Can We Stop Heart Failure at Its Source?

In this segment from the latest episode of Moving the Needle in Medicine, host Alex Hajduczok, MD, a cardiologist and heart failure specialist at Oklahoma Heart Institute, sits down with Philip Adamson, MD, MSc, chief medical officer at CVRx, to discuss Adamson’s perspective on the recent advancements in heart failure care and the ongoing trials of future treatment techniques.

Check out the full episode on Adamson’s full cardiology career here.

The conversation begins with a reflection on the evolution of Adamson’s career and the continuity of his scientific focus despite transitioning across different areas of cardiovascular medicine. He explains that, although others have viewed these shifts as changes in specialty, his underlying objective has remained constant: understanding the fundamental mechanisms of disease. Emphasizing the importance of viewing medicine through the lens of pathophysiology rather than rigid sub-specialization, he argues that cardiovascular disorders cannot be fully understood in isolation. Instead, clinicians should recognize the complex interplay between the electrical, mechanical, autonomic, and circulatory systems that collectively influence cardiac function and disease progression.

The discussion then turns to the historical evolution of heart failure management, highlighting the shift from a hemodynamic model of disease to the now well-established neurohormonal hypothesis. Recalling the early 1990s, Adamson describes how the recognition that maladaptive neurohormonal activation drives heart failure progression fundamentally transformed therapeutic strategies. He reflects on the initial skepticism surrounding beta-blocker therapy, noting that many clinicians doubted the failing heart could improve structurally. Subsequent clinical evidence demonstrating reverse ventricular remodeling and improved survival, however, validated the concept that interventions targeting disease mechanisms could modify the natural history of heart failure rather than simply relieve symptoms.

Building on this framework, Adamson explains the physiologic role of the carotid baroreceptors as the body's primary sensors of circulatory status. He describes how reduced cardiac performance leads to diminished baroreceptor signaling, causing the brain to misinterpret heart failure as a state of hypovolemia or hemorrhage. This perceived threat initiates a cascade of maladaptive responses, including sympathetic nervous system activation, renin-angiotensin-aldosterone system stimulation, and inflammatory signaling. While current guideline-directed medical therapies effectively block many of these downstream pathways, he characterizes them as protecting target organs from the consequences of persistent neurohormonal activation rather than addressing its central origin.

The conversation subsequently focuses on baroreceptor activation therapy (BAT) as a novel strategy designed to intervene earlier in this pathophysiologic cascade. By electrically stimulating the carotid sinus nerve, BAT restores afferent signaling to central autonomic control centers, reducing sympathetic outflow, enhancing parasympathetic activity, and attenuating inflammatory responses. Adamson contrasts this approach with conventional pharmacologic therapies, describing it as an opportunity to reduce the neurohormonal "storm" itself rather than simply shielding organs from its downstream effects. He suggests that directly modulating the autonomic nervous system may provide a more comprehensive strategy for slowing heart failure progression.

To conclude the discussion, attention shifts to the ongoing Benefit HF trial, which Adamson notes is expected to enroll approximately 2,500 randomized patients, making it the largest device-based heart failure trial conducted to date. He explains that the study aligns with emerging perspectives reflected in recent heart failure consensus statements, which emphasize defining heart failure according to impaired cardiac function and underlying pathophysiology rather than relying solely on ejection fraction thresholds. By evaluating BAT in patients with ejection fractions below 50%, the trial seeks to determine whether earlier autonomic modulation can improve clinical outcomes across a broader population of patients with heart failure and further redefine the role of device-based therapies within contemporary heart failure management.

Editors’ Note: Hajduczok reports disclosures with CVRx, Edwards Lifesciences, and Impulse Dynamics. Adamson reports employment with CVRx.