Obstructive Sleep Apnoea

Consequences of OSA

For more information on studies linking OSA with Heart Disease and Diabetes visit the Clinical Data – Study Area

In contrast with the normal physiologic effect of sleep on the cardiovascular system, the acute haemodynamic consequences of OSA include: systemic and pulmonary hypertension; bradycardia at the onset of apnoea and tachycardia at the resumption of ventilation; decreased cardiac output and increased left ventricular after-load. These changes are primarily the result of sympathetic stimulation, alterations in intrathoracic pressure, hypoxia and hypercapnia (Roux et al., 2000). Thus, patients with SBD are thought to be 'at risk' of a range of severe medical complications. Although the review undertaken by Wright et al. (1997) on the health effects of OSA dismissed the relationship between SBD and cardiovascular disease, citing the lack of controlled prospective studies and the major difficulty in adjusting for confounding factors such as obesity, hypertension, diabetes mellitus, smoking and ageing. A prospective longitudinal randomised placebo-controlled study design could be regarded as being unethical for withholding quality of life improvement, resulting from reduced hypersomnolence, but in addition randomization of OSA subjects to a placebo treatment could potentially increase their risk of cardiovascular morbidity. Several recent epidemiologic studies (Lindberg et al., 1988; Grote et al., 1999; Lavie et al., 2000) and trials (Worsnop et al., 1998; Davies et al., 2000) have demonstrated an association between SBD and cardiovascular disease.

Hypertension

During an apnoeic event OSA patients show an increase in blood pressure, which then returns to normal levels as the obstruction clears. The resulting hypoxia and sympathetic discharge leads to peripheral vasoconstriction, bradycardia and decrease in cardiac output (Brown, 1994). Millman et al. (1991) concluded that the high prevalence of hypertension in OSA subjects was primarily related to age and obesity. Davies et al. (2000), however, in comparing OSA subjects with closely matched controls, found diastolic blood pressure to be increased during both the day and night together with an increase in nocturnal systolic pressure. The evidence supporting a possible cause and effect relationship between OSA and hypertension comes primarily from intervention studies, which have reported reductions in blood pressure following treatment (Faccenda et al., 2001; Pepperell et al., 2002). If OSA is a causative factor in hypertension, the proposed mechanism is the repeated hypoxia or arousals during sleep leading to increased sympathetic activity during both the awake and sleeping states (Brown, 1994). The findings of a prospective longitudinal population based study, suggested that snoring and upper airways resistance syndrome may be associated with an increased risk of cardiovascular disease (Lindberg et al., 1988).

Coronary heart disease

Andreas et al. (1996) reported a higher incidence of OSA amongst subjects suffering from coronary heart disease, with OSA being implicated as a risk factor in accelerating atherosclerosis of the coronary vessels. Confirmation of this theory has been provided by Peker et al. (1999), who found an independent association between OSA and coronary artery disease, once the results had been adjusted for the presence of other variables including age, obesity, hypertension, smoking and diabetes mellitus. This study may be criticized for its case-control design and a true population based prospective design may have been preferable.

Heart failure

Inspiration against a closed upper airway in OSA subjects generates a significant negative intra-thoracic pressure leading to a decrease in right atrial pressure and an increase in venous return to the right ventricle. This in turn can lead to isolated right ventricular hypertrophy and heart failure (Sanner et al., 1997).

Cerebrovascular disease

It is reported that approximately one-third of strokes take place during sleep, with snoring being identified as a potential risk factor (Palomaki et al., 1989). Marler et al. (1989), reported SBD as being associated with a three-fold increase in the risk of stroke. However, from these studies it is not clear whether SBD were an independent risk factor for stroke or if the increased stroke risk was due to the associated hypertension. SBD affect cerebral haemodynamics, with an estimated 50 per cent reduction in cerebral blood flow, related to the duration of apnoea, hypopnoea and consequent degree of oxygen desaturation (Roux et al., 2000).

Sudden death

This may be the result of a myocardial infarction or a cerebrovascular accident, as outlined above. Alternatively, sufferers of SBD are at risk of falling asleep whilst driving with lethal consequences (Haraldsson et al., 1990).

Thus, early diagnosis of SBD and, in particular, OSA with the instigation of suitable therapy not only offers symptomatic improvement but also improves long-term health prospects.