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Background Many patients with obstructive sleep rrrrrrrrnapnea syndrome (OSAS) have complicated with hypertension and may be prescribed rrrrrrrrnwith antihypertension medications to control their blood pressure But whether rrrrrrrrnantihypertension medications can also decrease arterial stiffness or control therrrrrrrrn blood pressure increasing following obstructive events is not well describedrrrrrrrrn This study aimed to investigate whether antihypertensive medications can ameliorrrrrrrrnraterrrrrrrrn the changes in arterial stiffness and blood pressure associated with OSA rrrrrrrrnrrrrrrrrnMethods Sixtyone OSAS patients [13 women, 48 men, mean rrrrrrrrnage (534±123) years], 26 normotensive patients (N), 7 hypertensive patientrrrrrrrrns on no antihypertension medications (H), and 28 hypertensive patients on variourrrrrrrrns combination antihypertension therapy (HM), were prospectively diagnosed with rrrrrrrrnstandard nocturnal polysomnography Beattobeat blood pressure was continuourrrrrrrrnsly recorded from the radial artery by applanation tonometry during baseline slerrrrrrrrnep As a measure of arterial stiffness, arterial augmentation index (AAI) was crrrrrrrrnalculated as the ratio of augmented systolic blood pressure (SBP) to pulse pressrrrrrrrrnure and expressed as a percentage for the following conditions: awakening, the frrrrrrrrnirst 10 (“early apnea”) and last 10 (“late apnea”) cardiac cycles of obstrucrrrrrrrrntive events (apnea or hypopnea), and the first 15 cardiac cycles following eventrrrrrrrrn termination (“post apnea”) for all events with nadir O2 saturation ≤89% rrrrrrrrnrrrrrrrrnResults Systolic blood pressure (SBP) postapnea [(1427rrrrrrrrn4±1306) mmHg (N), (13706±2656) mmHg (H), (13694±141) mmHg (HM)] warrrrrrrrns significantly increased from awakening [(13576±1476) mmHg (N), (13558rrrrrrrrn±2317) mmHg (H), (12977±1400) mmHg (HM)], early apnea [(13053±126rrrrrrrrn5) mmHg (N), (12447±2497) mmHg (H), (12604±1312) mmHg (HM)], and latrrrrrrrrne apnea [(1298±1268) mmHg(N), (12478±2515) mmHg (H), (12448±1382rrrrrrrrn) mmHg (HM)] respectively (P<0001, repeated measures ANOVA) AAI was sigrrrrrrrrnnificantly increased for the N group (P<0001) from awakening to late apnearrrrrrrrn [(1045±262)% vs (1443±321)%] and from early apnea to late apnea [rrrrrrrrn(1061±234)% vs (1443±321)%], and also for H group (P<005) fromrrrrrrrrn awakening to late apnea [(1123±387)% vs (1632±802)%] and from earlyrrrrrrrrn apnea to late apnea [(1175±379)% vs (1632±802)%] Meanwhile, no sirrrrrrrrngnificant differences in AAI among awakening, early apnea, late apnea, and postrrrrrrrrnapnea conditions were found in HM group rrrrrrrrnConclusions The current data demonstrate that systemic bloorrrrrrrrnd pressure increases significantly during the postapneic phase of OrrrrrrrrnSAS, comparrrrrrrrnred with that during awakening and intraapnea phases even with the use of rrrrrrrrncombrrrrrrrrnined antihypertensive therapy which could normalize BP during awakening in the hrrrrrrrrnypertensive patients However, increases in arterial stiffness during obstructirrrrrrrrnve events could be ameliorated by combined antihypertension medications
Background Many patients with obstructive sleep r r r r r r r r napnea syndrome (OSAS) have complicated with hypertension and may be prescribed r r r r r r r r nwith antihypertension medications to control their blood pressure But whether r r r r r r r nantihypertension medications can also decrease arterial stiffness or control the r r r r r r r r n blood pressure increasing following obstructive events is not well described r r r r r r r n This study aimed to investigate whether antihypertensive medications can amelio r r r r r r r r nrate r r r r r r r r n the changes in arterial stiffness and blood pressure associated with OSA r r r r r r r n r r r r r r r nMethods Sixty-OSAS patients [13 women, 48 men, r r r r r r nage (53.4 ± 12.3 years), 26 normotensive patients (N), 7 hypertensive patient r r r r r r r ns on no antihypertension medications (H), and 28 hypertensive patients on variou r r r r r r r ns combination antihypertension th erapy (HM), were prospectively diagnosed with r r r r r r r nstandard nocturnal polysomnography Beattobeat blood pressure was continuou r r r r r r r r nsly recorded from the radial artery by applanation tonometry during baseline sle r r r r r r nep As a measure of arterial stiffness, arterial augmentation index (AAI) was c r r r r r r r r nalculated as the ratio of augmented systolic blood pressure (SBP) to pulse press r r r r r r r nure and expressed as a percentage for the following conditions: awakening, the f r r r r r r n first 10 (“early apnea ”) and last 10 apnea “) cardiac cycles of obstruc r r r r r r r n ntive events (apnea or hypopnea), and the first 15 cardiac cycles following event r r r r r r r r n termination ( ”post apnea ") for all events with nadir O2 saturation ≤89% r r r r r r r n r r r r r r r r nResults Systolic blood pressure (SBP) postapnea [(1427 r r r r r r r n4 ± 1306) mmHg (N), (13706 ± 2656) mmHg ( H), (136.94 ± 14.1) mmHg (HM)] wa r r r r r r r r ns significantly increased from awakening [(135.76 ± 14.76) mmHg (N), (135.58 r r r r r r r n ± 2317) mmHg (H), (12977 ± 1400) mmHg (HM)], early apnea [(13053 ± 126 r r r r r r (H), (12604 ± 1312) mmHg (HM)], and lat r r r r (1298 ± 1268) mmHg (N), (12478 ± 2515) mmHg (H), (12448 ± 1382 r) (P <0001, repeated measures ANOVA) AAI was sig r r r r r r r r r r r r r r r nnificantly increased for the N group (P <0001) from awakening to late apnea r r r r r r r n [(1045 ± 262)% vs (1443 ± 321)%] and from early apnea to late apnea [ r r r r r r r n 34)% vs (1443 ± 321)%], and also for H group (P <005) from r r r r r r r n awakening to late apnea [(1123 ± 387)% vs (1632 ± 802)%] and from early r r r r r r r n apnea to late apnea [(1175 ± 379)% vs (1632 ± 802)%] Meanwhile, no si r r r r r r r n nificificant differences in AAI among awakening, early apnea, late apnea, and post r r r r r r r n Λapnea conditions were found in HM group. R r r r r r r nConclusions The current data demonstrate that systemic bloo r r r r r r r r nd pressure increases significantly during the postapneic phase of O r r r r r r r nSAS, compa r r r r r r r nred with that during awakening and intraapnea phases even with the use of r r r r r r r r ncomb r r r r r r r r nined antihypertensive therapy which could normalize BP during awakening in the h r r r r r r r nypertensive patients. However, increases in arterial stiffness during obstructi r r r r r r r r nve events could be ameliorated by combined antihypertension medications