Jump to comment:

• OSA patients with metabolic syndrome
  Murat Enoz
  Published on: 31 March 2005

• Published on: 31 March 2005

  OSA patients with metabolic syndrome

  • Murat Enoz, Department of Otolaryngology, Head&Neck Surgery

  Dear Editor,

  Obstructive sleep apnea (OSA) is a common disorder associated with an increased risk of cardiovascular disease and stroke. As it is strongly associated with known cardiovascular risk factors, including obesity, insulin resistance, and dyslipidemia, OSA is an independent risk factor for hypertension and has also been implicated in the pathogenesis of congestive cardiac failure, pulmonary hypertension...

  Show More

  Dear Editor,

  Obstructive sleep apnea (OSA) is a common disorder associated with an increased risk of cardiovascular disease and stroke. As it is strongly associated with known cardiovascular risk factors, including obesity, insulin resistance, and dyslipidemia, OSA is an independent risk factor for hypertension and has also been implicated in the pathogenesis of congestive cardiac failure, pulmonary hypertension, arrhythmias, and atherosclerosis [1].

  Obstructive sleep apnea is part of a spectrum of sleep-related breathing disorders that includes snoring, upper airway resistance syndrome (increased respiratory effort without apnea or hypopnea), and central sleep apnea (CSA) (apnea without respiratory effort). The OSA syndrome is the combination of obstructive apneas with daytime tiredness or recurrent awakenings or gasping episodes [1].

  Clinical suspicion of OSA is usually raised by complaints of snoring and daytime tiredness, despite an adequate duration of sleep. Mainly, OSA patients are managed clinically by sleep physicians with a background in respiratory medicine or neurology. Atypical presentations are not uncommon, however, and result in OSA patients presenting to a variety of medical specialists.

  Obstructive sleep apnea is now recognized to be an independent risk factor for daytime hypertension. An association between OSA and hypertension was suggested by a series of population and cohort studies, observational studies in patients attending hypertension clinics and sleep clinics [2,3]. Increased variability of blood pressure and loss of the nocturnal blood pressure dip were also reported [4]. A recent prospective, randomized, placebo-controlled comparison between therapeutic and subtherapeutic CPAP reported a reduction in blood pressure, particularly in those with more severe OSA [5].

  Patients with OSA have many features in common with the “metabolic syndrome,” including systemic hypertension, central obesity [6], and insulin resistance [7]. The AHI correlates with BMI, waist-to-hip ratio, hypertension, and diabetes, whereas trends toward lower high-density lipoprotein and elevated triglycerides are reported for OSA subjects <_65 years="years" old="old" _8.="_8." p="p"/> The role of sleep-disordered breathing in arrhythmias in heart failure is still being defined. In a study of 81 males with stable heart failure, incidences of atrial fibrillation and ventricular tachycardia were significantly higher in sleep apnea subjects (AHI The risk of experiencing angina or an acute coronary syndrome is increased in the hours after waking from sleep. In OSA, cyclical variations in heart rate and blood pressure are dramatic [12], more so than many hemodynamic stresses in daily life, and occur during sleep, a time when in normal subjects blood pressure and heart rate are the lowest and least variable. In OSA, increased peripheral sympathetic nerve activity during sleep persists during wakefulness at approximately twice the normal levels [13] and may affect acute coronary events in the early hours of the day.

  Patients with heart failure can have a combination of CSA and OSA, which can vary during sleep or over time. In one study, within-night changes were documented with progression from predominantly OSA early in the night to CSA, presumably due to the fall in the arterial pCO2 level to below the apneic threshold [14].

  Positive airway pressure has been known to help acute cardiogenic pulmonary edema for decades. The beneficial effects are thought to operate via an increased intrathoracic pressure and reduced left ventricular transmural pressure gradient, increased lung volume, assistance to inspiratory respiratory muscles and stabilisation of the upper airway. Cardiac work is reduced as a result [15].

  In patients with established congestive heart failure is likely to be a marker of advanced disease, via the mechanisms of impaired cardiac output and elevated sympathetic activity, hyperventilation, reduced lung volume and circulatory delay. Importantly, such patients who have not responded to maximal medical therapy might be responsive to positive airway pressure.

  Sincerely

  Dr. Murat Enoz

  References

  1- The report of an American Academy of Sleep Medicine Task Force. Sleep-related breathing disorders in adults: recommendations for syndrome definition and measurement techniques in clinical research. Sleep 1999;22:667–89.

  2- Gislason T, Almqvist M. Somatic diseases and sleep complaints: an epidemiological study of 3,201 Swedish men. Acta Med Scand 1987;221:475–81.

  3- Worsnop CJ, Naughton MT, Barter CE, Morgan TO, Anderson AI, Pierce RJ. The prevalence of obstructive sleep apnea in hypertensives. Am J Respir Crit Care Med 1998;157:111–5.

  4- Wilcox I, Grunstein RR, Collins FL, Doyle JM, Kelly DT, Sullivan CE. Circadian rhythm of blood pressure in patients with obstructive sleep apnea. Blood Press 1992;1:219–22.

  5- Pepperell JCT, Ramdassingh-Dow S, Crosthawaite N, et al. Ambulatory blood pressure after therapeutic and subtherapeutic nasal positive airway pressure for obstructive sleep apnoea: a randomised parallel trial. Lancet 2001;359:204–10.

  6- Grunstein R, Wilcox I, Yang TS, Gould Y, Hedner J. Snoring and sleep apnoea in men: association with central obesity and hypertension. Int J Obes Relat Metab Disord 1993;17:533–40.

  7- Elmasry A, Lindberg E, Berne C, et al. Sleep-disordered breathing and glucose metabolism in hypertensive men: a population-based study. J Intern Med 2001;249:153–61.

  8- Newman AB, Nieto FJ, Guidry U, et al. Relation of sleep-disordered breathing to cardiovascular disease risk factors: the Sleep Heart Health Study. Am J Epidemiol 2001;154:50–9.

  9- Javaheri S, Parker TJ, Liming JD, et al. Sleep apnea in 81 ambulatory male patients with stable heart failure: types and their prevalences, consequences, and presentations. Circulation 1998;97:2154–9.

  10- Javaheri S. Effects of continuous positive airway pressure on sleep apnea and ventricular irritability in patients with heart failure. Circulation 2000;101:392–7.

  11- Garrigue S, Bordier P, Jais P, et al. Benefit of atrial pacing in sleep apnea syndrome. N Engl J Med 2002;346:404–12.

  12- Mayer J, Becker H, Brandenburg U, Penzel T, Peter JH, von Wichert P. Blood pressure and sleep apnea: results of long-term nasal continuous positive airway pressure therapy. Cardiology 1991;79:84–92.

  13- Carlson JT, Hedner J, Elam M, Ejnell H, Sellgren J, Wallin BG. Augmented resting sympathetic activity in awake patients with obstructive sleep apnea. Chest 1993;103:1763–8.

  14- Tkacova R, Niroumand M, Lorenzi-Filho G, Bradley TD. Overnight shift from obstructive to central apneas in patients with heart failure: role of PCO2 and circulatory delay. Circulation 2001;103:238–43.

  15- Kaye, D.M. et al. (2004) Continuous positive airway pressure decreases myocardial oxygen consumption in heart failure. Clin. Sci. (Lond.) 106, 599–603.

  Show Less

  Conflict of Interest:
  None declared.

  • Back to top