ABSTRACT
The respiratory and cardiovascular systems must act in concert to transfer oxygen (O2) and carbon dioxide (CO2) between the atmosphere and the cells. Accordingly, their control systems must be integrated to ensure that the metabolic needs of the tissues are met under varying conditions in response to demands. Both cyclic changes in breathing and sustained changes in alveolar ventilation exert important effects on the cardiovascular system (1). These effects are particularly prominent in patients with obstructive sleep apnea (OSA), who experience recurrent episodes of asphyxia during sleep associated with cyclic fluctuations in heart rate, blood pressure, cardiac output, and systemic O2 delivery (2). Therefore, it is not surprising that from the beginning of clinical research in sleep apnea, an association between OSA and cardiovascular disease was recognized. Initially, a high prevalence of nocturnal cardiac arrhythmias, systemic and pulmonary hypertension, and cor pulmonale among patients with OSA was described (3-6). More recently, there is a growing body of evidence implicating OSA in the development or progression of left ventricular (LV) hypertrophy and dysfunction (7,8). For example, a study from our laboratory has demonstrated an association between OSA and certain cases of LV
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heart failure of otherwise unknown etiology (9). Moreover, the treatment of these patients with continuous positive airway pressure (CPAP) was associated with an improvement in cardiac function measured during the day. These data indicate, first, that elimination of OSA by CPAP was responsible for the improvement in LV function and, second, that OSA was contributing to the development of LV dysfunction in these patients (9).
