Zuzana Dorková, Ružena Tkáčová
Recent epidemiologic studies suggest that obstructive sleep apnea (OSA) is an independent risk factor of arterial hypertension, stroke and ischemic heart disease. In patients with congestive heart failure, sleep apnea is a risk factor for the progression of left ventricular dysfunction. In the pathogenesis of the negative cardiovascular consequences of OSA, following mechanisms are involved: sympathetic activation and parasympathetic withdrawal resulting from intermitent hypoxemia at night and arousals from sleep, increases in left ventricular afterload due to increases in systemic blood pressure at the termination of apnea, and endothelial dysfunction. In addition, oxidative stress, systemic inflammation, hormonal changes and impairment in the hemocoagulation system may be involved. Noninvasive ventilation is the cornerstone in the management of OSA. In patients with coexisting sleep apnea and arterial hypertension or heart failure, the therapeutic goal is to reduce nocturnal sympathetic nervous system activity and blood pressure by improving the pharmacological therapy of these diseases, and elimination of sleep apnea by noninvasive ventilation.