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Prof. Costas Tsioufis,
At the present session we had the chance to review the current data regarding sleep apnea and its close relationship to cardiovascular disease. As analysed by Dr. McNicholas, sleep apnea is the main representative of sleep disordered breathing and is divided into the central (central sleep apnea-CSA) and obstructive type (obstructive sleep apnea-OSA), the latter accounting for most cases. While the two conditions may overlap, screening for OSA is based on loud snoring, daytime sleepiness and presence of obesity and hypertension while CSA is characterised by loss of ventilator drive and is often in patients with heart failure or stroke. An accurate diagnosis is provided by a full overnight polysomnography, that will also allow for titration of continuous positive airway pressure (CPAP). Dr. Arzt presented a thorough analysis of the relation of sleep apnea with heart failure. Both OSA and CSA are very common in patients with either systolic or diastolic heart failure. The close link between OSA and new or progressing heart failure seems to be based on long-standing, high -especially nocturnal- blood pressure, raised sympathetic activity, an increased right and left ventricular afterload and cardiac metabolic mismatch. Fluid migration from leg oedema to the neck when lying down may be a mechanism that leads to OSA in heart failure patients. CSA, more often in the form of Cheynes-Stokes respiration usually follows heart failure. There is evidence that CPAP improves ejection fraction and lowers sympathetic activity in these patients, yet its effect on mortality is unclear. The strongest association between OSA and cardiovascular disease has been with increased blood pressure, as reviewed by Dr. Narkiewicz. Patients with OSA are often non-dippers and exhibit hypertension that may be resistant to treatment. Sustained hypertension in these patients is thought to be mediated by increased sympathetic activity and chemoreflex/baroreflex derangement that follow the repetitive triads of hypoxia-arousal-intrathoracic pressure swings. The effect of CPAP on BP however, as assessed from multiple randomized trials, has been rather mild, while daytime sleepiness constitutes a possibly important clinical criterion for a more prominent BP response. A recent prospective cohort study that also accounted for changes in BMI reported that use of CPAP in patients with OSA reduces the risk of incident hypertension. Aldosterone-mediated fluid retention may justify the use of spironolactone in patients with resistant hypertension. The nighttime BP swings, accelerated atherosclerosis and decreased cerebral blood flow may serve as the pathophysiological background relating sleep apnea to stroke. Yet, epidemiological studies regarding such an association have not provided conclusive results, and it is not easy to identify whether sleep apnea precipitates or is the consequence of stroke. CSA rather than OSA seems to be present more often at the acute phase of a stroke. As Dr. van de Borne presented, a wide array of nocturnal arrhythmias has been reported in patients with OSA that ranges from sinus arrest to premature ventricular contractions and nonsustained ventricular tachycardia. Bradycardia as well as bradyarrhythmias such as atrioventricular block and asystole may develop during sleep, while CPAP is an effective treatment. OSA may be associated with atrial fibrillation, perhaps through atrial enlargement, while atrial fibrillation is common in patients with CSA with or without left-ventricular systolic dysfunction. Presence of OSA may be associated with an increased risk of atrial fibrillation recurrence after cardioversion. It is unclear whether OSA is associated with an increased risk of sudden cardiac death during sleep.
Sleep apnea is a major unrecognised cardiovascular risk factor
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