Increased Sympathetic Activity as Possible Etiology of Hypertension and Left Ventricular Hypertrophy in Patients with Obstructive Sleep Apnea

Abstract

A high prevalence of systemic hypertension in subjects suffering from obstructive sleep apnea syndrome (OSAS) is indicated from several recent reports [1-3]. Retrospective epidemiological studies indicate that hypertension is also overrepresented among habitual snorers [4–6], although the pathophysiological role of habitual snoring in systemic hypertension has been debated [7]. Pulmonary hypertension and cardiac arrhythmias seem to be other cardiovascular complications associated with OSAS [8, 9]. Although the pathogenetic link between snoring and/or apneic events and hypertension remains to be resolved, both metabolic (hypoxia during apnea) and physical (negative intrathoracic pressure during apnea) mechanisms may be implicated in the genesis of long-term changes in hemodynamics and cardiac function. Intermittent apneic breathing during sleep is hemodynamically associated with a complicated pattern of events, involving cyclic shifts between bradycardia and tachycardia [10, 11], biphasic changes in central pressures, and cardiac output [12, 13]. The cyclic variations are not seen in patients with defective autonomic nervous control of the heart (e.g., heart transplanted patients) [10], indicating that the accelerative phase of the cardiac rate response is associated with increased sympathetic outflow. Thus, there is a potential basis for cardiac structural changes as well as development of systemic hypertension.

This research was supported by grants from the Swedish Heart and Lung Foundation and from Lundberg’s Research Foundation.