Impact of Sleep-disordered Breathing on Vascular Dysfunction and Ventricular Arrhythmias in Heart Failure Patients

Abstract

Breathing disorders have recently received particular attention, because periodic and non-periodic irregular breathing are frequently observed in patients with chronic heart failure and seem to be linked to autonomic dysfunction and worsening heart failure. Pathophysiologic problems of these respiratory instabilities in heart failure are sympathetic nerve activation, carbon dioxide chemoreflex hypersensitivity, and hemodynamic deterioration. Generally, the instability of the negative feedback system such as respiratory control arises from delayed signaling and high controller gain, which could correspond to circulatory delay caused by low cardiac output and enhanced chemosensitivity in heart failure. Clinical data suggest that sympathoexcitation is one of the important causes of chemoreflex hypersensitivity. On the other hand, the enhanced chemosensitivity facilitates unstable respiration such as Cheyne-Stokes respiration, which augments sympathetic tone further. Another type of respiratory instabilty is the non-periodic irregular respiration which is likely caused by nonchemical ventilatory modulation such as stimulation of afferent vagal endings by the elevation of pulmonary artery pressure and lung congestion. These respiratory instabilities are not only related to severity of cardiac dysfunction and functional capacity, but the key to enforce vicious circle of sympathetic and chemoreflex augmentation and eventually worsening hemodynamics. These findings indicate that respiratory instability faithfully reflects worsening heart failure and that respiratory stabilization therapy could improve heart failure through the suppression of chemosensitivity and sympathetic nerve activity.