Normal sleep is associated with state changes in heart rate, blood pressure and neural circulatory control. During slow wave sleep, heart rate, blood pressure and sympathetic activity decrease whereas during REM sleep, sympathetic traffic to blood vessels increases significantly and heart rate and blood pressure are very labile. While these changes are physiologic, they may have implications for ischemia and arrhythmias in people with an underlying vulnerable substrate. While the overall decline in blood pressure during sleep is physiologic, subjects in whom the blood pressure decline is blunted or absent (non-dippers) are often at higher risk for cardiac and vascular events. Conversely, excessive nocturnal blood pressure decline has also been associated with cardiovascular risk including development of lacunar infarction. REM sleep has been linked to significant arrhythmias including asystole. REM has also been associated with coronary vasospasm and with angina (with ST depression) that causes waking from sleep. REM may also contribute to arrhythmogenesis in patients with ion-channelopathies. Indeed in patients with Long QT2 and Long QT3 syndromes, there is a markedly increased risk of fatal arrhythmic events occurring during sleep. Patients with Brugada syndrome also have a high risk of sleep-related sudden death. Interestingly these patients may have a higher than expected prevalence of obstructive sleep apnea. Disturbed sleep may also predispose to cardiac ischemia, arrhythmias and death. Obstructive sleep apnea (OSA) has been implicated in nocturnal angina and in myocardial infarction presenting during the nighttime hours. Apneic episodes have also been linked to bradyarrhythmias, including cardiac asystole. OSA patients have a higher risk of experiencing sudden death at night, and of receiving nighttime shocks from implanted defibrillators.
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