains. A dual effect by providing supportive cardiac care (control of fluid overload providing a slow ultrafiltration) and, perhaps, a diseasemodifying treatment (ultrafiltration of light-chains) makes this technique a promissory alternative for the treatment of cardiac AL. Further studies might be needed in order to reproduce our findings, and to clarify the pathophysiological mechanisms by which peritoneal dialysate exerted this favorable effect on this patient. Supplementary data to this article can be found online at http://dx. doi.org/10.1016/j.ijcard.2016.08.255.
J. Núñez et al. / International Journal of Cardiology 223 (2016) 807–809
809
Fig. 2. Hematological response. A. Red lines represent the reference interval limits and the blue one represents the SFLC ratio evolution. Following CAPD onset serum free light-chains kappa/lambda ratio increased and remained within normal values. B and C. Serum (B) and urine (C) immunofixation electrophoresis images. The lanes are broad and there is a gradual and smooth reduction in the color density toward the edges of the lane with no narrow dense band with sharp borders identified within the lane. Monoclonal protein was not detected. D. Peritoneal dialysate immunofixation electrophoresis image. A narrow band with sharp borders (arrow) can be identified in the lambda light chain lane, which implies the presence of a monoclonal protein. CAPD: Continuous ambulatory peritoneal dialysis; SFLC: serum free light-chains. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)
Conflict of interest The authors have no conflicts of interest to declare. Funding This work was supported in part by grants from Instituto de Salud Carlos III, Red de Investigación Cardiovascular, Programa 7 (RD12/ 0042/0010), FEDER and PIE15/00013. References [1] M. Grogan, A. Dispenzieri, M. Grogan, A. Dispenzieri, Natural history and therapy of AL cardiac amyloidosis, Heart Fail. Rev. 20 (2015) 155–162. [2] S.K. Kumar, M.A. Gertz, M.Q. Lacy, D. Dingli, S.R. Hayman, F.K. Buadi, et al., Recent improvements in survival in primary systemic amyloidosis and the importance of an early mortality risk score, Mayo Clin. Proc. 86 (2011) 12–18.
[3] S. Kumar, A. Dispenzieri, M.Q. Lacy, S.R. Hayman, F.K. Buadi, C. Colby, et al., Revised prognostic staging system for light chain amyloidosis incorporating cardiac biomarkers and serum free light chain measurements, J. Clin. Oncol. 30 (2012) 989–995. [4] J. Núñez, M. González, G. Miñana, R. Garcia-Ramón, J. Sanchis, V. Bodí, et al., Continuous ambulatory peritoneal dialysis as a therapeutic alternative in patients with advanced congestive heart failure, Eur. J. Heart Fail. 14 (2012) 540–548. [5] J. Núñez, M. González, G. Miñana, R. Garcia-Ramón, J. Sanchis, V. Bodí, et al., Continuous ambulatory peritoneal dialysis and clinical outcomes in patients with refractory congestive heart failure, Rev. Esp. Cardiol. (Engl. Ed.) 65 (2012) 986–995. [6] R. Lu, M.J. Muciño-Bermejo, L.C. Ribeiro, E. Tonini, C. Estremadoyro, S. Samoni, et al., Peritoneal dialysis in patients with refractory congestive heart failure: a systematic review, Cardiorenal Med. 5 (2015) (145–56). [7] T. Nakahashi, T. Arita, K. Yamaji, K. Inoue, T. Yokota, Y. Hoshii, et al., Impact of clinical and echocardiographic characteristics on occurrence of cardiac events in cardiac amyloidosis as proven by endomyocardial biopsy, Int. J. Cardiol. 176 (2014) 753–759.