Heart failure with preserved ejection fraction (HFpEF) is comprised of a seeming multitude of pathophysiologic processes including diastolic dysfunction, impaired ventricular-arterial coupling, atrial pathology, endothelial dysfunction, and myocardial fibrosis. While this apparent dizzying complexity exists, the core pathology, the sine qua non, of HFpEF is left heart congestion leading to elevated pulmonary venous pressures and exercise intolerance. Despite its obligatory presence, defining and employing invasive measurements of left heart congestion in the assessment of HFpEF remains challenging.

Increased total blood volume and excessive redistribution of blood to the central circulation are thought to be major contributors to increased pulmonary and cardiac filling pressures in patients with heart failure, especially during exercise. These factors are considered important determinants to exercise limitations and decompensation events in heart failure.1 While total blood volume can be influenced by diuretic therapy, redistribution of blood between peripheral and central circulations, which is mainly attributed to excessive sympathetic tone leading to constriction of splanchnic veins and reduction of splanchnic capacity, has recently been recognized as a potential target to improve heart failure outcomes.

Adverse autonomic nervous system activation, characterized by neural and hormonal sympathetic overactivity and parasympathetic withdrawal, plays an important role in disease progression of heart failure (HF) with reduced ejection fraction (HFrEF).1 Carotid baroreflex activation therapy (BAT, Barostim™) is an emerging therapy for HFrEF that modulates baroreceptor nerve activity, restoring baroreflex sensitivity and rebalancing systemic autonomic control systems. BAT consists of an implantable pulse generator that delivers continuous electrical stimulation of carotid baroreceptors through a lead sutured on the carotid sinus.