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  • Title: Hypertension, cardiac arrhythmias, myocardial infarction, and stroke in relation to obstructive sleep apnea.
    Author: Shepard JW.
    Journal: Clin Chest Med; 1992 Sep; 13(3):437-58. PubMed ID: 1521412.
    Abstract:
    The cyclical changes in heart rate and systemic blood pressure that accompany apneic events are predominantly mediated by fluctuations in the activity of the autonomic nervous system. Increased vagal efferent parasympathetic activity is responsible for the cyclical reductions in heart rate during apnea. In contrast, the cyclical elevations in systemic blood pressure are believed to result from recurrent peripheral vasoconstriction mediated by repetitive activation of the sympathetic nervous system. Maximal activation and pressures coincide with apnea termination and brief arousal from sleep. These cyclical elevations in systemic pressure during sleep increase ventricular workload and, thereby, may contribute to the development of ventricular hypertrophy. Systemic hypertension is present during wakefulness in approximately 50% of patients with OSA. Although age and obesity are the predominant risk factors for diurnal hypertension, OSA probably makes an independent contribution in younger obese men. Sinus bradycardia, Mobitz type 1 second-degree heart block, and prolonged sinus arrest have all been documented in association with the apneic events. Increased ventricular ectopy has been observed with oxyhemoglobin desaturations below 60%. Myocardial ischemia, infarction, sudden death, and stroke all demonstrate similar circadian variations in time of onset. Peak frequencies occur between 6 AM and noon, generally within several hours of awakening. Although sleep is associated with decreased frequencies of these adverse cardiovascular events in the general population, evidence exists linking REM sleep to an increased risk of myocardial ischemia. In men who habitually snore, epidemiologic data have detected an increased risk for ischemic heart disease and stroke. Habitual snoring has also been associated with an increased risk of sudden death during sleep. In patients with clinically significant OSA, there is reasonable information indicating excessive mortality in the absence of treatment. This mortality is predominantly cardiovascular and tends to occur during sleep.
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