[The effect of nasal continuous positive airway pressure on endothelial function in obstructive sleep apnea-hypopnea syndrome with coronary heart disease].

OBJECTIVE

To study the association between the indices of endothelial function in obstruction sleep apnea-hypopnea syndrome (OSAHS) and coronary heart disease (CHD) and the effect of nasal continuous positive airway pressure (nCPAP) on the combination of OSAHS and CHD.

METHODS

A total of 80 subjects were prospectively recruited into four groups including control, OSAHS, CHD, OSAHS with CHD groups, with 20 subjects each. The indices of sleep apnea, serum nitric oxide (NO), and plasma endothelial-1 (ET-1) were measured. The changes of concentration of ET-1 and NO were compared before and after nCPAP therapy. The associations between ET-1 and NO and MSpO2, CT90 were analyzed.

RESULTS

(1) Multi-variable logistic analysis showed that OSAHS was one of the risk factors for CHD (OR = 0.511). (2) Compared with the control subjects and CHD group, there were significantly higher values of CT90, concentrations of ET-1 and lower values of MSpO2, concentrations of NO in both OSAHS and OSAHS with CHD groups (P < 0.01). There were no significant difference in sleep apnea indices between OSAHS and OSAHS with CHD groups (P > 0.05). However, in the group of OSAHS with CHD, the plasma ET-1 was significantly higher, whereas the serum NO was significantly lower than that in the group of OSAHS alone (P < 0.01). (3) The concentration of serum NO in the group of OSAHS was positively correlated with MSpO2 (r = 0.519, P < 0.05) and inversely correlated with CT90 (r = -0.529, P < 0.05). In addition, the concentration of plasma ET-1 was inversely correlated with MSpO2 (r = -0.457, P < 0.05) and positively correlated with CT90 (r = 0.476, P < 0.05). (4) In the groups of OSAHS and OSAHS with CHD, MSpO2, NO and NO/ET-1 after nCPAP therapy were higher than those before therapy, while CT90 and ET-1 were lower than those before therapy (P < 0.01).

CONCLUSIONS

OSAHS is one of the risk factors for CHD. Endothelial function was significantly impaired in OSAHS patients, and more severe in patients with OSAHS with CHD. The impairment of endothelial function may be one of the main mechanisms for the development or deterioration of CHD in OSAHS patients. The vascular endothelial dysfunction can be ameliorated by nCPAP treatment, which is correlated with improvement of nocturnal hypoxemia.