Effects of antihypertensives on arterial responses associated with obstructive sleep apneas

Many patients with obstructive sleep apnea syndrome (OSAS) have complicated with hypertension and may be prescribed with antihypertension medications to control their blood pressure. But whether antihypertension medications can also decrease arterial stiffness or control the blood pressure increasing following obstructive events is not well described. This study aimed to investigate whether antihypertensive medications can ameliorate the changes in arterial stiffness and blood pressure associated with OSA.

Sixty-one OSAS patients [13 women, 48 men, mean age (53.4 +/- 12.3) years], 26 normotensive patients (N), 7 hypertensive patients on no antihypertension medications (H), and 28 hypertensive patients on various combination antihypertension therapy (HM), were prospectively diagnosed with standard nocturnal polysomnography. Beat-to-beat blood pressure was continuously recorded from the radial artery by applanation tonometry during baseline sleep. As a measure of arterial stiffness, arterial augmentation index (AAI) was calculated as the ratio of augmented systolic blood pressure (SBP) to pulse pressure and expressed as a percentage for the following conditions: awakening, the first 10 ("early apnea") and last 10 ("late apnea") cardiac cycles of obstructive events (apnea or hypopnea), and the first 15 cardiac cycles following event termination ("post apnea") for all events with nadir O2 saturation

Systolic blood pressure (SBP) post-apnea [(142.74 +/- 13.06) mmHg (N), (137.06 +/- 26.56) mmHg (H), (136.94 +/- 14.1) mmHg (HM)] was significantly increased from awakening [(135.76 +/- 14.76) mmHg (N), (135.58 +/- 23.17) mmHg (H), (129.77 +/- 14.00) mmHg (HM)], early apnea [(130.53 +/- 12.65) mmHg (N), (124.47 +/- 24.97) mmHg (H), (126.04 +/- 13.12) mmHg (HM)], and late apnea [(129.8 +/- 12.68) mmHg (N), (124.78 +/- 25.15) mmHg (H), (124.48 +/- 13.82) mmHg (HM)] respectively (P < 0.001, repeated measures ANOVA). AAI was significantly increased for the N group (P < 0.001) from awakening to late apnea [(10.45 +/- 2.62)% vs (14.43 +/- 3.21)%] and from early apnea to late apnea [(10.61 +/- 2.34)% vs (14.43 +/- 3.21)%], and also for H group (P < 0.05) from awakening to late apnea [(11.23 +/- 3.87)% vs (16.32 +/- 8.02)%] and from early apnea to late apnea [(11.75 +/- 3.79)% vs (16.32 +/- 8.02)%]. Meanwhile, no significant differences in AAI among awakening, early apnea, late apnea, and post-apnea conditions were found in HM group.

The current data demonstrate that systemic blood pressure increases significantly during the post-apneic phase of OSAS, compared with that during awakening and intra-apnea phases even with the use of combined antihypertensive therapy which could normalize BP during awakening in the hypertensive patients. However, increases in arterial stiffness during obstructive events could be ameliorated by combined antihypertension medications.