- Email: [email protected]
Management of Heart Failure With Outpatient Technology
Management of Heart Failure With Outpatient Technology Natalie Murphy, PhD, FNP-BC, Margaret Shanks, MSN, FNP-BC, and Pamela Alderman, MSLIS ABSTRACT
Approximately 6.5 million Americans have heart failure, and the cost is projected to reach $70 billion annually by the year 2020. Hospital systems and providers are tasked with effectively managing this condition to prevent readmission from exacerbations. In fact, if patients are readmitted within 30 days of discharge, payers limit reimbursement for the care. Traditional clinic markers and monitoring systems have failed to reduce hospital readmission rates because these systems rely on patient symptoms, which too often present late in the decompensation process. Newer technology shows promise at identifying heart failure earlier and may reduce readmission rates. Keywords: heart failure, HFrEF, HFpEF, management, technology Ó 2018 Elsevier Inc. All rights reserved.
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pproximately 6.5 million Americans have heart failure (HF), and this figure will grow as society ages. HF-related hospital admissions appear to be equally divided by the underlying cause, with half resulting from HF with reduced ejection fraction (HFrEF) and the other 50% being caused by HF with preserved ejection fraction (HFpEF).1 The expected incidence of HF is projected to nearly double by the year 2020. With this rising incidence, the financial burden increases exponentially as well. By 2020, the cost of HF care is projected to grow by 127% to nearly $70 billion dollars annually.2 In 2012, the Centers for Medicare and Medicaid Services, as part of the Affordable Care Act, began penalizing hospitals by reducing payments for service if patients are readmitted with HF within 1 month of initial discharge.3 Readmission rates became a performance measure by which hospitals are reimbursed and graded. This new pay-forperformance atmosphere has forced providers and health systems to focus not only on treatment of the exacerbations but also on the prevention of acute decompensations that result in readmission. In a disease process fraught with exacerbations and remissions, the task is to recognize HF patients at www.npjournal.org
greatest danger of acute decompensation and treat them early enough to prevent admission. The purpose of this article is to explore the underlying pathophysiology of HF, examine the causes of HF, review evidence on outpatient monitoring systems and the technology developed to identify fluid shifts, and discuss the effect of this technology on readmission rates. PATHOPHYSIOLOGY OF HF
HF is the result of the heart’s incapacity to propel an adequate supply of blood to satisfy metabolic requirements and is mediated by the body’s neurohormonal response. The ventricles are unable to pump effectively enough to eject blood (systolic failure) and/or they fail to relax well and subsequently do not fill with blood properly (diastolic failure). HF causes hemodynamic changes and, ultimately, permanently changes the structure of the heart muscle, which is called myocardial remodeling. In HF, the sympathetic nervous system, the reninangiotensin- aldosterone cascade, the tumor necrosis factor alpha, and vasodilator peptides called atrial natriuretic peptide and brain natriuretic peptide are triggered, causing a vicious cycle of fluid shifts and The Journal for Nurse Practitioners - JNP
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continued deterioration of overall heart function. Ultimately, patients present with dyspnea, edema, exercise intolerance, sleep disorders, nocturnal cough, orthopnea, and fatigue.4,5 As the understanding of the pathophysiology of HF evolves, treatment approaches are changing. In the past, treatment focused on salt consumption and subsequent fluid retention. Although sodium does play a role, acute symptoms may be related instead to a redistribution of blood volume within the circulatory system and not as a result of a volume overload. Monitoring of weight has been a key management strategy that has largely failed to provide clinically relevant information to providers and has not decreased admission rates. Most patients do not experience any significant change in weight in the weeks preceding an acute exacerbation.6 Blood volume is contained within the circulatory system. The veins are considered to be capacitance, or reservoir, vessels and generally house 70% of the blood volume. Veins in the abdomen, referred to as the splanchnic system, hold 20% to 50% of the volume at any given time. These vessels are mediated by complicated passive and active systems, which include numerous baroreceptors, hormones, and the sympathetic nervous system. The capacitance vessels regulate preload by constriction. Acute exacerbation of HF is now believed to be related to dysregulation of the splanchnic system, which results in the vessels failing to hold onto the normal stored volume. Subsequently, blood volume shifts from the veins of the abdomen into the cardiac and pulmonary system, resulting in extravascular edema. This likely is the result of neurohormonal mediation by the cardiorenal and hepatorenal systems. Interestingly, both angiotensin-converting enzyme inhibitors and nitrates increase splanchnic capacitance, which is perhaps the reason they improve HF symptoms.6,7
dilated cardiomyopathies; genetic cardiomyopathies; hypertension; cardiomyopathies related to endocrine and metabolic disorders such as obesity, diabetes, thyroid disease, and acromegaly; cardiomyopathies caused by heart toxins such as alcohol, cocaine, and chemotherapy; and tachycardia-induced cardiomyopathy. In addition, myocarditis, connective tissue disorders, peripartum cardiomyopathy, iron overload, amyloidosis, sarcoidosis, valvular disorders, and stress can also cause HFrEF.8-10 The remaining patients have HFpEF, which is broadly defined as having HF with an EF greater than 40% to 45%. This is a more perplexing diagnosis with less clear-cut causes. Essentially, the diagnosis is usually made when a patient presents with signs and symptoms of HF, all other noncardiac causes for the symptoms have been excluded, and evidence of diastolic dysfunction has been documented via either cardiac catheterization or Doppler echocardiogram. Newer evidence suggests that symptomatic patients with HFpEF may not have visible diastolic dysfunction on echocardiogram, and there are additional causative factors at play.11 This type of HF is most commonly noted in elderly women with a significant history of hypertension. Most patients with HFpEF also have a history of diabetes mellitus, hyperlipidemia, coronary artery disease, atrial fibrillation, smoking, and obesity. These comorbidities are believed to cause systemic inflammation, which causes oxidative stress within the microvasculature of the myocardium. Eventually, this causes heart muscle cells to hypertrophy and stiffen. Current therapies available to treat diastolic HF have not proven effective.8,9,11 It is important to understand that HFrEF and HFpEF can and do occur together.8,9
TYPES AND CAUSES OF HF
OUTPATIENT STRATEGIES TO PREVENT READMISSION Telehealth
In general, a normal left ventricular ejection fraction (EF) is 55% or greater. About half of the population has HFrEF, which is defined as an EF of less than 40%. The causes of this systolic dysfunction are numerous, but the primary cause is ischemic heart disease leading to myocardial infarction, which impairs left ventricular function. Other causes include
Telehealth has been used for years in an effort to prevent HF readmissions. Very simply stated, this noninvasive endeavor consists of telephone support provided by nurses who assess for the presence of edema and other symptoms consistent with cardiac decompensation. Systems generally measure parameters such as body weight, vital signs, and telemetry
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rhythm strips.2 Worsening parameter changes then prompt an intervention aimed at reducing acute symptoms. Unfortunately, evidence suggests that although telehealth systems may benefit patients from a quality of life standpoint, overall the systems are not effective at decreasing hospital readmission rates.12-16 The systems have failed because the symptoms targeted occur too late in the decompensation process to be addressed aggressively enough in an outpatient setting to prevent admission.17 Changes in weight and symptoms may occur because of clinical changes such as cardiac cachexia and arrhythmias, leaving telehealth monitoring poorly sensitive as a predictor of decompensation.16 Despite no reduction in readmission rates, outpatient telemonitoring has merit. This noninvasive system can be used to monitor all patients regardless of HF type or New York Heart Association (NYHA) Functional Classification17 (Table) and appears to enhance preventative care and selfawareness in many patients. Phone support from providers, whether a registered nurse or advanced practice nurse, also offers an opportunity to build trusting relationships and reinforce appropriate HF education. Invasive Devices
Although implanted devices, such as implanted cardioverter defibrillators (ICDs), have historically served an important role in the management of cardiac electrical dysfunction, researchers wondered if the technology might also assist HF management. Approximately 2 weeks before the development of weight gain and edema, intrathoracic impedance has been shown to change.18,19 Essentially, impedance is Table. New York Heart Association Functional Classification17 Class
Presentation of Symptoms
I
No symptoms at rest, asymptomatic except during severe exertion
II
No symptoms at rest, symptoms start with moderate exertion
III
No symptoms at rest, symptoms start with minimal exertion
IV
Symptomatic even at rest
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a measurement of resistance to the flow of electrical current along a device lead wire. Although increases in impedance can indicate a lead fracture, a change in impedance can also suggest a change in volume, which is useful information to providers managing HF. Thoracic tissue provides a higher degree of resistance than body fluid and blood, which offer less hindrance to the flow of electrical current. In an HF patient with an ICD, a drop in impedance may be 1 of the first indicators that decompensation is occurring.19 Early studies on impedance led to the development of Optival, which was then marketed by Medtronic (Minneapolis, MN) in 2004. Devices equipped with this technology detect impedance amid the right ventricular defibrillating coil and the ICD device.18 As left ventricular filling pressure rises, intrathoracic fluid increases and impedance drops. There was excitement that this implanted technology could improve HF care and reduce admission rates, but multiple studies have revealed no clear, consistent reduction in readmission rates with the device.20 Unfortunately, false alarms can be triggered because other comorbidities can impact impedance such as the presence of pneumonia, pneumothorax, and positive-pressure ventilation. When the device is set to achieve lower false-positive alarms, sensitivity is then sacrificed.18 Before a decrease in intrathoracic impedance, left ventricular filling pressures increase. Detection of this event could potentially allow for treatment changes earlier along the decompensation continuum. The COMPASS-HF (Chronicle Offers Management to Patient with Advanced Signs and Symptoms of Heart Failure) study used an implanted device to continuously record hemodynamic measurements of NYHA functional class III and IV patients with both HFrEF and HFpEF. The device, with a transvenous recording lead, was inserted subcutaneously in the anterior chest. The Medtronic Chronicle device stored pulmonary artery diastolic pressure and data such as vital signs and activity. The data recorded guided HF therapy of those in the treatment arm of the trial. This cohort had more therapy adjustments than patients in the control arm, which led to a 21% decrease in HF exacerbations. Retrospective examination of the data discovered a 36% fall in the risk of primary HF hospitalization in the treatment cohort.20 The Journal for Nurse Practitioners - JNP
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Information gathered in the Multisensor Chronic Evaluation in Ambulatory Heart Failure Patients (MultiSENSE) clinical trial led to the development of a treatment algorithm called HeartLogic. In addition to measuring impedance, researchers also analyzed vital signs, heart sounds, tidal volume measurements, and patient activity level. These data allowed accurate prediction of future HF events. The algorithm was applied to implanted cardiac resynchronization defibrillator technology, which allows providers to intervene much earlier in the decompensation cycle. Regrettably, these devices are invasive and applicable only to HFrEF patients with ICDs. The devices are not placed in patients who have HFpEF, so they offer no value to this class of HF. Like previous devices, the newer ICDs have poor sensitivity and can be adversely affected by comorbid conditions.21 The Hemodynamically Guided Home SelfTherapy in Severe Heart Failure Patients (HOMEOSTASIS) trial was an observational study that followed NYHA class III and IV clients irrespective of EF for up to 38 months with an implanted left atrial pressure monitor. The data collected by the device guided therapy, which resulted in neurohormonal blockade being up-titrated more frequently. There was a greater reduction in loop diuretic doses as well. Researchers found positive improvements in left atrial pressure, NYHA functional class, and left ventricular EF. Hospital readmission rates were not measured.22 The CardioMEMS Heart Sensor Allows Monitoring of Pressure to Improve Outcomes in NYHA Class III Heart Failure Patients (CHAMPION) trial evaluated the impact of treatment guided by data collected by the wireless CardioMEMS (Abbott Laboratories, St. Jude Medical, St. Paul, Minnesota, United States) device. The device implanted in the pulmonary artery allowed for even earlier identification of those at risk for decompensation. Five hundred fifty patients with HFpEF and HFrEF were registered in 64 centers. Participants in the treatment arm appreciated a 37% decrease in HF-related hospitalizations, a lower risk of death, and lower pulmonary artery pressures than those in the control group.23 Upon completion of the randomization period, researchers opened access and used data to guide therapy in the original control cohort. The 4
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results showed an impressive reduction in hospitalizations in this group as well and sustained benefit in the former treatment group.24 After Food and Drug Administration approval in 2014, CardioMEMS received a great deal of attention. The results of the original trial have been reproduced.25-27 An additional retrospective analysis of data recorded from the first 2,000 patients to undergo an implant revealed similar results and provided support for the device in an older population that was comprised of more women and more HFpEF patients than the original CHAMPION trial.28 Other studies on CardioMEMS documented an improvement in functional status, suggesting data from the device result in more frequent adjustments of vasodilators, neurohormonal agents, and diuretics without a detriment to renal function.25,26 Additionally, CardioMEMS-guided therapy is likely to lessen HF costs.25 The device may also be effective when used in those with chronic obstructive pulmonary disease, an important subgroup of patients in whom other technology falls short.27 Although CardioMEMS has been shown to be a safe and potentially effective device in both HFrEF and HFpEF cohorts, there are shortcomings. First, as an implanted device, an invasive procedure is required. Second, treatment with aspirin and clopidogrel for 1 month after implantation is required in those who are not otherwise anticoagulated, which increases the risk of bleeding.23 Lastly, CardioMEMS is an expensive device with an estimated cost over $17,000. The implantation procedure cost is more than $1,000, and monthly monitoring is approximately $30. Although it has been Food and Drug Administration approved, it has not achieved nationwide Medicare reimbursement at this time.29 Noninvasive Devices
Noninvasive devices that accurately measure lung impendence have also been developed. The IMPEDANCE-HF (Non Invasive Lung IMPEDANCE-guided Preemptive Treatment in Patients with Chronic Heart Failure) study revealed that participants had a surge in pulmonary congestion approximately 14 days before their HF admissions. The most pronounced change in impedance Volume
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occurred approximately 3 days before hospitalization. By then, intensification of therapy was too late to prevent HF admission. Statistical analysis showed that when used to guide therapy earlier in the decompensation process, this device reduced hospitalizations, mortality, and improved functional status. Interestingly, evaluation of lung impedance on the day of discharge revealed that as many as 80% of those admitted with HF exacerbation were being discharged with residual congestion.30 Essentially, this suggests patients are being discharged too soon and while still decompensated, which would certainly raise the chances of readmission within a 30-day window. The newest potential player in the world of remote monitoring is a noninvasive, wearable vest. The device uses ReDS (Sensible Medical, Tenafly, NJ, United States) (remote dielectric sensing) which is technology originally used in military defense, and dielectric principles to estimate fluid levels in the lung. These principles refer to a material’s ability to conduct electricity. Air possesses a low dielectric coefficient, whereas water possesses a very high coefficient. This multiuse vest has 2 sensors positioned on the anterior and posterior thoracic areas to transmit and intercept low-power electromagnetic signals through lung tissue. The sensors do not require skinto-skin contact and can be placed over clothing. The sensors calculate fluid volume within 90 seconds.31 Data from the vest allow providers to estimate the fluid balance in the lungs and potentially identify decompensation before weight gain or symptoms of congestion occur. The ability of the device to identify lung fluid was demonstrated in the laboratory using pigs who were subjected to myocardial infarction by comparing the ReDS data with serial chest computed tomographic scans results.31 Researchers then validated the device on humans by comparing ReDS data with the physical examinations, laboratory data, chest radiographs, and intake/output of both HF patients and healthy volunteers. Another observational study that compared ReDS values with computed tomographic scan results of patients admitted with and without acutely decompensated HF also identified that the ReDS system accurately estimates lung fluid volume.32 This work then led to a www.npjournal.org
subsequent small study that used the data obtained from the vest to guide the therapy of 50 acutely decompensated HF patients after discharge from the hospital. During the management period, the treatment cohort appreciated an 87% reduction in readmission. When therapy with the vest was discontinued, readmission rates rose. This small group of patients was comprised of both HFrEF and HFpEF patients, 38% of whom were women.33 Consequently, this vest shows promise in managing both types of HF with less risk than an implanted device. Similar to data found in the IMPEDANCE-HF trial, another study on the ReDS device found that HF patients are likely being discharged before the acute decompensation is truly resolved. The ReDS vest was used to guide the timing of discharge of clients hospitalized with decompensated HF. When deemed ready for discharge based on existing clinical markers, volume status was then evaluated using the ReDS technology. Data were collected, and those in the control arm were discharged regardless of the ReDS value. If the vest discovered the patient appeared to still be decompensated, those in the treatment arm remained admitted and further intravenous diuresis was administered. The increased use of intravenous diuretics did not appear to cause greater renal insufficiency. Results indicated that despite documentation of thorough diuresis by traditional methods (intake/output, symptoms, physical assessment, and weight loss), over 30% of the patients deemed ready for discharge were still inadequately decongested, which increased the risk of readmission.34 Patients are simply being discharged too soon, and existing clinical markers are not as accurate as previously believed to be. DISCUSSION
As evidence grows on the underlying pathophysiology of HF, it becomes apparent that the key to reducing acute cardiac decompensation, which results in hospital admission, is early identification. Symptoms historically monitored by providers or telehealth systems such as worsening edema, weight gain, exercise intolerance, or dyspnea occur late in the process. In fact, the occurrence is so late even aggressive The Journal for Nurse Practitioners - JNP
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outpatient treatment often fails to prevent further decompensation. Consequently, efforts to reduce readmission by this method have largely failed.12-14,27 Newer technology shows promise in more effective management of HF simply because the devices identify volume shifts early enough in the decompensation continuum to allow for appropriate medication adjustment. Noninvasive devices appear safe. Trials using these devices suggest a reduction in readmission rates and also indicate that HF patients are often discharged before decompensation is fully resolved.33 Although ongoing, larger clinical trials are needed to build additional evidence, these devices offer hope for improved HF outcomes.
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CONCLUSION
Increasing HF incidence and the resulting physical, emotional, and financial cost to patients, society, and the health care system is alarming. Acute HF decompensation begins to occur weeks before subjective and objective symptoms present. Subsequently, the traditional methods of surveillance have failed to reduce hospital readmission rates. Innovative technology offers a new path to identifying decompensation early enough to initiate therapy that may reduce readmission rates and improve overall HF outcomes.
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21. References 1. Benjamin EJ, Virani SS, Callaway CW, et al. Heart disease and stroke statistics—2018 update: a report from the American Heart Association. Circulation. 2018;137(12):e67-e492. https://doi.org/10.1161/CIR. 0000000000000558. 2. Fraiche A, Eapen Z, McClellan MB. Moving beyond the walls of the clinic. JACC Heart Fail. 2017;5(4):297-304. https://doi.org/10.1016/j.jchf.2016.11.013. 3. Centers for Medicare & Medicaid Services. Readmission reduction program (HRRP). https://www.cms.gov/Medicare/Medicare-Fee-for-Service-Payment/ AcuteInpatientPPS/Readmissions-Reduction-Program.html. March 20, 2018. Accessed April 23, 2018. 4. Keller KB, Sabatino D, Winland-Brown JE, Porter BO, Keller MB. Cardiovascular problems. In: Dunphy L, Winland-Brown J, Porter B, Thomas D, eds. Primary Care: The Art and Science of Advanced Practice Nursing. Philadelphia, PA: FA Davis Company; 2015:430-503. 5. Nicholson C. Chronic heart failure: pathophysiology, diagnosis, and treatment. Nurs Older People. 2014;26:29-38. https://doi.org/10.7748/nop.26.7. 29.e584. 6. Fudim M, Hernandez A, Felker M. Role of volume redistribution in the congestion of heart failure. J Am Heart Assoc. 2017;6:e006817. https://doi.org/ 10.1161/JAHA.117.006817. 7. McDonald, Ashley EA, Fedak PW, et al. Mind the gap: current challenges and the future state of heart failure care. Can J Cardiol. 2017;33(11):1434-1449. https://doi.org/10.1016/j.cjca.2017.08.023. 8. Yancy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2013;128:e240-e327. https://doi.org/10.1161/CIR. 0b013e31829e8776. 9. Yancy CW, Jessup M, Bozkurt B, et al. 2017 ACC/AHA/HFSA focused update of the 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology/American Heart Association
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Task Force on Clinical Practice Guidelines and the Heart Failure Society of America. J Card Fail. 2017;23(8):628-651. https://doi.org/10.1016/j.cardfail. 2017.04.014. Ponikowski P, Voors AA, Anker SD, et al. 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure: the Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC) Developed with the special contribution of the Heart Failure Association (HFA) of the ESC. Eur Heart J. 2016;37(27):2129-2200. https://doi.org/10.1093/eurheartj/ehw128. Upadhya U, Kitzman D. Management of heart failure with preserved ejection fraction: current challenges and future directions. Am J Cardiovasc Drugs. 2017;17(4):283-298. https://doi.org/10.1007/s40256-017-0219-2. Kitsiou S, Pare G, Jaana M. Effects of home telemonitoring interventions on patients with chronic heart failure: an overview of systemic reviews. J Med Internet Res. 2015;17(3):e63. https://doi.org/10.2196/jmir.4174. Kraii I, deVries A, Vermeulen L, et al. The value of telemonitoring and ICTguided disease management in heart failure: results from the IN TOUCH study. Int J Med Inform. 2016;85:53-60. https://doi.org/10.1016/j.ijmedinf.2015 .10.001. Ong M, Romano P, Edington S, Aronow H. Effectiveness of remote patient monitoring of hospitalized patients with heart failure: the better effectiveness after transition-heart failure (BEAT-HF) randomized clinical trial. JAMA Intern Med. 2016;176:310-318. https://doi.org/10.1001/ jamainternmed.2015.7712. Varon C, Alao M, Minter J, et al. Telehealth on heart failure results of the Recap project. J Telemed Telecare. 2015;21(6):340-347. Sandhu AT, Goldhaber-Fiebert JD, Owens DK, Turakhia MP, Kaiser DW, Heidenreich PA. Cost-effectiveness of implantable pulmonary artery pressure monitoring in chronic heart failure. JACC Heart Fail. 2016;4(5):368-375. https:// doi.org/10.1016/j.jchf.2015.12.015. The Criteria Committee of the New York Heart Association. In: Dolgin M, ed. Nomenclature and Criteria for the Diagnosis of the Heart and Great Vessels. 9th ed. Boston, MA: Little, Brown & Co; 1994:253-256. Mooney D, Fung E, Doshi R, Shavelle D. Evolution from electrophysiologic to hemodynamic monitoring: the story of left atrial and pulmonary artery pressure monitors. Front Physiol. 2015;6:271. https://doi.org/10.3389/fphys .2015.00271. Tang WH, Tong W. Measuring impedance in congestive heart failure: current options and clinical applications. Am Heart J. 2008;157(3):402-411. https://doi. org/10.1016/j.ahj.2008.10.016. Bourge RC, Abraham WT, Adamson PB, et al. Randomized controlled trial of an implantable continuous hemodynamic monitor in patients with advanced heart failure. J Am Coll Cardiol. 2008;51(11):1073-1079. https://doi.org/ 10.1016/j.jacc.2007.10.061. Boehmer J, Hariharan R, Devecchi F, et al. A multisensor algorithm predicts heart failure events in patients with implanted devices. JACC Heart Fail. 2017;5(3):216-225. https://doi.org/10.1016/j.jchf.2016.12.011. Ritzema J, Troughton R, Melton I, et al. Physician-directed patient selfmanagement of left atrial pressure in advanced chronic heart failure. Circulation. 2010;121:1086-1095. https://doi.org/10.1161/CIRCULATIONAHA .108.800490. Abraham WT, Adamson PB, Bourge RC, et al. Wireless pulmonary artery haemodynamic monitoring of chronic heart failure: a randomised controlled trial. Lancet. 2011;377:658-666. https://doi.org/10.1016/S0140-6736(11) 60101-3. Abraham WT, Adamson PB, Bourge RC, et al. Hemodynamic monitoring in advanced heart failure: results from the LAPTOP-HF trial. J Card Fail. 2016;22(11):940. https://doi.org/10.1016/j.cardfail.2016.09.012. Costanzo M, Stevenson LW, Adamson PB, et al. Interventions linked to decreased heart failure hospitalizations during ambulatory pulmonary artery pressure monitoring. JACC Heart Fail. 2016;4(5):333-344. https://doi.org/ 10.1016/j.jchf.2015.11.011. Jermyn R, Alam A, Kvasic J, Saeed O, Jorde U. Hemodynamic-guided heart-failure management using a wireless implantable sensor: infrastucture, methods, and results in a community heart failure diseasemanagement program. Clin Cardiol. 2017;40:170-176. https://doi.org/10. 1002/clc.22643. Vanoli E, D’Elia E, La Rovere M, Gronda E. Remote heart function monitoring: role of the CardioMEMS HF system. J Cardiovas Med. 2016;17(7):518-523. https://doi.org/10.2459/JCM.0000000000000367. Heywood JT, Jermyn R, Shavelle D, et al. Impact of practice based management of pulmonary artery pressures in 2000 patients implanted with the CardioMEMS sensor. Circulation. 2017;135:1509-1517. https://doi.org/ 10.1161/CIRCULATIONAHA.116.026184.
29. Casey T. Cost effectiveness of the CARDIOMEMS device for heart failure remains questionable. http://www.cardiovascularbusiness.com/topics/ healthcare-economics/cost-effectiveness-cardiomems-device-heart-failureremains-questionable. September 8, 2016. Accessed April 23, 2018.
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30. Shochat M, Shotan A, Blondheim D, et al. Non-invasive lung IMPEDANCEGuided preemptive treatment in chronic heart failure patients: a randomized controlled trial (IMPEDANCE-HF Trial) [published erratum appears in J Card Fail. 2017;23(6):512-513. J. Card Fail. 2016;22:713-722. https://doi.org/10.1016/ j.cardfail.2016.03.015. 31. Amir O, Rappaport D, Zafir B, Abraham WT. A novel approach to monitoring pulmonary congestion in heart failure: initial animal and clinical experiences using remote dielectric sensing technology. Congest Heart Fail. 2013;19(3):149-155. https://doi.org/10.1111/chf.12021. 32. Amir O, Azzam Z, Gaspar T, et al. Validation of remote dielectric sensing (ReDS) technology for quantification of lung fluid status: Comparison of high resolution chest computed tomography in patients with and without acute heart failure. Int J Cardiol. 2016;221:841-846. https://doi.org/10.1016/j.ijcard. 2016.06.323. 33. Amir O, Ben-Gal T, Weinstein J, et al. Evaluation of remote dielectric sensing (ReDS) technology- guided therapy for decreasing heart failure re-hospitalizations. Int J Cardiol. 2017;240:279-284. https://doi.org/10.1016/j.ijcard.2017.02.120. 34. Bensimhon D, McLean D, Chase P, Wood D, Garman V, Curran L. Readiness for discharge of heart failure patients based on ReDS lung fluid measurement. J Card Fail. 2017;23(8):S66. http://www.onlinejcf.com/article/ S1071-9164(17)30405-0/pdf.
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Natalie Murphy, PhD, FNP-BC, is an associate teaching professor at the University of Missouri, St Louis University in St Louis. She is available at [email protected]. Margaret Shanks, MSN, FNP-BC, ACGNP-BC, is a heart failure nurse practitioner at Penn Cardiology at Penn Presbyterian Medical Center, University of Pennsylvania in Philadelphia. Pamela Alderman, MSLIS, HBOI, is a library director at Florida Atlantic University in Ft Pierce. In compliance with national ethical guidelines, the authors report no relationships with business or industry that would pose a conflict of interest. 1555-4155/18/$ see front matter © 2018 Elsevier Inc. All rights reserved. https://doi.org/10.1016/j.nurpra.2018.07.004
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Approximately 6.5 million Americans have heart failure, and the cost is projected to reach $70 billion annually by the year 2020. Hospital systems and providers are tasked with effectively managing this condition to prevent readmission from exacerbations. In fact, if patients are readmitted within 30 days of discharge, payers limit reimbursement for the care. Traditional clinic markers and monitoring systems have failed to reduce hospital readmission rates because these systems rely on patient symptoms, which too often present late in the decompensation process. Newer technology shows promise at identifying heart failure earlier and may reduce readmission rates. Keywords: heart failure, HFrEF, HFpEF, management, technology Ó 2018 Elsevier Inc. All rights reserved.
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pproximately 6.5 million Americans have heart failure (HF), and this figure will grow as society ages. HF-related hospital admissions appear to be equally divided by the underlying cause, with half resulting from HF with reduced ejection fraction (HFrEF) and the other 50% being caused by HF with preserved ejection fraction (HFpEF).1 The expected incidence of HF is projected to nearly double by the year 2020. With this rising incidence, the financial burden increases exponentially as well. By 2020, the cost of HF care is projected to grow by 127% to nearly $70 billion dollars annually.2 In 2012, the Centers for Medicare and Medicaid Services, as part of the Affordable Care Act, began penalizing hospitals by reducing payments for service if patients are readmitted with HF within 1 month of initial discharge.3 Readmission rates became a performance measure by which hospitals are reimbursed and graded. This new pay-forperformance atmosphere has forced providers and health systems to focus not only on treatment of the exacerbations but also on the prevention of acute decompensations that result in readmission. In a disease process fraught with exacerbations and remissions, the task is to recognize HF patients at www.npjournal.org
greatest danger of acute decompensation and treat them early enough to prevent admission. The purpose of this article is to explore the underlying pathophysiology of HF, examine the causes of HF, review evidence on outpatient monitoring systems and the technology developed to identify fluid shifts, and discuss the effect of this technology on readmission rates. PATHOPHYSIOLOGY OF HF
HF is the result of the heart’s incapacity to propel an adequate supply of blood to satisfy metabolic requirements and is mediated by the body’s neurohormonal response. The ventricles are unable to pump effectively enough to eject blood (systolic failure) and/or they fail to relax well and subsequently do not fill with blood properly (diastolic failure). HF causes hemodynamic changes and, ultimately, permanently changes the structure of the heart muscle, which is called myocardial remodeling. In HF, the sympathetic nervous system, the reninangiotensin- aldosterone cascade, the tumor necrosis factor alpha, and vasodilator peptides called atrial natriuretic peptide and brain natriuretic peptide are triggered, causing a vicious cycle of fluid shifts and The Journal for Nurse Practitioners - JNP
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continued deterioration of overall heart function. Ultimately, patients present with dyspnea, edema, exercise intolerance, sleep disorders, nocturnal cough, orthopnea, and fatigue.4,5 As the understanding of the pathophysiology of HF evolves, treatment approaches are changing. In the past, treatment focused on salt consumption and subsequent fluid retention. Although sodium does play a role, acute symptoms may be related instead to a redistribution of blood volume within the circulatory system and not as a result of a volume overload. Monitoring of weight has been a key management strategy that has largely failed to provide clinically relevant information to providers and has not decreased admission rates. Most patients do not experience any significant change in weight in the weeks preceding an acute exacerbation.6 Blood volume is contained within the circulatory system. The veins are considered to be capacitance, or reservoir, vessels and generally house 70% of the blood volume. Veins in the abdomen, referred to as the splanchnic system, hold 20% to 50% of the volume at any given time. These vessels are mediated by complicated passive and active systems, which include numerous baroreceptors, hormones, and the sympathetic nervous system. The capacitance vessels regulate preload by constriction. Acute exacerbation of HF is now believed to be related to dysregulation of the splanchnic system, which results in the vessels failing to hold onto the normal stored volume. Subsequently, blood volume shifts from the veins of the abdomen into the cardiac and pulmonary system, resulting in extravascular edema. This likely is the result of neurohormonal mediation by the cardiorenal and hepatorenal systems. Interestingly, both angiotensin-converting enzyme inhibitors and nitrates increase splanchnic capacitance, which is perhaps the reason they improve HF symptoms.6,7
dilated cardiomyopathies; genetic cardiomyopathies; hypertension; cardiomyopathies related to endocrine and metabolic disorders such as obesity, diabetes, thyroid disease, and acromegaly; cardiomyopathies caused by heart toxins such as alcohol, cocaine, and chemotherapy; and tachycardia-induced cardiomyopathy. In addition, myocarditis, connective tissue disorders, peripartum cardiomyopathy, iron overload, amyloidosis, sarcoidosis, valvular disorders, and stress can also cause HFrEF.8-10 The remaining patients have HFpEF, which is broadly defined as having HF with an EF greater than 40% to 45%. This is a more perplexing diagnosis with less clear-cut causes. Essentially, the diagnosis is usually made when a patient presents with signs and symptoms of HF, all other noncardiac causes for the symptoms have been excluded, and evidence of diastolic dysfunction has been documented via either cardiac catheterization or Doppler echocardiogram. Newer evidence suggests that symptomatic patients with HFpEF may not have visible diastolic dysfunction on echocardiogram, and there are additional causative factors at play.11 This type of HF is most commonly noted in elderly women with a significant history of hypertension. Most patients with HFpEF also have a history of diabetes mellitus, hyperlipidemia, coronary artery disease, atrial fibrillation, smoking, and obesity. These comorbidities are believed to cause systemic inflammation, which causes oxidative stress within the microvasculature of the myocardium. Eventually, this causes heart muscle cells to hypertrophy and stiffen. Current therapies available to treat diastolic HF have not proven effective.8,9,11 It is important to understand that HFrEF and HFpEF can and do occur together.8,9
TYPES AND CAUSES OF HF
OUTPATIENT STRATEGIES TO PREVENT READMISSION Telehealth
In general, a normal left ventricular ejection fraction (EF) is 55% or greater. About half of the population has HFrEF, which is defined as an EF of less than 40%. The causes of this systolic dysfunction are numerous, but the primary cause is ischemic heart disease leading to myocardial infarction, which impairs left ventricular function. Other causes include
Telehealth has been used for years in an effort to prevent HF readmissions. Very simply stated, this noninvasive endeavor consists of telephone support provided by nurses who assess for the presence of edema and other symptoms consistent with cardiac decompensation. Systems generally measure parameters such as body weight, vital signs, and telemetry
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rhythm strips.2 Worsening parameter changes then prompt an intervention aimed at reducing acute symptoms. Unfortunately, evidence suggests that although telehealth systems may benefit patients from a quality of life standpoint, overall the systems are not effective at decreasing hospital readmission rates.12-16 The systems have failed because the symptoms targeted occur too late in the decompensation process to be addressed aggressively enough in an outpatient setting to prevent admission.17 Changes in weight and symptoms may occur because of clinical changes such as cardiac cachexia and arrhythmias, leaving telehealth monitoring poorly sensitive as a predictor of decompensation.16 Despite no reduction in readmission rates, outpatient telemonitoring has merit. This noninvasive system can be used to monitor all patients regardless of HF type or New York Heart Association (NYHA) Functional Classification17 (Table) and appears to enhance preventative care and selfawareness in many patients. Phone support from providers, whether a registered nurse or advanced practice nurse, also offers an opportunity to build trusting relationships and reinforce appropriate HF education. Invasive Devices
Although implanted devices, such as implanted cardioverter defibrillators (ICDs), have historically served an important role in the management of cardiac electrical dysfunction, researchers wondered if the technology might also assist HF management. Approximately 2 weeks before the development of weight gain and edema, intrathoracic impedance has been shown to change.18,19 Essentially, impedance is Table. New York Heart Association Functional Classification17 Class
Presentation of Symptoms
I
No symptoms at rest, asymptomatic except during severe exertion
II
No symptoms at rest, symptoms start with moderate exertion
III
No symptoms at rest, symptoms start with minimal exertion
IV
Symptomatic even at rest
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a measurement of resistance to the flow of electrical current along a device lead wire. Although increases in impedance can indicate a lead fracture, a change in impedance can also suggest a change in volume, which is useful information to providers managing HF. Thoracic tissue provides a higher degree of resistance than body fluid and blood, which offer less hindrance to the flow of electrical current. In an HF patient with an ICD, a drop in impedance may be 1 of the first indicators that decompensation is occurring.19 Early studies on impedance led to the development of Optival, which was then marketed by Medtronic (Minneapolis, MN) in 2004. Devices equipped with this technology detect impedance amid the right ventricular defibrillating coil and the ICD device.18 As left ventricular filling pressure rises, intrathoracic fluid increases and impedance drops. There was excitement that this implanted technology could improve HF care and reduce admission rates, but multiple studies have revealed no clear, consistent reduction in readmission rates with the device.20 Unfortunately, false alarms can be triggered because other comorbidities can impact impedance such as the presence of pneumonia, pneumothorax, and positive-pressure ventilation. When the device is set to achieve lower false-positive alarms, sensitivity is then sacrificed.18 Before a decrease in intrathoracic impedance, left ventricular filling pressures increase. Detection of this event could potentially allow for treatment changes earlier along the decompensation continuum. The COMPASS-HF (Chronicle Offers Management to Patient with Advanced Signs and Symptoms of Heart Failure) study used an implanted device to continuously record hemodynamic measurements of NYHA functional class III and IV patients with both HFrEF and HFpEF. The device, with a transvenous recording lead, was inserted subcutaneously in the anterior chest. The Medtronic Chronicle device stored pulmonary artery diastolic pressure and data such as vital signs and activity. The data recorded guided HF therapy of those in the treatment arm of the trial. This cohort had more therapy adjustments than patients in the control arm, which led to a 21% decrease in HF exacerbations. Retrospective examination of the data discovered a 36% fall in the risk of primary HF hospitalization in the treatment cohort.20 The Journal for Nurse Practitioners - JNP
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Information gathered in the Multisensor Chronic Evaluation in Ambulatory Heart Failure Patients (MultiSENSE) clinical trial led to the development of a treatment algorithm called HeartLogic. In addition to measuring impedance, researchers also analyzed vital signs, heart sounds, tidal volume measurements, and patient activity level. These data allowed accurate prediction of future HF events. The algorithm was applied to implanted cardiac resynchronization defibrillator technology, which allows providers to intervene much earlier in the decompensation cycle. Regrettably, these devices are invasive and applicable only to HFrEF patients with ICDs. The devices are not placed in patients who have HFpEF, so they offer no value to this class of HF. Like previous devices, the newer ICDs have poor sensitivity and can be adversely affected by comorbid conditions.21 The Hemodynamically Guided Home SelfTherapy in Severe Heart Failure Patients (HOMEOSTASIS) trial was an observational study that followed NYHA class III and IV clients irrespective of EF for up to 38 months with an implanted left atrial pressure monitor. The data collected by the device guided therapy, which resulted in neurohormonal blockade being up-titrated more frequently. There was a greater reduction in loop diuretic doses as well. Researchers found positive improvements in left atrial pressure, NYHA functional class, and left ventricular EF. Hospital readmission rates were not measured.22 The CardioMEMS Heart Sensor Allows Monitoring of Pressure to Improve Outcomes in NYHA Class III Heart Failure Patients (CHAMPION) trial evaluated the impact of treatment guided by data collected by the wireless CardioMEMS (Abbott Laboratories, St. Jude Medical, St. Paul, Minnesota, United States) device. The device implanted in the pulmonary artery allowed for even earlier identification of those at risk for decompensation. Five hundred fifty patients with HFpEF and HFrEF were registered in 64 centers. Participants in the treatment arm appreciated a 37% decrease in HF-related hospitalizations, a lower risk of death, and lower pulmonary artery pressures than those in the control group.23 Upon completion of the randomization period, researchers opened access and used data to guide therapy in the original control cohort. The 4
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results showed an impressive reduction in hospitalizations in this group as well and sustained benefit in the former treatment group.24 After Food and Drug Administration approval in 2014, CardioMEMS received a great deal of attention. The results of the original trial have been reproduced.25-27 An additional retrospective analysis of data recorded from the first 2,000 patients to undergo an implant revealed similar results and provided support for the device in an older population that was comprised of more women and more HFpEF patients than the original CHAMPION trial.28 Other studies on CardioMEMS documented an improvement in functional status, suggesting data from the device result in more frequent adjustments of vasodilators, neurohormonal agents, and diuretics without a detriment to renal function.25,26 Additionally, CardioMEMS-guided therapy is likely to lessen HF costs.25 The device may also be effective when used in those with chronic obstructive pulmonary disease, an important subgroup of patients in whom other technology falls short.27 Although CardioMEMS has been shown to be a safe and potentially effective device in both HFrEF and HFpEF cohorts, there are shortcomings. First, as an implanted device, an invasive procedure is required. Second, treatment with aspirin and clopidogrel for 1 month after implantation is required in those who are not otherwise anticoagulated, which increases the risk of bleeding.23 Lastly, CardioMEMS is an expensive device with an estimated cost over $17,000. The implantation procedure cost is more than $1,000, and monthly monitoring is approximately $30. Although it has been Food and Drug Administration approved, it has not achieved nationwide Medicare reimbursement at this time.29 Noninvasive Devices
Noninvasive devices that accurately measure lung impendence have also been developed. The IMPEDANCE-HF (Non Invasive Lung IMPEDANCE-guided Preemptive Treatment in Patients with Chronic Heart Failure) study revealed that participants had a surge in pulmonary congestion approximately 14 days before their HF admissions. The most pronounced change in impedance Volume
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occurred approximately 3 days before hospitalization. By then, intensification of therapy was too late to prevent HF admission. Statistical analysis showed that when used to guide therapy earlier in the decompensation process, this device reduced hospitalizations, mortality, and improved functional status. Interestingly, evaluation of lung impedance on the day of discharge revealed that as many as 80% of those admitted with HF exacerbation were being discharged with residual congestion.30 Essentially, this suggests patients are being discharged too soon and while still decompensated, which would certainly raise the chances of readmission within a 30-day window. The newest potential player in the world of remote monitoring is a noninvasive, wearable vest. The device uses ReDS (Sensible Medical, Tenafly, NJ, United States) (remote dielectric sensing) which is technology originally used in military defense, and dielectric principles to estimate fluid levels in the lung. These principles refer to a material’s ability to conduct electricity. Air possesses a low dielectric coefficient, whereas water possesses a very high coefficient. This multiuse vest has 2 sensors positioned on the anterior and posterior thoracic areas to transmit and intercept low-power electromagnetic signals through lung tissue. The sensors do not require skinto-skin contact and can be placed over clothing. The sensors calculate fluid volume within 90 seconds.31 Data from the vest allow providers to estimate the fluid balance in the lungs and potentially identify decompensation before weight gain or symptoms of congestion occur. The ability of the device to identify lung fluid was demonstrated in the laboratory using pigs who were subjected to myocardial infarction by comparing the ReDS data with serial chest computed tomographic scans results.31 Researchers then validated the device on humans by comparing ReDS data with the physical examinations, laboratory data, chest radiographs, and intake/output of both HF patients and healthy volunteers. Another observational study that compared ReDS values with computed tomographic scan results of patients admitted with and without acutely decompensated HF also identified that the ReDS system accurately estimates lung fluid volume.32 This work then led to a www.npjournal.org
subsequent small study that used the data obtained from the vest to guide the therapy of 50 acutely decompensated HF patients after discharge from the hospital. During the management period, the treatment cohort appreciated an 87% reduction in readmission. When therapy with the vest was discontinued, readmission rates rose. This small group of patients was comprised of both HFrEF and HFpEF patients, 38% of whom were women.33 Consequently, this vest shows promise in managing both types of HF with less risk than an implanted device. Similar to data found in the IMPEDANCE-HF trial, another study on the ReDS device found that HF patients are likely being discharged before the acute decompensation is truly resolved. The ReDS vest was used to guide the timing of discharge of clients hospitalized with decompensated HF. When deemed ready for discharge based on existing clinical markers, volume status was then evaluated using the ReDS technology. Data were collected, and those in the control arm were discharged regardless of the ReDS value. If the vest discovered the patient appeared to still be decompensated, those in the treatment arm remained admitted and further intravenous diuresis was administered. The increased use of intravenous diuretics did not appear to cause greater renal insufficiency. Results indicated that despite documentation of thorough diuresis by traditional methods (intake/output, symptoms, physical assessment, and weight loss), over 30% of the patients deemed ready for discharge were still inadequately decongested, which increased the risk of readmission.34 Patients are simply being discharged too soon, and existing clinical markers are not as accurate as previously believed to be. DISCUSSION
As evidence grows on the underlying pathophysiology of HF, it becomes apparent that the key to reducing acute cardiac decompensation, which results in hospital admission, is early identification. Symptoms historically monitored by providers or telehealth systems such as worsening edema, weight gain, exercise intolerance, or dyspnea occur late in the process. In fact, the occurrence is so late even aggressive The Journal for Nurse Practitioners - JNP
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outpatient treatment often fails to prevent further decompensation. Consequently, efforts to reduce readmission by this method have largely failed.12-14,27 Newer technology shows promise in more effective management of HF simply because the devices identify volume shifts early enough in the decompensation continuum to allow for appropriate medication adjustment. Noninvasive devices appear safe. Trials using these devices suggest a reduction in readmission rates and also indicate that HF patients are often discharged before decompensation is fully resolved.33 Although ongoing, larger clinical trials are needed to build additional evidence, these devices offer hope for improved HF outcomes.
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CONCLUSION
Increasing HF incidence and the resulting physical, emotional, and financial cost to patients, society, and the health care system is alarming. Acute HF decompensation begins to occur weeks before subjective and objective symptoms present. Subsequently, the traditional methods of surveillance have failed to reduce hospital readmission rates. Innovative technology offers a new path to identifying decompensation early enough to initiate therapy that may reduce readmission rates and improve overall HF outcomes.
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21. References 1. Benjamin EJ, Virani SS, Callaway CW, et al. Heart disease and stroke statistics—2018 update: a report from the American Heart Association. Circulation. 2018;137(12):e67-e492. https://doi.org/10.1161/CIR. 0000000000000558. 2. Fraiche A, Eapen Z, McClellan MB. Moving beyond the walls of the clinic. JACC Heart Fail. 2017;5(4):297-304. https://doi.org/10.1016/j.jchf.2016.11.013. 3. Centers for Medicare & Medicaid Services. Readmission reduction program (HRRP). https://www.cms.gov/Medicare/Medicare-Fee-for-Service-Payment/ AcuteInpatientPPS/Readmissions-Reduction-Program.html. March 20, 2018. Accessed April 23, 2018. 4. Keller KB, Sabatino D, Winland-Brown JE, Porter BO, Keller MB. Cardiovascular problems. In: Dunphy L, Winland-Brown J, Porter B, Thomas D, eds. Primary Care: The Art and Science of Advanced Practice Nursing. Philadelphia, PA: FA Davis Company; 2015:430-503. 5. Nicholson C. Chronic heart failure: pathophysiology, diagnosis, and treatment. Nurs Older People. 2014;26:29-38. https://doi.org/10.7748/nop.26.7. 29.e584. 6. Fudim M, Hernandez A, Felker M. Role of volume redistribution in the congestion of heart failure. J Am Heart Assoc. 2017;6:e006817. https://doi.org/ 10.1161/JAHA.117.006817. 7. McDonald, Ashley EA, Fedak PW, et al. Mind the gap: current challenges and the future state of heart failure care. Can J Cardiol. 2017;33(11):1434-1449. https://doi.org/10.1016/j.cjca.2017.08.023. 8. Yancy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2013;128:e240-e327. https://doi.org/10.1161/CIR. 0b013e31829e8776. 9. Yancy CW, Jessup M, Bozkurt B, et al. 2017 ACC/AHA/HFSA focused update of the 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology/American Heart Association
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29. Casey T. Cost effectiveness of the CARDIOMEMS device for heart failure remains questionable. http://www.cardiovascularbusiness.com/topics/ healthcare-economics/cost-effectiveness-cardiomems-device-heart-failureremains-questionable. September 8, 2016. Accessed April 23, 2018.
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30. Shochat M, Shotan A, Blondheim D, et al. Non-invasive lung IMPEDANCEGuided preemptive treatment in chronic heart failure patients: a randomized controlled trial (IMPEDANCE-HF Trial) [published erratum appears in J Card Fail. 2017;23(6):512-513. J. Card Fail. 2016;22:713-722. https://doi.org/10.1016/ j.cardfail.2016.03.015. 31. Amir O, Rappaport D, Zafir B, Abraham WT. A novel approach to monitoring pulmonary congestion in heart failure: initial animal and clinical experiences using remote dielectric sensing technology. Congest Heart Fail. 2013;19(3):149-155. https://doi.org/10.1111/chf.12021. 32. Amir O, Azzam Z, Gaspar T, et al. Validation of remote dielectric sensing (ReDS) technology for quantification of lung fluid status: Comparison of high resolution chest computed tomography in patients with and without acute heart failure. Int J Cardiol. 2016;221:841-846. https://doi.org/10.1016/j.ijcard. 2016.06.323. 33. Amir O, Ben-Gal T, Weinstein J, et al. Evaluation of remote dielectric sensing (ReDS) technology- guided therapy for decreasing heart failure re-hospitalizations. Int J Cardiol. 2017;240:279-284. https://doi.org/10.1016/j.ijcard.2017.02.120. 34. Bensimhon D, McLean D, Chase P, Wood D, Garman V, Curran L. Readiness for discharge of heart failure patients based on ReDS lung fluid measurement. J Card Fail. 2017;23(8):S66. http://www.onlinejcf.com/article/ S1071-9164(17)30405-0/pdf.
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Natalie Murphy, PhD, FNP-BC, is an associate teaching professor at the University of Missouri, St Louis University in St Louis. She is available at [email protected]. Margaret Shanks, MSN, FNP-BC, ACGNP-BC, is a heart failure nurse practitioner at Penn Cardiology at Penn Presbyterian Medical Center, University of Pennsylvania in Philadelphia. Pamela Alderman, MSLIS, HBOI, is a library director at Florida Atlantic University in Ft Pierce. In compliance with national ethical guidelines, the authors report no relationships with business or industry that would pose a conflict of interest. 1555-4155/18/$ see front matter © 2018 Elsevier Inc. All rights reserved. https://doi.org/10.1016/j.nurpra.2018.07.004
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