الفهرس 
Aim of the workOnly 14 pages are availabe for public view
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Abstract
Obstructive sleep apnea (OSA) is sleep disorder that involves cessation or significant decrease in air flow in the presence of breathing effort. It is the most common type of sleep-disordered breathing (SDB) and is characterized by recurrent episodes of upper airway collapse during sleep. This collapse leads to loud snoring, arousal with or without oxygen desaturation, sleep fragmentation, excessive daytime sleepiness, and poor quality of life.1
The prevalence of OSA is high and its prevalence rates are also expected to increase in the future owing to an aging population, and also because obesity, which is strongly associated with OSA, is increasing dramatically in both children and adults.13
The gold standard to assess OSA is polysomnography or multichannel respiratory polygraphy (―sleep study‖).8
The apnea-hypopnea index (AHI), which is standard metric of sleep disordered breathing, is defined as the number of apneas or hypopneas that occur during sleep divided by the sleep time in hours. The American Academy of Sleep Medicine (AASM) classifies OSA severity in according to AHI as mild (5-15 events per hour), moderate (>15-30 events per hour), or severe (>30 events per hour).23
Strong connection is established between cardiovascular complications and OSA. Three major pathological changes are considered to be the contributors to acute adverse cardiovascular complications: hypoxemia, the generation of excessive negative intrathoracic pressure against an occluded pharynx and its effects on right and left ventricular (LV) function, and repeated arousals from sleep. The main effects of these changes include sympathetic nervous system activation, leading to surges in HR and BP, increased atrial and ventricular wall stress, myocardial workload and myocardial oxygen demand (and possibly myocardial ischemia), as well as decreased myocardial contractility and cardiac output. All these changes may promote the development of arrhythmias.28
One serious complication of OSA is sudden cardiac death (SCD).5complex ventricular arrhythmias reported in OSA patient may trigger spontaneous cardiac impulse formation and predispose to cardiac electrical repolarization changes that facilitate initiation of VF, the main arrhythmia associated with SCD.71
Evaluation of OSA patients with high risk of arrhythmia is crucial. It is possible that SCD in OSA is in part mediated by changes in ventricular repolarization in this population. Among the parameters that can be used to evaluate ventricular repolarization are QT interval (QT), corrected QT interval (QTc), QT dispersion, and transmural dispersion of repolarization. Moreover, the time interval from the peak to the end of the T wave electrocardiographically referred to as Tp-e appears as an index for transmural dispersion of ventricular repolarization. Tp-e/QT and Tp-e/QTc ratios are among the other electrocardiographic indices representing ventricular arrhythmogenic potential.6