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Clinical Policy Bulletin:
Peripheral Ultrafiltration for Acute Decompensated Heart Failure
Number: 0741


Policy

Aetna considers ultrafiltration medically necessary for the acute management of members hospitalized with acutely decompensated congestive heart failure (CHF) who have dyspnea at rest or with minimal activity. 

Aetna considers intermittent peripheral ultrafiltration in persons who are not acutely decompensated or scheduled repetitive peripheral ultrafiltration experimental and investigational, as is use of peripheral ultrafiltration for all other indications becauses of insufficient evidence of their effectiveness.

See also CPB 0610 - Biventricular Pacing (Cardiac Resynchronization Therapy)/Combination Resynchronization-Defibrillation Devices for Congestive Heart Failure, and CPB 0709 - Nesiritide (Natrecor).



Background

Approximately 5 million Americans are currently diagnosed with heart failure (HF), and more than 500,000 new cases are diagnosed each year.  Heart failure is the leading cause of hospitalizations in the United States (U.S.) and is associated with significant morbidity, mortality and resource utilization.  The New York Heart Association (NYHA)'s classification of HF was the first rating system developed to quantify the degree of functional limitations exhibited by patients with HF.  It is a 4-tier system that categorizes patients based on subjective impression of the degree of functional compromise.  The 4 NYHA functional classes are as follows:

Class I

Patients with cardiac disease but without resulting limitation of physical activity.  Ordinary physical activity does not cause undue fatigue, palpitation, dyspnea, or anginal pain.  Symptoms only occur on severe exertion.

Class II:

Patients with cardiac disease resulting in slight limitation of physical activity.  They are comfortable at rest.  Ordinary physical activity (e.g., moderate physical exertion such as carrying shopping bags up several flights or stairs) results in fatigue, palpitation, dyspnea, or anginal pain.

Class III:

Patients with cardiac disease resulting in marked limitation of physical activity.  They are comfortable at rest.  Less than ordinary activity (i.e., mild exertion) causes fatigue, palpitation, dyspnea, or anginal pain.

Class IV:

Patients with cardiac disease resulting in inability to carry on any physical activity without discomfort.  Symptoms of cardiac insufficiency or of the anginal syndrome may be present even at rest.  If any physical activity is undertaken, discomfort is increased.

The NYHA's functional classification of HF entails a continuum of increasing symptom severity, in which patients in Class I report no symptoms of HF, while those in Class IV exhibit severe symptomatology at rest.  Patients with acute decompensated heart failure (ADHF) are usually characterized by an acute change in their baseline NYHA status (usually NYHA Class I or II) to NYHA Class IV disease (Hunt et al, 2001).  Although no formal definition of ADHF exists, traditional signs of ADHF include pitting edema greater than 2 mm, presence of rales on pulmonary examination, pulmonary capillary wedge pressure (greater than 18 mm Hg), elevated right atrial pressure (greater than 10 mm Hg), and an increase in body weight (greater than 4.5 kg for patients below 5 feet in height or greater than 6.8 kg for patients over 5 feet in height).  The level of brain B-type natriuretic peptide is now recommended to confirm the diagnosis of ADHF, with a level greater than 80 pg/ml being indicative of decompensation.  While ADHF can occur in patients with almost any stage of HF, episodes occur frequently in those with structural heart disease and either a history or current symptoms of HF (Bleske et al, 1998; Gottlieb et al, 1998; Hunter et al, 2001).

In contrast to chronic HF, where there have been numerous advances in care and corresponding decreases in morbidity and mortality, treatment for patients with ADHF remains largely empiric, and outcomes of these patients have remained relatively unchanged with an approximate 10 % 30-day mortality and almost 40 % 1-year re-hospitalization rate (Howlett, 2005).  Acute decompensated heart failure is an important milestone in the clinical course of HF.  It is an event associated with a significant deterioration in the prognosis of HF (Onwuanyi and Taylor, 2007).

Allen and O'Connor (2007) stated that ADHF represents a heterogeneous group of disorders that typically present as dyspnea, edema and fatigue.  Despite the high prevalence of this condition and its associated major morbidity and mortality, diagnosis can be difficult, and optimal treatment remains poorly defined.  Identification of the acute triggers for the decompensation as well as non-invasive characterization of cardiac filling pressures and output is central to management.  Diuretics, vasodilators, continuous positive airway pressure and inotropes can be used to alleviate symptoms.  However, few agents currently available for the treatment of ADHF have been definitively shown in large prospective randomized clinical trials to provide meaningful improvements in intermediate-term clinical outcomes.  Multiple novel therapies are being developed, but previous treatment failures indicate that progress in the management of ADHF is likely to be slow.

The therapeutic objective in patients with ADHF is volume and sodium removal, and the restoration of diuretic sensitivity.  A number of drugs have been demonstrated to lower morbidity and mortality in patients with chronic HF.  Despite these advances, the frequency of hospitalization for HF has continued to rise, and evidence is lacking in demonstrable benefit of pharmacotherapy for patients hospitalized with ADHF.  In particular, Sackner-Bernstein and Aaronson (2007) noted that nesiritide is approved by the U.S. Food and Drug Administration (FDA) for the treatment of patients with ADHF who suffer from symptoms at rest or with minimal exertion.  Its approval was based on a clinical development program that focused on surrogates and short-term effects on symptoms rather than clinical outcomes.  Aggregate data analysis has suggested that it may be associated with a risk of excess mortality and worsening renal insufficiency.  The association between its use and subsequent risk of death raises the question of whether the endpoints assessed in the clinical development program were adequate, and provides the opportunity to evaluate the process of weighing risks with benefits.  The authors concluded that with nesiritide, the risks of therapy outweigh the benefits demonstrated to date.

Several percutaneous/peripheral devices have been developed to improve symptoms and clinical outcomes in patients hospitalized with HF.  These include devices such as continuous aortic flow augmentation and ultrafiltration (UF) devices.  Peripheral UF therapy offers the potential of greater volume and sodium removal as compared with conventional therapies in a more expeditious manner.  Ultrafiltration differs from dialysis because it acts via convection rather than diffusion, which lowers the risk for induced metabolic abnormalities.  Conventional UF devices required central venous access with a double lumen catheter, monitoring by a dialysis technician, and specialized hospital units.  More recently, devices have been developed that allow UF to be carried out via large peripheral venous catheters (CTAF, 2007).

One device for ultrafiltration is the Aquadex FlexFlow system; Aquapheresis is the trademarked term for removal of salt and water with the Aquadex system.  The Aquadex FlexFlow technology received initial 510(k) marketing clearance from the FDA in June 2002.  An updated/amended 510(k) clearance (classified as a high permeability dialysis system) was given in February 2006 following some modifications.  That Aquadex FlexFlow System is indicated for temporary (up to 8 hours) ultrafiltration treatment of patients with fluid overload who have failed diuretic therapy, and extended (longer than 8 hours) ultrafiltration treatment of patient with fluid overload who have failed diuretic therapy and require hospitalization.

Costanzo (2006) stated that 90 % of one million annual hospitalizations for HF in the U.S. are due to symptoms of volume over-load.  Hypervolemia contributes to HF progression and mortality.  Current treatment guidelines recommend that therapy for patients with HF be aimed at achieving euvolemia.  Intravenous loop diuretics induce a rapid diuresis that reduces lung congestion and dyspnea.  However, the effectiveness of loop diuretics decreases with repeated treatments.  Unresolved congestion may contribute to high re-hospitalization rates.  Furthermore, loop diuretics may be associated with increased morbidity and mortality due to deleterious effects on neuro-hormonal activation, electrolyte balance, as well as cardiac and renal function.  Peripheral UF is an alternative method of sodium and water removal that may improve hemodynamics in patients with HF.

Bart et al (2005) evaluated the safety and effectiveness of UF in patients admitted with decompensated congestive HF (CHF).  Ultrafiltration for CHF is usually reserved for patients with renal failure or those unresponsive to pharmacological management.  These researchers performed a randomized trial of UF versus usual medical care using a simple UF device that does not require special monitoring or central intravenous access.  Patients admitted for CHF with evidence of volume over-load were randomized to a single, 8-hour UF session in addition to usual care or usual care alone.  The primary end point was weight loss 24 hours after the time of enrollment.  A total of 40 patients were enrolled (20 UF, 20 usual care).  Ultrafiltration was successful in 18 of the 20 patients in the UF group.  Fluid removal after 24 hours was 4,650 ml and 2,838 ml in the UF and usual care groups, respectively (p = 0.001).  Weight loss after 24 hours, the primary end point, was 2.5 kg and 1.86 kg in the UF and usual care groups, respectively (p = 0.240).  Patients tolerated UF well.  The authors concluded that the early application of UF for patients with CHF was feasible, well-tolerated, and resulted in significant weight loss and fluid removal.  They noted that a larger trial is underway to determine the relative effectiveness of UF versus standard care in ADHF.

In a case-series study, Dahle and colleagues (2006) reported the feasibility and effectiveness of performing large volume UF via peripherally inserted standard intravenous catheters in hospitalized patients with ADHF (n = 9).  The mean length of time of peripheral UF therapy was 33.3 +/- 20.0 hours with a mean volume removed of 7.0 +/- 4.9 L.  All patients experienced a statistically significant mean weight loss of 6.2 +/- 5.0 kg (p = 0.01).  There was no statistically significant change in renal function.  The authors noted that this was the first successful implementation of UF via standard peripheral intravenous catheters to remove a large volume of fluid over an extended period of time reliably in a small group of patients.  The ability to use peripheral UF therapy via intravenous catheters will potentially allow this therapy to be implemented more easily in a variety of care settings to treat patients with refractory HF.

Costanzo and associates (2007) compared the safety and effectiveness of peripheral (veno-venous) UF and standard intravenous diuretic therapy for patients with hypervolemic HF.  Patients hospitalized for HF with greater than or equal to 2 signs of hypervolemia were randomized to UF or intravenous diuretics.  Primary end points were weight loss and dyspnea assessment at 48 hours after randomization.  Secondary end points included net fluid loss at 48 hours, functional capacity, HF re-hospitalizations, and unscheduled visits in 90 days.  Safety end points included changes in renal function, electrolytes, and blood pressure.  A total of 200 patients (138 men and 62 women, mean age of 63 +/- 15 years, 71 % ejection fraction less than or equal to 40 %) were randomized to UF or intravenous diuretics.  At 48 hours, weight loss (5.0 +/- 3.1 kg versus 3.1 +/- 3.5 kg; p = 0.001) and net fluid loss (4.6 versus 3.3 L; p = 0.001) were greater in the UF group.  Dyspnea scores were similar.  At 90 days, the UF group had fewer patients re-hospitalized for HF (16 of 89 [18 %] versus 28 of 87 [32 %]; p = 0.037), HF re-hospitalizations (0.22 +/- 0.54 versus 0.46 +/- 0.76; p = 0.022), re-hospitalization days (1.4 +/- 4.2 versus 3.8 +/- 8.5; p = 0.022) per patient, and unscheduled visits (14 of 65 [21 %] versus 29 of 66 [44 %]; p = 0.009).  No serum creatinine differences occurred between groups.  Nine deaths occurred in the UF group and 11 in the diuretics group.  The authors concluded that in patients with decompensated HF, peripheral UF safely produces greater weight and fluid loss than intravenous diuretics, reduces 90-day resource utilization for HF, and is an effective alternative therapy.

In an editorial that accompanied the afore-mentioned study, Elkayam et al (2007) stated that "[t]he use of this therapy should be considered early in patients not responding to intravenous diuretics and vasoactive medications and in patients in whom such therapy is discontinued or reduced because of worsening of renal function or other drug-induced complications".  Furthermore, Guglin and Polavaram (2007) stated that managing volume over-load is essential for the treatment of symptomatic HF.  Traditionally, it is achieved via oral and intravenous diuretics.  Alternatively, the excess fluid can be removed via UF.  Advent in technology has made UF more feasible than before for routine clinical practice.  Zevitz (2006) stated that patients with HF who are fluid over-loaded should be treated with diuretics, or, if necessary in patients with renal failure, hemodialysis with UF.

In contrast, in an editorial regarding the efficacy of vasopressin antagonism in heart failure outcome study with tolvaptan (EVEREST) clinical trials program, Yancy (2007) noted that UF represents at best an emerging technology with intriguing preliminary data but limited applications.

There is also a lack of consensus among several specialty societies and a technology assessment agency regarding the clinical value of peripheral UF in the treatment of patients with ADHF.  The European Society of Cardiology Task Force's guidelines on the diagnosis and treatment of acute HF (Dickstein et al, 2008) stated that ultrafiltration should be considered to reduce fluid overload in selected patients, and to correct hyponatremia in symptomatic patients that are refractory to diuretics.  The guidelines noted, however, that the appropriate selection criteria for UF have not been established.  The Heart Failure Society of America's guidelines on evaluation and management of patients with ADHF (2006) stated that when congestion fails to improve in response to diuretic therapy, UF may be considered (strength of evidence = C [expert opinion, observational studies, epidemiologic findings, safety reporting from large-scale use in practice]).  Furthermore, the Institute for Clinical Systems Improvement's guidelines on HF in adults (2006) noted that patients with persistent volume over-load may be candidates for continuous intravenous diuretics, UF, or hemodialysis (all out of guideline).

On the other hand, a technology assessment on peripheral UF for the management of ADHF by the California Technology Assessment Forum (CTAF, 2007) concluded that the use of peripheral UF does not meet Technology Assessment Criterion 3, 4 and 5 for safety, effectiveness and improvement in health outcomes when used to treat ADHF.  The CTAF assessment also discussed a number of methodological issues regarding the study by Costanzo et al (2007).  These issues include a lack of blinding for patients, investigators, staff, or those evaluating and adjudicating outcomes as well as inadequate reporting of recruitment and follow-up.  Furthermore, data for the primary endpoints (weight loss at 48 hours and dyspnea scores at 48 hours) were only available on 80 % to 84 % of the patients randomized.  This high rate of incomplete data 48 hours after randomization in a hospitalized patient population was not explained by the researchers.  Also, patients studied in this trial did not meet the FDA indication for peripheral UF as they had not previously failed diuretic therapy.  The authors of the CTAF assessment noted that the benefits of peripheral UF remain to be proven; and the findings by Costanzo et al (2007) need to be replicated before they can be accepted with confidence.

The McGill University Health Center Technology Assessment Unit (Pan and Dendukuri, 2010) found that there is sufficient evidence to conclude that UF is an effective technology for the management of ADHF, and is the method of choice when patients have become resistant to diuretics or have developed secondary renal failure.  The assessment found limited evidence that UF may have long-term health benefits including improved exercise performance for up to 3, and possibly 6 months, and that these effects are associated with a reduction in re-hospitalization rates.

An assessment of UF for HF by the Veterans Health Administration Technology Assessment Program (Flynn, 2010) found no recently published evidence to materially change conclusions from a previous report by the Centre for Evidence-based Purchasing (CEP) of the UK National Health Services, which found: “CEP finds that UF has significant potential to become a routine therapy for excess fluid removal in patients with CHF.  However, further work is needed to establish the patient groups who would benefit most, the optimal rates of fluid removal, the conditions for termination of therapy, and the cost savings associated with long-term quality of life benefits.”

The VATAP report stated that these conclusions can be transferred to the United States in 2010 (Flynn, 2010).  Additional shortcomings of the available literature include those elaborated by the CEP report: lack of blinding, which may be understandably difficult in the case of a bulky bedside device; lack of explicit power calculations and correspondingly small numbers of patients in clinical trials, which may reflect the relative lack of reliable estimates of clinically significant effects for UF in available research on which such calculations would be based; lack of follow-up beyond 2 to 3 months; reliance on intermediate or surrogate outcomes such as fluid volume removed or weight lost, rather than longer term outcomes such as quality of life or HF-specific mortality.  The VATAP report noted that the device manufacturer is a significant presence in the only published (Costanzo et al, 2007; Costanzo et al, 2010) and ongoing trials.  The VATAP report found that systematic reviews and assessments do not report significant adverse events or safety concerns with ultrafiltration for HF, but studies may not have been adequately powered or followed patients for long enough to detect uncommon adverse events.  Post-marketing surveillance for a device only available since late 2006 may also be inadequate for detecting uncommon or late adverse events.  The VATAP report notes that kidney dysfunction with over-zealous volume reduction has been observed and is under investigation for UF.

The American College of Cardiology/American Heart Association's updated guidelines on the diagnosis and management of chronic HF in adults (Hunt et al, 2005) did not discuss the use of peripheral UF as a therapeutic option for patients at various stages of HF.  Similarly, the National Heart Foundation of Australia/the Cardiac Society of Australia and New Zealand's guidelines on the prevention, detection and management of chronic HF (2006) did not address the use of peripheral UF as a therapeutic option.

The potential for peripheral UF devices to normalize underlying cardiac function and thus improve long-term clinical outcomes in patients with ADHF needs to be further investigated.

Fiaccadori et al (2011) stated that fluid over-load is a key pathophysiologic mechanism underlying both the acute decompensation episodes of HF and the progression of the syndrome.  Moreover, it represents the most important factor responsible for the high re-admission rates observed in these patients and is often associated with renal function worsening, which by itself increases mortality risk.  In this clinical context, UF has been proposed as an alternative to diuretics to obtain a quicker relief of pulmonary/systemic congestion.  These researchers reviewed technical issues, mechanisms, efficacy, safety, costs, and indications of UF in HF.  The available evidence does not support the widespread use of UF as a substitute for diuretic therapy.  Owing to its operative characteristics, UF can not be expected to directly influence serum electrolyte levels, azotemia, and acid-base balance, or to remove high-molecular-weight substances (e.g., cytokines) in clinically relevant amounts.  Ultrafiltration should be used neither as a quicker way to achieve a sort of mechanical diuresis nor as a remedy for an inadequately prescribed and administered diuretic therapy.  Instead, it should be reserved to selected patients with advanced HF and true diuretic resistance, as part of a more complex strategy aiming at an adequate control of fluid retention.

 
CPT Codes / HCPCS Codes / ICD-9 Codes
There are no specific CPT or HCPCS codes for peripheral ultrafiltration:
ICD-9 codes not covered for indications listed in the CPB:
428.0 Congestive heart failure


The above policy is based on the following references:
  1. Bleske BE, Welage LS, Kramer WG, Nicklas JM. Pharmacokinetics of torsemide in patients with decompensated and compensated heart failure. J Clin Pharmacol. 1998;38(8):708-714.
  2. Gottlieb SS, Khata M, Wentworth D, et al. The effect of diuresis on the pharmacokinetics of the loop diuretics furosemide and torsemide in patients with heart failure. Am J Med. 1998;104(6):533-538.
  3. Hunt SA, Baker DW, Chin MH, et al; American College of Cardiology/American Heart Association. ACC/AHA guidelines for the evaluation and management of chronic heart failure in the adult: Executive summary. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to revise the 1995 Guidelines for the Evaluation and Management of Heart Failure). J Am Coll Cardiol. 2001;38(7):2101-2113.
  4. Howlett JG. Acutely decompensated congestive heart failure: New therapies for an old problem. Expert Rev Cardiovasc Ther. 2005;3(5):925-936.
  5. Bart BA, Boyle A, Bank AJ, et al. Ultrafiltration versus usual care for hospitalized patients with heart failure: The Relief for Acutely Fluid-Overloaded Patients With Decompensated Congestive Heart Failure (RAPID-CHF) trial. J Am Coll Cardiol. 2005;46(11):2043-2046.
  6. Hunt SA, Abraham WT, Chin MH, et al. ACC/AHA 2005 guideline update for the diagnosis and management of chronic heart failure in the adult. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure). Bethesda, MD: American College of Cardiology Foundation (ACCF); August 2005. Available at: http://content.onlinejacc.org/cgi/reprint/46/6/e1. Accessed September 10, 2007.
  7. Gura V, Beizai M, Ezon C, et al. Continuous renal replacement therapy for congestive heart failure: The wearable continuous ultrafiltration system. ASAIO J. 2006;52(1):59-61.
  8. Costanzo MR. The role of ultrafiltration in the management of heart failure. Curr Treat Options Cardiovasc Med. 2006;8(4):301-309.
  9. Dahle TG, Blake D, Ali SS, et al. Large volume ultrafiltration for acute decompensated heart failure using standard peripheral intravenous catheters. J Card Fail. 2006;12(5):349-352.
  10. Zevitz ME. Heart failure. eMedicine Medicine Topic 3552. Omaha, NE: eMedicine.com; January 2, 2006. Available at: http://www.emedicine.com/med/topic3552.htm. Accessed September 10, 2007.
  11. Heart Failure Society of America. Evaluation and management of patients with acute decompensated heart failure. J Card Fail. 2006;12(1):e86-e103. Available at: http://www.heartfailureguideline.com/. Accessed Septmeber 10, 2007.
  12. Institute for Clinical Systems Improvement (ICSI). Heart failure in adults. ICSI Healthcare Guidelines. Bloomington, MN: Institute for Clinical Systems Improvement (ICSI); August 2006. Available at: http://www.icsi.org/guidelines_and_more/guidelines__order_sets___protocols/. Accessed September 10, 2007.
  13. National Heart Foundation of Australia, Cardiac Society of Australia and New Zealand, Chronic Heart Failure Guidelines Expert Writing Panel. Guidelines for the prevention, detection and management of chronic heart failure in Australia, 2006. Sydney, NSW: National Heart Foundation of Australia; November 2006. Available at: http://www.heartfoundation.com.au/document/NHF/CHF_2006_Guidelines_NHFA-CSANZ_WEB_PDF-1.2MB.pdf. Accessed September 10, 2007.
  14. Onwuanyi A, Taylor M. Acute decompensated heart failure: Pathophysiology and treatment. Am J Cardiol. 2007;99(6B):25D-30D.
  15. Allen LA, O'Connor CM. Management of acute decompensated heart failure. CMAJ. 2007;176(6):797-805.
  16. Sackner-Bernstein J, Aaronson KD. Nesiritide for acute decompensated heart failure: Does the benefit justify the risk? Curr Cardiol Rep. 2007;9(3):187-193.
  17. Costanzo MR, Guglin ME, Saltzberg MT, et al. Ultrafiltration versus intravenous diuretics for patients hospitalized for acute decompensated heart failure. J Am Coll Cardiol. 2007;49(6):675-683.
  18. Elkayam U, Hatamizadeh P, Janmohamed M. The challenge of correcting volume overload in hospitalized patients with decompensated heart failure. J Am Coll Cardiol. 2007;49(6):684-686.
  19. Guglin M, Polavaram L. Ultrafiltration in heart failure. Cardiology in Review. 2007;15(5):226-230.
  20. Yancy CW. Climbing the mountain of acute decompensated heart failure. The EVEREST trials. JAMA. 2007;297(12):1374-1376.
  21. National Horizon Scanning Centre (NHSC). Ultrafiltration for acute decompensated heart failure: Horizon scanning technology briefing. Birmingham, UK: NHSC; 2006.
  22. California Technology Assessment Forum (CTAF). Peripheral ultrafiltration for the management of acute decompensated heart failure: A technology assessment. San Francisco, CA: CTAF; June 20, 2007. Available at: http://ctaf.org/content/general/detail/740. Accessed September 10, 2007.
  23. Peterangelo M. Incorporating aquapheresis into the hospital setting: A practical approach. Prog Cardiovasc Nurs. 2008;23(4):168-172.
  24. Rogers HL, Marshall J, Bock J, et al. A randomized, controlled trial of the renal effects of ultrafiltration as compared to furosemide in patients with acute decompensated heart failure. J Card Fail. 2008;14(1):1-5.
  25. Haas GJ, Pestritto VM, Abraham WT. Ultrafiltration for volume control in decompensated heart failure. Heart Fail Clin. 2008;4(4):519-534.
  26. Dickstein K, Cohen-Solal A, Filippatos G, et al.; Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2008 of the European Society of Cardiology.  ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2008. Eur J Heart Fail. 2008;10(10):933-989. 
  27. Jaski BE, Romeo A, Ortiz B, et al. Outcomes of volume-overloaded cardiovascular patients treated with ultrafiltration. J Card Fail. 2008;14(6):515-520.
  28. Wertman BM, Gura V, Schwarz ER. Ultrafiltration for the management of acute decompensated heart failure. J Card Fail. 2008;14(9):754-759.
  29. Colechin ES, Bower L, Sims AJ. Ultrafiltration therapy for fluid overload in heart failure. Report. CEP 07016. Newcastle Upon Thyne; UK: Centre for Evidence-based Purchasing, Policy and Innovation Directorate, UK National Health Services; 2007.
  30. Menes J, Bousfield D, Colechin E, et al. CHF Solutions Aquadex Flexflow ultrafiltration system. Report. CEP 07017. Newcastle Upon Thyne, UK: Centre for Evidence-based Purchasing, Policy and Innovation Directorate, UK National Health Services; 2008.
  31. Bart BA. Treatment of congestion in congestive heart failure: Ultrafiltration is the only rational initial treatment of volume overload in decompensated heart failure. Circ Heart Fail. 2009; 2(5):499-504.
  32. Shin JT, Dec GW. Ultrafiltration should not replace diuretics for the initial treatment of acute decompensated heart failure. Circ Heart Fail. 2009;2(5):505-511.
  33. Pan I, Dendukuri N. Efficacy, safety and cost of ultrafiltration for the management of acute decompensated heart failure. Report No 47. Montreal, QC: Technology Assessment Unit of the McGill University Health Centre (MUHC); May 31, 2010.
  34. Costanzo MR, Agostoni P, Marenzi G. Extracorporeal fluid removal in heart failure patients. Contrib Nephrol. 2010;164:173-198.
  35. Andrade JG, Stadnick E, Virani SA. The role of peripheral ultrafiltration in the management of acute decompensated heart failure. Blood Purif. 2010;29(2):177-182.
  36. Flynn K. Brief overview: Ultrafiltration for decompensated heart failure. Boston, MA: Technology Assessment Program (VATAP), Office of Patient Care Services, Veterans Health Administration; January 2010. 
  37. De Maria E, Pignatti F, Patrizi G, et al. Ultrafiltration for the treatment of diuretic-resistant, recurrent, acute decompensated heart failure: Experience in a single center. J Cardiovasc Med (Hagerstown). 2010;11(8):599-604.
  38. Fiaccadori E, Regolisti G, Maggiore U, et al. Ultrafiltration in heart failure. Am Heart J. 2011;161(3):439-449.


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Copyright Aetna Inc. All rights reserved. Clinical Policy Bulletins are developed by Aetna to assist in administering plan benefits and constitute neither offers of coverage nor medical advice. This Clinical Policy Bulletin contains only a partial, general description of plan or program benefits and does not constitute a contract. Aetna does not provide health care services and, therefore, cannot guarantee any results or outcomes. Participating providers are independent contractors in private practice and are neither employees nor agents of Aetna or its affiliates. Treating providers are solely responsible for medical advice and treatment of members. This Clinical Policy Bulletin may be updated and therefore is subject to change.
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