Role of Device Therapy in Complementing Contemporary Medical Management

Device-based therapies for heart failure (HF) have evolved significantly since 1962, when Liotta et al. first reported the surgical implantation of a pneumatic pump serving as a left ventricular (LV) ‘artificial corollary.’¹ Demonstrating the therapeutic benefit of devices is challenging due to the diversity of different endpoints used in trials, in addition to the costs and time-intensive nature of robust and well-designed trials.² In an effort to address these barriers and expedite the translation of innovative technologies into clinical practice, the Food and Drug Administration (FDA) launched the Expedited Access Pathway in 2015. This initiative later restructured into the Breakthrough Devices Program in 2018 to accelerate the development and review of novel technologies aimed at treating high-impact conditions such as HF. To increase accessibility to these device therapies, the Centers for Medicare and Medicaid Services increased hospital reimbursement for these innovations. As a result, there has been a surge of device therapies and their respective trials in the past decade.³

Despite optimal medical management and lifestyle modifications, many patients continue to experience persistent symptoms and impaired quality of life, with some facing progression to end-stage HF and increased mortality.⁴ In this context, device-based interventions offer a therapeutic bridge or an adjunct for symptom relief and functional improvement. There has been difficulty in proving mortality benefit, as discussed below in the Limitations and Future Directions section.

This review aims to provide clinicians with an overview of current novel non-surgical device therapies for HF (Figures 1 and 2). For the purposes of the paper, we exclude discussions on ICDs, CRT, both temporary or durable forms of mechanical circulatory support, and devices that are surgically implanted or in the investigational phase.

Pressure Sensor Monitoring Devices

Cardiopulmonary congestion is the leading cause of hospitalization among HF patients. Hence, early detection and management can be critical to help improve patient outcomes.⁵ In this context, pressure sensor monitoring devices have emerged as promising tools that enable continuous or intermittent remote monitoring to guide volume management and reduce HF-related hospitalizations. Notable devices in this category include the CardioMEMS (Abbott) and Cordella (Endotronix) pulmonary artery (PA) sensors (Figure 1). These devices are generally considered safe but can be associated with serious adverse events, including vascular complications, bleeding, arrhythmias, and PA injury, which can occur in <1% of patients (Supplementary Table 1).⁶

CardioMEMS HF System

The CardioMEMS HF system is a wireless pressure sensor implanted in a distal PA branch via right heart catheterization. Approved by the FDA in 2014, the device allows for continuous monitoring of PA pressures through patient-initiated data transmissions using an external unit.^7,8 Common indications for implantation include symptomatic HF with elevation in natriuretic biomarkers or a history of HF hospitalization (HFH).⁹ Clinicians often use these readings to guide individualized diuretic adjustments.^7,8,10

The pivotal CHAMPION trial demonstrated a 39% reduction in HFH among patients in the device group compared with standard of care.¹⁰ Additional benefits of CardioMEMS include improvement in quality of life, with a significant increase in the Kansas City Cardiomyopathy Questionnaire (KCCQ) score at 12 months.⁷ The GUIDE-HF study expanded inclusion criteria to New York Heart Association (NYHA) class II–IV HF patients with either recent HFH or elevated biomarkers and reported a trend towards a reduction in HFH, urgent visits, and all-cause mortality.⁸ Major limitations of the aforementioned trials include selection of patients who were already being followed closely, a lack of standardized PA pressure-guided therapy, and a lack of blinding (i.e. investigators and participants knew who had the device). Clinicians should consider CardioMEMS for patients with symptomatic HF and recurrent HFH despite medication adherence. Ideally, patients should be capable of regular and reliable data transmission and communication with their clinician (Figure 3).

Cordella PA Pressure Sensor

The Cordella PA pressure sensor functions similarly to CardioMEMS in its ability to remote monitor PA pressures.¹¹ A distinguishing feature of the Cordella system is its integration of additional physiological data, including blood pressure, oxygen saturation, weight, and heart rate. The sensor is typically placed in the right PA. In 2024, Cordella received FDA premarket approval. The PROACTIVE- HF trial reported a composite event rate of 0.15 for HFH or all-cause mortality at 6 months, significantly lower than the prespecified performance goal of 0.43 (p<0.0001).¹¹ Clinicians should consider Cordella for patients who may benefit not only from PA pressure monitoring, like with CardioMEMS, but also from integrated daily vitals such as weight, blood pressure, and heart rate for a more comprehensive approach to remote management.

Therapeutic Devices

In this section, we discuss device-based therapies for patients with valvular heart disease, mainly in patients with severe mitral or tricuspid valve regurgitation.

Percutaneous Mitral Valve Interventions

Mitral valve pathology, most notably mitral regurgitation (MR), can contribute to the pathophysiology of HF by exacerbating volume overload, promoting pulmonary and systemic congestion, and impairing cardiac output. Non-surgical mitral valve interventions have emerged as important therapeutic modalities for HF patients and concomitant MR who remain symptomatic despite being on optimal guideline-directed medical therapy (GDMT; Figure 2; Supplementary Table 1).⁹

MitraClip

The MitraClip (Abbott) is a mitral transcatheter edge-to-edge repair system approved by the FDA in 2013. MitraClip reduces the severity of MR by percutaneously approximating the anterior and posterior mitral valve leaflets using a clip mechanism, thereby reducing regurgitant volume.¹²

The landmark COAPT trial demonstrated that MitraClip reduced all-cause mortality and HFH at 2 and 5 years in patients with HF with reduced ejection fraction (HFrEF).^12–14 In contrast, the MITRA-FR trial was a smaller randomized controlled trial that did not show statistically significant differences in all-cause mortality or HFH at 12 months.¹⁵ One proposed explanation for the discordant results between COAPT and MITRA-FR lies in the differences in patient selection and trial design. COAPT enrolled patients with more severe MR relative to LV dilation, representing so called ‘disproportionate’ MR, making these patients more likely to benefit from mitral intervention.¹⁶ In contrast, MITRA-FR participants had greater degrees of LV dilation and less severe MR, suggesting that the regurgitation was more a consequence of LV dilation rather than a cause of HF.¹⁶ Additional differences between the two trials include higher GDMT optimization, greater operatory experience and longer follow-up duration in COAPT.¹⁶ MitraClip has demonstrated a favorable safety profile, with a 97% freedom-from-adverse events rate at 12 months reported in COAPT.¹² Procedural complications, such as intra-cardiac injury, device failure, and infection, occurred in fewer than 5% of participants.¹¹

Clinicians should consider MitraClip in patients with symptomatic HFrEF and severe MR, taking into consideration the patient’s comorbidities, life expectancy, and the need for any other cardiac procedures to ensure they are an appropriate candidate and were represented in clinical trials (Figure 3).

Tricuspid Valve

Tricuspid valve pathology, predominantly tricuspid regurgitation (TR), contributes to systemic congestion, volume overload, and compromised cardiac outputs in patients with HF. Historically underdiagnosed and undertreated, TR is increasingly recognized as a therapeutic target. In patients with severe TR who are deemed high risk for surgery, transcatheter options, such as TriClip (Abbott) and EVOQUE (Edwards Lifesciences), have emerged as viable alternatives (Figure 2 and Supplementary Table 1).⁹

TriClip

The TriClip transcatheter tricuspid valve repair system, approved by the FDA in 2024, uses a percutaneous transcatheter edge-to-edge repair technique adapted from the MitraClip to reduce TR severity. The TRILUMINATE trial evaluated TriClip in 350 patients with severe symptomatic TR who were considered high risk for surgery and were on stable GDMT for at least 30 days.¹⁷ At 12-month follow-up, the rates of HFH and all-cause mortality were similar between the TriClip group and the control group.¹⁷ However, the TriClip group experienced meaningful clinical improvements, including significant reductions in TR severity (by 1–2 grades) and enhanced quality of life, as reflected in KCCQ scores.¹⁷ The procedure was generally safe, although severe bleeding occurred in 11% of participants.¹⁷ There were no reported cases of periprocedural death, device embolization, stroke, or MI; single leaflet attachment was observed in 7% of patients.¹⁷ Major limitations of TRILUMINATE include its short follow-up (12 months) for a chronic condition such as HF, the lack of sham-controlled placebo, and the lack of statistical significance between groups in objective outcomes such as mortality and hospitalization. Clinicians should consider TriClip for patients with symptomatic HF and moderate-to-severe TR who remain symptomatic despite GDMT, particularly if they are at high surgical risk and meet anatomical criteria for transcatheter tricuspid valve repair (Figure 3).

EVOQUE

EVOQUE, also approved by the FDA in 2024, is the first transcatheter tricuspid valve replacement system designed for tricuspid position. The TRISCEND and TRISCEND II trials evaluated the EVOQUE tricuspid valve replacement system in patients with TR.^18,19 TRISCEND noted improvements in NYHA classification, KCCQ, and the 6-minute walk test (6MWT) after tricuspid valve replacement.²⁰ TRISCEND II, a randomized trial comparing a device group plus optimal medical therapy (OMT) versus OMT alone, reported superior quality of life outcomes (NYHA, KCCQ and 6MWT) in the device group at 6 months in the first 150 patients recruited to the trial.¹⁹ Notably, the TRISCEND trial saw a 27% major adverse events rate at 30 days, including direct device complications, the need for a pacemaker, and severe bleeding (15% in the device group versus 5% with OMT alone).²⁰ The limitations of the TRISCEND trials also include a short follow-up, lack of sham placebo, and an open-label design. These limitations are especially pronounced in subjective or patient-reported outcomes, such as quality of life or symptoms, rather than objective outcomes. When choosing between EVOQUE and TriClip, anatomic considerations are critical. EVOQUE may be preferred in patients with larger coaptation gaps or more complex anatomy not amenable to edge-to-edge repair.²⁰

Aortic Valve

The relationship between HF and aortic valve diseases is driven by the pathophysiological alterations in LV structure and function. Aortic stenosis leads to pressure overload and concentric hypertrophy, whereas aortic insufficiency causes volume overload and eccentric remodeling. Both conditions can lead to myocardial dysfunction and HF symptoms (Figure 2 and Supplementary Table 1).²¹

Transcatheter Aortic Valve Replacement

Transcatheter aortic valve replacement (TAVR) has become a well-established therapeutic option for patients with symptomatic aortic stenosis, particularly in those deemed at increased surgical risk. Currently, three FDA-approved devices are available:

• Evolut FX (Medtronic): a supra-annular, self-expanding system;
• Sapien S3 Ultra (Edwards Lifesciences): a balloon-expandable, intra-annular valve; and
• Navitor (Abbott): a newer self-expanding, intra-annular valve.

These devices have demonstrated procedural efficiency, lower complication rates, and clinical outcomes comparable or superior to surgical aortic valve replacement.^22–26 Given the extensive literature and numerous high-quality reviews already available on TAVR and other aortic valve interventions, these therapies are not addressed in this review.

Autonomic Nervous System Modulators

Baroreflex-activation Therapy: BaroStim

Baroreflex-activation therapy is an emerging neuromodulation therapy that targets the autonomic imbalance achieved via an implanted pulse generator in the pectoral region, which modulates sympathetic and parasympathetic pathways.²⁷ The BaroStim system (CVRx) received FDA approval in 2019 for patients with NYHA class III symptoms, and LV ejection fraction (LVEF) ≤35%, who are stable on GDMT for at least 4 weeks and are not candidates for CRT.²⁷ The BeAT-HF trial reported improved quality of life outcomes and reduced N-terminal pro B-type natriuretic peptide levels at 6 months in patients treated with the BaroStim.²⁷ The trial was not powered to detect statistically significant differences in HFH or mortality. Baroreflex-activation therapy has demonstrated a favorable safety profile, with 97% of patients free from major adverse events.²⁸ The most common complication was non-life-threatening bleeding, whereas serious events, such as device embolization, were rare.²⁸ Major caveats of the BeAT-HF trial include significant between-group differences in medication adjustments, the lack of a sham control, and an open-label design. Clinicians should consider BaroStim for patients who remain symptomatic or have recurrent HFH despite OMT and who are not candidates for CRT (Figure 3).

Cardiac Contractility Modulation Therapy: IMPULSE

Cardiac contractility modulation is a novel device-based approach aimed at improving functional capacity in patients with HFrEF by enhancing cardiac contractility through non-excitatory electrical stimulation. The IMPULSE Optimizer device received FDA approval in 2019 for patients with NYHA class III, LVEF between 25% and 45%, and narrow QRS duration and without an indication for CRT.³ This device delivers high-voltage, non-excitatory impulses to the right ventricular septum during the absolute refractory period of diastole, which eventually can enhance contractility through modulation of intracellular calcium dynamics.²⁹

The FIX-HF-5C trial was a multicenter RCT that demonstrated significant improvement in peak oxygen consumption, quality of life, NYHA functional class, and exercise tolerance among patients receiving cardiac contractility modulation compared with those on OMT.²⁹ The limitations of the FIX-HF-5C trial are similar to the other trials mentioned here; for example, the lack of a sham control, short follow-up, and an open-label design. In addition, the FIX-HF-5C trial used prior FIX-HF-5 subgroup data, which may have introduced potential bias in interpretation. Clinicians should consider IMPULSE for patients with HFrEF (LVEF <45%) who remain symptomatic or have recurrent HFH despite OMT and who are not candidates for CRT (Figure 3).

Limitations and Future Directions

Effective implementation of device therapies for HF are challenged by both patient-related and systemic barriers.⁹ At the patient level, access to device therapies may be restricted by geographic limitations, particularly in patients residing in rural or underserved areas lacking proximity to specialized centers. At the provider and institutional level, barriers include variability in experience with device technologies, complex authorization process and insurance coverage, and high upfront costs.

Clinical research faces notable limitations, as many of the trials included in this review are relatively small, which can affect the statistical power to determine meaningful significant differences. In addition, mortality benefit remains particularly challenging due to low event rates of death, prompting the use of composite endpoints. The lack of head-to-head trials directly comparing the safety and efficacy of various device therapies can impede clinicians’ ability to select the most appropriate intervention for a given patient. In addition, there is insufficient evidence guiding the optimal timing of device implementation, particularly in relation to initiation or escalation of GDMT. Addressing these gaps through larger, more inclusive trials, comparative studies, and economic analyses will be helpful in refining the role of device therapies in HF management. Expanding access, streamlining training and approval processes, and refining clinical practice guidelines will be an important step in integrating device therapies into routine HF care.

Conclusion

A growing range of device-based therapies is available to reduce HF-related mortality, improve quality of life and reduce HFH. Although GDMT and lifestyle modifications remain the foundation of HF management, certain device therapies are now approved by the FDA for use in well-selected patient populations who remain symptomatic despite OMT or who are unable to tolerate the conventional therapies. Most of these devices demonstrate favorable safety profiles, with procedural complications, such as device embolization, malfunction, infection, bleeding, and vascular or cardiac injury, being uncommon yet important to recognize. Ongoing research and real-world data will be essential to fully realize the potential of these device therapies within broader HF therapies.

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