Sleep Apnea and Cardiovascular Disease

Abstract

Obstructive sleep apnea (OSA), a widely prevalent disease, is the most frequent form of sleep-disordered breathing encountered by adults of all age groups and is associated with serious medical, public health, and economic sequelae. During the last 2 decades, the cardiovascular consequences associated with OSA continue to unfold. These include hypertension, coronary artery disease, congestive heart failure, arrhythmia, stroke, insulin resistance/diabetes, and pulmonary hypertension. The association with systemic hypertension is most compelling and believed to be causal. Increasing evidence accrues for the remaining cardiovascular spectrum. Myocardial infarction, stroke, arrhythmia, and death appear to be more common or premature in those afflicted with OSA than the general population. Although the mechanisms underpinning the relationships with cardiovascular disease are not fully elucidated, investigators propose that the consequences of chronic, intermittent hypoxemia, and repetitive apnea include fluctuations in sympathetic drive, endothelial dysfunction, and inflammatory mediators. A large proportion of patients remain undiagnosed and untreated despite an increasing understanding of the deleterious health and economic effects of OSA.T he advancement in our understanding of cardiovascular pathophysiology has led to the recognition of the importance of sleep-disordered breathing (SDB) and its role in cardiovascular disease. Positive cardiovascular outcomes have been reported anecdotally by treating sleep apnea with tracheostomies. 1,2 Since then, the field of sleep and cardiovascular medicine has exploded with a multitude of experimental, cross-sectional, case-controlled, randomized, and longitudinal studies to address a range of associations between the 2 disease entities. The main areas of interest have focused on SDB's link with several cardiovascular disorders including hypertension, coronary artery disease (CAD), and congestive heart failure (CHF), as well as potential mechanisms of association such as endothelial dysfunction, inflammation, and hypercoagulability.A number of factors have hampered the establishment of associations and causality in the field of SDB and cardiovascular disease. First, the definition of SDB, especially hypopneas, has not been standardized. In addition, the cut-off point for a given number of apnea events to define a sleep disorder is inconsistent. Further complication is anticipated with increasing demand for evaluation and the resultant expansion in use of home-based diagnostic techniques. Cardiovascular disease and SDB populations share many common attributes such as body mass index (BMI), age, and sex that can confound interpretations and results. Moreover, sleep apnea, in and of itself, is a disorder that is plagued by under diagnosis and lack of an aggressive approach to treatment. 3 Nonetheless, the relationship between SDB and cardiovascular disease is clinically relevant since patients with SDB have a 13.4% increased risk for developing a cardiovascular event over a peri...

Chronobiological Aspects of Impact of Apnoic Episode and Reoxygenation on the Electrical Myocardial Properties and Autonomic Nervous System Activity in Wistar Rats

“…Apneic episodes significantly (p<0,001) decreased the VAT in both light parts of the day and eliminated LD differences. The results clearly demonstrate and confirm the pro-arrhythmogenic effects of apneic episodes(Budhiraja and Quan, 2005;Schulz et al, 2006;Aronow, 2007;Patel and Rosen, 2007; Arias and Sanchez, 2007). In our model, we initially stated that the pro-arrhythmogenic effects of apneic episodes act in the same manner regardless of whether they are in the light (non-active) or dark (active) part of the day for rats (figure 2).…”

“…However, establishing the pathogenic mechanisms are not clear and precise contribution of OSA or CSA in the development of cardiovascular disease is not fully understood (Arias and Sanchez, 2007). Increased sympathetic activity induced by hypoxia, blood viscosity, inflammation (Chowdhuri et al, 2007;Patel and Rosen, 2007) or increased oxidative stress (Schulz et al, 2006) may mediate establishing pathogenesis. In both of these disorders are described serious complications significantly increasing the risk of arterial hypertension, coronary heart disease, heart rhythm disorders, including myocardial infarction.…”

“…Apnea episodes produce not only short-term systemic hypoxia as well as hypercapnia and acidosis, where not only the myocardium is suffering disorders (Budhiraja and Quan, 2005;Schulz et al, 2006;Aronow, 2007;Patel and Rosen, 2007;Arias and Sanchez, 2007), but also the central nervous system. These clinical trials unambiguously ascribe the increased risk of cardiac events to apneic episodes occuring during sleep.…”