Remote Measurement of Volume Status in Heart Failure

Abstract

Heart failure admissions are driven by elevated cardiac filling pressures culminating in symptoms of congestion and result in a significant burden to both patients and society. Traditional strategies of monitoring changes in weight and symptoms to trigger adjustments in therapy, even when combined with telemedicine services, have failed to improve outcomes. Implantable hemodynamic monitors allow clinicians to obtain meaningful, objective data, with an opportunity for early intervention to improve outcomes. Patients with concomitant kidney disease represent a particularly vulnerable population with higher rates of hospitalization compared with patients with heart failure and normal kidney function. Several studies have demonstrated a reduction in hospitalization rates with the use of ambulatory hemodynamic monitors. In the following review, we discuss the existing literature, including studies in patients with kidney disease, and highlight future innovations in the field.

Introduction

The prevalence of heart failure in the United States is expected to rise significantly in the next several years,¹ correlating with higher rates of comorbidities, such as obesity and hypertension. Despite significant advancements in heart failure management, both hospitalization and rehospitalization rates continue to increase,² projecting an economic burden of approximately $160 billion.³ Patients with CKD are particularly vulnerable with rates of heart failure hospitalization inversely associated with GFR.⁴

The transition from compensated to decompensated heart failure is strongly correlated with elevated intracardiac pressures,^5–7 which do not consistently correspond with, and can occur independently of, the traditionally used metric of weight changes.⁸ In addition, increased cardiac pressures may precede symptoms of congestion, the most common indication for admission, by days to weeks.^7,9 As such, interventions relying on weights and patient-reported symptoms, even in combination with telemedicine, have failed to improve outcomes.^10,11 Implantable systems for monitoring intracardiac and pulmonary pressures may provide opportunities for early intervention and reduction in hospitalization rates.

The purpose of this review is to provide an overview of the benefits, various options, and rationale for remote hemodynamic monitoring in patients with heart failure, with a specific emphasis on patients with CKD.

Clinical Trials of Implantable Hemodynamic Monitors

Remote monitoring of heart failure using surrogate, noninvasive measures of volume status, such as weights and symptoms, has not demonstrated clinical benefit.¹¹ However, implantable hemodynamic monitors allow clinicians to use objective, clinically meaningful, and actionable measures to improve outcomes in patients with heart failure (Figure 1). The feasibility and benefit of implantable hemodynamic monitoring has been demonstrated by multiple studies using a wireless, battery-free sensor that lies in either the left or right pulmonary artery (PA).^12–15 This allows for daily recordings of PA pressures (PAPs), which are sensitive to volume status and reflect left-sided intracardiac filling pressures, a critically important hemodynamic target in heart failure management.

Figure 1.

Flow chart of indications for and outcomes of postimplantable PAP monitors. GDMT, guideline-directed medical therapy; HF, heart failure; NYHA, New York Heart Association.

The pivotal CHAMPION study¹² was a randomized controlled trial of 550 patients with heart failure (irrespective of left ventricular ejection fraction, New York Heart Association (NYHA) class 3 symptoms, and a heart failure hospitalization within the prior 12 months. All patients received implant of the CardioMEMS PAP sensor (Abbott Laboratories, Abbott Park, IL) and were randomized 1:1 to PAP-guided management versus control. Patients in the PAP-guided management group had demonstrated both clinical and hemodynamic benefits compared with the control. The cohort with PAP-guided management had a 37% reduction in heart failure hospitalizations over 15 months. In addition, PAP-guided management showed a significant decrease in PAPs over time (mean area under the curve of change in PAP versus time=−156), while patients randomized to the control group had a rise in PAP (mean area under the curve=+33) during the study period, likely due to the progressive nature of heart failure. These findings, in combination, demonstrate the importance and feasibility of ambulatory hemodynamic management in patients with heart failure. Subsequent analyses of CHAMPION demonstrated that the benefit included both patients with heart failure with reduced¹⁶ and preserved¹⁷ ejection fraction. This was followed by the GUIDE-Heart Failure (HF) study,¹³ which studied a broader group of heart failure patients, including those with NYHA classes 2–4 and those without recent heart failure hospitalization, but elevated natriuretic peptide levels. In GUIDE-HF, 1000 patients were randomized to receive PAP-guided management versus usual care, which involved a robust protocol of telephone monitoring without hemodynamic data. GUIDE-HF was performed between 2018 and 2020, and consequently, about 25% of the trial data were affected by the coronavirus disease 2019 (COVID-19) pandemic and widespread lockdowns. A prespecified pre–COVID-19 analysis of the GUIDE-HF study demonstrated that the PAP-monitored group had a 19% reduction in the primary outcome of mortality and heart failure hospitalizations at 1 year. The benefit was largely due to a 28% decrease in hospitalization in patients with NYHA classes 2 and 3 heart failure. The COVID-19 pandemic appeared to have a significant effect on this trial, primarily by substantially decreasing the event rate in the control group by 21%. In the overall analysis, hemodynamic-guided management failed to reduce the cumulative incidence of heart failure events (0.85, 0.70–1.03; P = 0.10).

In addition to these two large randomized controlled trials, observational studies have shown that the benefit of PAP monitoring may be even greater in a real-world population than that seen in a more restrictive clinical trial cohort.^18,19 Even as heart failure medical therapy continues to advance (with increasing utilization of angiotensin receptor neprilysin inhibitors and sodium-glucose cotransporter 2 inhibitors), the benefit of PAP-guided management persists.¹⁵

The benefit of PAP-guided management extends beyond its effect on heart failure hospitalizations. The MONITOR-HF study showed that PAP-guided management improves heart failure–related quality of life (QOL).¹⁴ No single randomized controlled trial has demonstrated a mortality benefit from implantable hemodynamic monitoring. However, a recent meta-analysis of three large studies (including both PAP and left atrial pressure [LAP] sensors) suggests the possibility that long-term hemodynamic management may improve mortality in patients with heart failure with reduced ejection fraction.²⁰

PAP monitoring allows for a robust measure of volume and heart failure status, but it is equally important to understand how treatment is affected by these data and how hemodynamics are affected by treatment. The predominant pharmacologic intervention in the PAP monitoring trials is diuretic adjustment, as hypervolemia is the dominant cause of elevated filling pressures in patients with heart failure. In the PAP-guided management arm of CHAMPION, there were significantly more changes (both increases and decreases) in diuretic therapy.²¹ The bidirectional nature of diuretic adjustments in patients receiving PAP-guided management underlies the concept that management of heart failure is not simply about increasing diuretics in heart failure patients who are wet but about tailoring diuretic therapy (both uptitrating and downtitrating) to patients based on an individual's dynamic hemodynamic state. Changes in vasodilator therapy (which reduce left-sided filling pressures by decreasing afterload) and other heart failure guideline-directed medical therapy (GDMT) were also more common in patients receiving PAP-guided management but still far less common than diuretic management. The net hemodynamic effect of tailored diuretic and vasodilator therapy is a sustained decrease in PAP over time, which translates into a reduction in hospitalizations and improvement in QOL. A summary of remote hemodynamic monitoring trials for the management of heart failure is presented in Table 1. The most recent American Heart Association guidelines have given implantable wireless PAP monitors a 2b recommendation, citing the need for additional data regarding clinical outcomes.

Table 1.

Summary of remote monitoring trials for management of heart failure

Trial Name	Sensor Location and Type	Trial Design	Population	Kidney Function Exclusion Criteria	GFR (or eGFR) in ml/min per 1.73 m2		Primary Outcome	Results
					Treatment	Control
CHAMPION12	PA—CardioMEMS	Randomized controlled trial	N=550 NYHA class 3 heart failure with HFH within 12 mo	GFR <25 ml/min per 1.73 m2	Mean 60±23	Mean 62±23	Rate of HFHs at 6 mo	37% reduction in HFHs in the treatment group
GUIDE-HF13	PA—CardioMEMS	Randomized controlled trial	N=1000 NYHA class 2–4 heart failure with HFH within 12 mo or elevated natriuretic peptides	GFR <25 ml/min per 1.73 m2 AND nonresponsive to diuretic therapy OR on receiving long-term dialysis	Median (IQR) 51.3 (39.3–65.3)	Median (IQR) 48.9 (38.1–64.8)	Composite: HFHs, urgent heart failure visits, and all-cause mortality at 12 mo	177 primary events in treatment group and 224 events in control group (HR, 0.81 [95% CI, 0.66 to 1.00]; P = 0.049)
MONITOR-HF14	PA—CardioMEMS	Open-label randomized controlled trial	N=348 NYHA class 3 heart failure with HFH within 12 mo	GFR <25 ml/min per 1.73 m2, refractory to diuretic therapy, or on long-term dialysis therapy	Median (IQR) 48 (35–60)	Median (IQR) 48 (38–63)	Mean difference in KCCQ score at 12 mo	Change in KCCQ of +7.05 in the intervention group and –0.08 in the control group. Between group difference of 7.13 (95% CI, 1.51 to 12.75; P = 0.013)
PROACTIVE-HF15	PA—Endotronix	Open-label, single-arm clinical trial	N=456 NYHA class 3 heart failure with HFH within 12 mo or elevated natriuretic peptides	GFR <25 ml/min per 1.73 m2 or on long-term dialysis therapy	Mean 54.7±19.7		Hospitalization for heart failure or all-cause mortality at 6 mo compared with historical trials	6-mo event rate of 0.15 events/patient was lower than historical performance goal of 0.43 events/patient
FIRE1 early feasibility study22	Inferior vena cava—FIRE1Foundry	Single-arm early feasibility study	N=15 Chronic heart failure with HFH within 12 mo, elevated natriuretic peptide and on ≥40 mg furosemide	GFR <25 ml/min per 1.73 m2	Mean 37.0±9.0		Safety of implantation and device-related complications; successful data transmission	NYHA functional class improved in 7/15 patients
VECTOR-HF23	Left atrium via interatrial septum—VLAP	Single-arm early feasibility study (n=24)	N=24 NYHA class 3 heart failure with HFH within 12 mo or elevated natriuretic peptides	GFR <25 ml/min per 1.73 m2	Mean 54.62±19.95		Successful deployment, ability to perform initial pressure measurements, safety outcomes	NYHA functional class improved in 40% of patients

CI, confidence interval; HF, heart failure; HFH, heart failure hospitalization; HR, heart rate; IQR, interquartile range; KCCQ, Kansas City Cardiomyopathy Questionnaire; NYHA, New York Heart Association; PA, pulmonary artery.

Implantation Technique

As the only US Food and Drug Administration (FDA)–approved devices for implantable hemodynamic monitoring are those that monitor the PAP (CardioMEMS and Cordella), we will focus on this technique. Implantation is typically performed under fluoroscopy in the catheterization laboratory. Venous access with a 12 French sheath typically is obtained in the femoral vein.^24–26 Alternative access through the internal jugular vein is possible as well. Before implantation, a right heart catheterization is usually performed with a PA catheter to evaluate the right atrial pressure (RAP), pulmonary arterial pressure, pulmonary capillary wedge pressure (PCWP), and cardiac output/index. Once the distal tip of the PA catheter is in a descending branch of the left PA, an angiogram with contrast is performed to assess the vascular anatomy. An adequate vessel for implantation should have a diameter of 7–15 mm and an angulation of <30°.^24–26 The left-sided PA branches are preferred over the right-sided branches as they have more of a posterior orientation, making interrogation of the MEMs device more effective. The PA catheter is exchanged for the delivery system over an 0.018″ guidewire. The pressure sensor is then deployed using the delivery system into the target vessel. The nitinol loops extending from the pressure sensor are critical to holding the pressure sensor in place in the target vessel. A PA catheter is then exchanged for the delivery system to calibrate the pressure sensor. The external electronic system is then placed in the appropriate anatomic position, usually along the patient's back, and used to calibrate the pressure sensor to the PAP of the PA catheter.

Complications of implantation can be divided into procedure-related complications, device-related complications, and diagnostic errors. Procedure-related events are uncommon, with an incidence of 1% in both the landmark clinical trial and the registry.^12,27 Procedural complications include access site complications such as groin hematoma (0.3%–0.7%), pulmonary hemorrhage, pulmonary infarction, arrhythmia, and perforation. Although there were no instances of pulmonary injury in the landmark trial, in the postmarketing surveillance, there were 28 reports out of 5500 implants of PA injury/hemoptysis leading to 14 intensive care unit stays, seven intubations, and six deaths.² Device-related complications are also uncommon, occurring in 1.1% in the CHAMPION trial and 0.3% in the postmarketing registry.^12,27 After implantation, sensor failure, malfunction, or migration occurred in 46 of 5500 implants.¹²

Considerations for Patient Selection

Before proceeding with implantable hemodynamic monitoring in patients with heart failure, several logistical, clinical, and procedural factors need to be considered. Adequate vascular access to accommodate a 12 French catheter is required in either the femoral or jugular vein.²⁸ Intracardiac devices such as pacemakers/defibrillators or a tricuspid valve repair/replacement can make implantation more complicated. Baseline hemodynamics demonstrating predominantly right ventricular failure or pulmonary hypertension may limit the yield of a PA sensor. In the cardiorenal syndrome population, an additional concern is contrast-associated nephropathy. In those with a lower GFR, the contrast necessary for implantation may result in the need for KRT. A risk score to evaluate risk of contrast-associated nephropathy before the case is helpful in discussing the risks of implantation.²⁹

There are logistical considerations as well when discussing implantable hemodynamic monitoring. The pressure sensor is not a therapy unto its own but a diagnostic tool. Unless patients can reliably submit readings and implement treatment modifications from the managing team, outcomes cannot be affected. Thus, factors such as access to high-speed internet and electricity as well as motivation to participate in more complex care are important when considering implantable hemodynamic monitoring. Those who have struggled with health care literacy, communication, and adherence to therapy may not be suitable for remote monitoring.

Despite initial FDA approval in May 2014, access to PAP sensors has been challenging due to mixed coverage from payers for PAP sensor implantation and management. However, in January 2025, the Centers for Medicare & Medicare Services provided a National Coverage Analysis for implantation of PAP sensors.³⁰ This provides coverage for patients with Medicare or Medicare Advantage who meet the Centers for Medicare & Medicare Services criteria—patients with chronic NYHA class 2 or 3 heart failure (regardless of ejection fraction) who have been on GDMT for at least 3 months and have either a heart failure hospitalization within 12 months or an elevated natriuretic peptide level within 30 days.

Establishing Hemodynamic Targets

The classic paradigm for the implantable PAP sensor is to optimize left ventricular preload or filling pressure. This is commonly accomplished through the establishment of a PA diastolic pressure range, a range of PA diastolic pressures at which one is thought to be euvolemic. This is because the PA diastolic pressure can be a surrogate for the LAP, PCWP, and left ventricular end diastolic pressure.^31,32 A PA diastolic pressure range is established once a normal diastolic pressure gradient (difference between the PA diastolic pressure and the PCWP) is confirmed. Using the diastolic pressure gradient, a PA diastolic range can be chosen to reflect a normal PCWP range of 6–18 mm Hg. Typically, the initial PA diastolic range is 8–20 mm Hg.¹³ However, this range is initially adjusted based on estimation of preload, afterload, and pulmonary vascular impedance. For instance, when there is an elevated pulmonary vascular resistance, transpulmonary gradient, or diastolic pressure gradient, this number needs to be adjusted (Figure 2). In the first few weeks after implantation, this range is often adjusted based on clinical judgment.

Figure 2.

Proposed algorithm for setting a PA diastolic target using baseline hemodynamics with implantable PAP monitors. In this algorithm, the two main decision points to determine the initial PA diastolic target range are the RA:PCWP ratio and the diastolic pulmonary gradient (A). An elevated RA:PCWP ratio is a sign of right heart failure and means that changes in PA diastolic and thus the PCWP are not as reflective of the RAP. Similarly, an elevated diastolic pulmonary gradient is usually due to precapillary pulmonary hypertension and means that the PA diastolic is not reflective of the PCWP. Those with a normal diastolic pulmonary gradient (≤5 mm Hg) can use the initial diastolic pulmonary gradient goal of 8–20 (B). However, an elevated diastolic pulmonary gradient (>5 mm Hg) needs to be considered when setting the initial PA diastolic target range (C). The initial PA diastolic target range usually requires adjustment over time based on clinical judgment. DPG, diastolic pulmonary gradient; LA, left atrium; PA, pulmonary artery; PAD, pulmonary artery diastolic; PADP, pulmonary artery diastolic pressure; PAP, pulmonary artery pressure; PCWP, pulmonary capillary wedge pressure; RA, right atrium; RAP, right atrial pressure; RV, right ventricle.

Application to Patients with CKD

The complex, bidirectional pathways between heart failure and kidney disease are well established. Patients with CKD have an estimated three-fold higher risk of incident heart failure compared with those without CKD.³³ CKD is a common and independent predictor of death and hospitalization in patients with heart failure, across the spectrum of left ventricular systolic function.³⁴ Like patients without CKD, congestion from elevated filling pressures is the primary driver of hospitalizations. However, GDMT and diuretics are underutilized due to concern for electrolyte abnormalities, azotemia, and worsening kidney function.³⁵ In addition, elevated central venous pressures can negatively affect GFR (Figure 3). The most robust data for remote hemodynamic monitoring in this population come from studies assessing the effect of PAP monitoring using the CardioMEMS system.

Figure 3.

Knowledge gaps with the use of remote hemodynamic monitoring, with both currently approved and developmental devices.

In the CHAMPION and MONITOR-HF trials, the average eGFR for participants was 60 and 48 ml/min per 1.73 m², respectively, and those with an eGFR <25 ml/min per 1.73 m² were excluded. The CHAMPION trial included 150 participants in the treatment group, compared with 147 participants in the control group with CKD at baseline. Consistent with prior data, patients with CKD had overall higher rates of heart failure hospitalization compared with the control population. Patients with CKD managed with PAP monitoring had reduced rates of hospitalization compared with those patients with CKD managed with standard of care (0.48 versus 0.83; heart rate, 0.58; P < 0.001). In addition, benefits of PAP monitoring in the CKD group were comparable with the overall treatment effect observed in the parent trial (0.48 versus 0.45; heart rate, 1.05; P = 0.69).³⁶

In a retrospective analysis of the CardioMEMS US postapproval study, which was a multicenter, prospective, open-label study assessing the use of PAP-guided management in a postmarket, real-world setting, the average eGFR was roughly 53 ml/min per 1.73 m², and similarly, patients with an eGFR <25 ml/min per 1.73 m² were excluded. In the retrospective analysis, patients were grouped in quartiles by baseline eGFR: eGFR >65 ml/min per 1.73 m² (Q1), eGFR >50 and ≤65 (Q2), >37 and ≤50 (Q3), and ≤37 (Q4). Hospitalization rates were lower in the 12 months after sensor implantation in each of the eGFR quartiles compared with the 12 months before enrollment, including a 47% reduction in the lowest eGFR quartile. Lower hospitalization rates were associated with lower PAPs. Diuretic dosing was the most frequently changed medical intervention in the study. These findings are limited by the open-label design and lack of control group.

In a separate retrospective real-world analysis of 117 patients, heart failure hospitalizations 1 year pre-CardioMEMS and post-CardioMEMS device insertion was assessed in patients with concomitant CKD. The 26 patients with a creatinine clearance ≤29 mL/min had higher preimplantation rates of heart failure admissions (2.42±1.63) compared with 91 patients with a creatinine clearance ≥30 mL/min (1.82±1.34). Hospitalization rates decreased in both groups postimplantation, 0.84±1.19 and 0.35±0.73, respectively, with no statistically significant difference between groups, P = 0.77.³⁷

Data regarding long-term kidney outcomes because of remote hemodynamic monitoring are limited. In the CardioMEMS US PAS study, 911 participants had follow-up kidney function data available. Of these, the majority (n=530) had stage 3 CKD and a minority (n=84) had stage 4 CKD or worse. In the 12-month follow-up period post–CardioMEMS implantation, participants with stage 4 or worse CKD had greater improvement in kidney function (39.3%) compared with those with stage 3 CKD (8.9%), which was defined as improvement by at least one CKD stage.³⁸ Unfortunately, specific data regarding granular changes in eGFR are not available.

It is worth noting that a high RAP, or central venous pressure, which reflects systemic venous congestion, is more directly associated with poor kidney outcomes as compared with PCWP^39–42; therefore, using a PA diastolic range to optimize left ventricular filling pressures may not represent the ideal hemodynamic variable to target when adjusting therapy in this population. Instead, a PA diastolic range could theoretically be chosen to reflect an ideal RAP range using the right atrium (RA):PCWP ratio at baseline. Typically, there is a linear relationship between the RAP and PCWP in those with heart failure with a RA:PCWP ratio of 0.62.⁴³ However, the relationship between the RAP and the pulmonary arterial pressure is complicated and sometimes unpredictable. An elevated RA:PCWP ratio will need to be considered when setting PA diastolic pressure goals. As with standard heart failure patients, the PA diastolic pressure range in patients with cardiorenal syndrome needs to be adjusted in the immediate period postimplantation based on clinical judgment. This paradigm may influence device selection as additional products become available.

Application to Patients on Hemodialysis

Volume excess is common among patients with kidney failure undergoing hemodialysis and can lead to comorbidities such as heart failure. Although the term dry weight lacks a consensus definition, studies have shown that a significant proportion of patients undergoing hemodialysis are above their prescribed dry weight.^23,44 Current tools to determine dry weight are inaccurate in most patients with currently used methods.²³ The common strategy of assessing pedal edema has been shown in studies to be of poor clinical utility.^45,46 Lung ultrasound has demonstrated promise,⁴⁷ although is limited to small studies, and furthermore requires operator expertise and can be time-consuming to incorporate during dialysis rounds. The use of remote hemodynamic monitoring in patients with concomitant heart failure and kidney failure requiring dialysis, in whom pulmonary hypertension has been shown to be an independent predictor of mortality,⁴⁸ is primarily relegated to sparse case reports, which have not reported meaningful outcomes.⁴⁹ A small prospective study of eight patients with kidney failure undergoing hemodialysis received a CardioMEMS system, which demonstrated elevated pulmonary pressures even when patients were at their prescribed “dry weight.”⁵⁰ In the PEPPER study, which was a single-center study out of Germany, patients with kidney failure requiring hemodialysis who had unexplained dyspnea underwent right heart catheterization prehemodialysis and posthemodialysis and were compared with patients with CKD not requiring dialysis. Elevated pulmonary pressures were identified in 25 of 31 (81%) patients before dialysis, as compared with 22 of 31 (71%) nondialysis CKD patients. Mean PAPs improved postdialysis (62±18 to 55±17); however, pulmonary hypertension (PH) persisted in 24/31 (77%) of participants, with 20/31 consistent with postcapillary PH. This likely represents persistent volume overload, which has been supported by the observation that PH improves after kidney transplantation.⁵¹ This study is limited by the fact that pulmonary pressures were only ascertained in patients with dyspnea and may not be broadly applicable. In addition, information regarding hemodialysis treatments and dry weights was not provided.

A technical consideration that may need to be considered is the possible hemodynamic effect of an arteriovenous fistula for dialysis access. Shunting of blood from the arterial to the venous system results in a significant decrease in systemic vascular resistance, leading to increased cardiac output. The increase in venous return must be accommodated by pulmonary vasculature. However, endothelial dysfunction as a consequence of kidney failure, pulmonary arterial disease, or chronic heart failure results in progressive pulmonary arterial disease.⁵² This may alter the relationship between right atrial, PA, and LAPs, and re-evaluation of PAPs targets may be warranted. Ultimately, the effectiveness of remote hemodynamic monitoring to improve outcomes in this population requires further study.

Future Innovations in Ambulatory Hemodynamic Monitoring

Previous studies using PAP sensors have provided foundational evidence to support the concept that ambulatory hemodynamic monitors improve hemodynamics and clinical outcomes in patients with heart failure. Currently, there are two PAP sensors that are FDA approved for management of patients with heart failure including CardioMEMS (Abbott Laboratories) and Cordella (Edwards Lifesciences). In addition, there are several novel devices and approaches to ambulatory hemodynamic monitoring. A LAP sensor can be deployed across the atrial septum to provide a direct intracardiac pressure measurement. Early safety concerns delayed development of this approach, but a new LAP sensor (VLAP, Vectorious Medical) is being studied in patients with heart failure.^53,54 A novel aspect of this study includes incorporation of patient self-management to minimize provider burden in patients with mild elevations in LAP.⁵² Another sensor that measures both left and RAPs had its first-in-man implantation in 2023 (Shifa Med, Adona).⁵⁵ This device also includes an adjustable intra-atrial shunt, which can shift volume from a stiff left atrium into a compliant right heart. Clinical experience is still in early development, but this may provide additional hemodynamic data in patients with biventricular heart failure or significant systemic venous congestion, which is not always accurately reflected by PAP or LAP sensors. Venous congestion may also be better captured by a novel inferior vena cava sensor (FIRE1Foundry) that measures changes in inferior vena cava diameter as a reflection of volume status. The first-in-man experience has been published,²² and future clinical trials to determine its clinical utility are expected.

In addition to implantable hemodynamic sensors, there are insertable, noninvasive, and wearable monitors under development.⁵⁶ They use a variety of technologies including electrocardiography, heart rate measurements, physical activity, respiratory rate, thoracic impedance, heart sounds, ballistocardiography, and impedance plethysmography, among others. Many of these devices have leveraged machine learning artificial intelligence to create algorithms and scores that inform clinicians of heart failure risk. Studies will be required to see if these signals are robust enough to influence management and allow for tailored approaches to diuretic and heart failure treatment. A single-arm study (MANAGE-HF)⁵⁷ using the HeartLogic algorithm embedded in Boston Scientific defibrillators has demonstrated the feasibility and safety of this approach, but an ongoing randomized controlled trial will help determine the clinical effectiveness.

Conclusion

Current strategies to monitor volume status in ambulatory patients with heart failure have failed to improve outcomes. Remote hemodynamic monitoring provides objective, real-time, and actionable data that have demonstrated a reduction in cardiac filling pressure, reduced hospitalization rates, and improved QOL, including in patients with concomitant CKD. Data in patients with kidney failure are lacking and sorely needed to address this particularly vulnerable population. PAP monitors have provided foundational data to pave the way for future innovations, including invasive and noninvasive systems, combined with artificial intelligence, which may allow for more personalized algorithms and further improve care.

Disclosures

Disclosure forms, as provided by each author, are available with the online version of the article at http://links.lww.com/JSN/F378.

Author Contributions

Writing – original draft: Nayan Arora, Christopher Chien, Conrad J. Macon.

Writing – review & editing: Nayan Arora.

Funding

None.