The emerging concept of glycocalyx damage as the trigger of heart failure onset and progression

Abstract

The suppression of adrenergic and renin-angiotensin-aldosterone system (RAAS) activity, exaggerated due to hypoperfusion-related hypoxia and/or sodium retention, is crucial for drugs’ efficacy in heart failure (HF). Both, insufficient oxygenation and excess sodium impair the glycocalyx-dependent microcroperfusion and peripheral metabolism, therefore enhancing the adrenergic and RAAS activity. The local renal and pulmonary RAAS activity and hypoxia increase sodium retention. Interstitial sodium accumulation activates interstitial inflammation and coagulation disorders that further diminish glycocalyx-supported microperfusion and peripheral metabolism. The main trigger of glycocalyx damage in reduced ejection fraction (EF) HF is hypoxia; whereas, in HF preserved EF sodium retention prevails; both stimulate left ventricular (LV) cardiac output (CO), however, impair microperfusion and metabolic heat production. Infrared-dependent, surface-induced flow (SIF) and diamagnetic properties of oxygenated haemoglobin; both improve non-Newtonian blood flow. Therefore, the temperature-driven SIF augments the deoxygenated erythrocytes' flow, while the pulmonary oxygenation of haemoglobin, by diamagnetic properties, enables frictionless erythrocytes’ flow in the oxygenated blood compartments complementing the cardiac function in HF.