Valo Misa, Wons Annette, Moeller Albert, Teupe Claudius
Department of Medicine, Center of Sleep Medicine, Sachsenhausen Hospital, Frankfurt, Germany.
Clin Cardiol. 2015 Aug;38(8):462-8. doi: 10.1002/clc.22419. Epub 2015 Jul 14.
Obstructive sleep apnea (OSA) is associated with an increased risk of cardiovascular complications. OSA and coronary artery disease (CAD) share the same risk factors and coexist in many patients. In previous studies, repeated nocturnal cardiac ischemic events in OSA patients with CAD have been reported.
We hypothesized that OSA may precipitate myocardial ischemia, evidenced by ST-segment depression and elevated N-terminal brain natriuretic peptide (NT-proBNP) and high-sensitivity troponin T (hs-TropT) levels in patients with severe OSA and concomitant CAD. We also aimed to evaluate if the effects could be reversed by continuous positive airway pressure (CPAP) therapy.
Twenty-one patients with severe OSA (apnea-hypopnea index >15/h, nadir oxygen desaturation ≤ 80%), and coexisting CAD underwent in-hospital polysomnography at baseline and under CPAP. Blood samples for hs-TropT and NT-proBNP measurements were drawn prior and immediately after sleep. ST-segment depression was measured at the time of maximum oxygen desaturation during sleep.
CPAP significantly decreased elevated NT-proBNP levels from 475 ± 654 pg/mL before sleep to 353 ± 573 pg/mL after sleep and attenuated ST-segment depression during sleep. hs-TropT was not elevated and did not differ after nocturnal oxygen desaturation at baseline and after CPAP.
CPAP significantly reduced NT-proBNP in patients suffering from severe OSA and coexisting CAD. Repeated nocturnal myocardial ischemia did not cause myocyte necrosis evidenced by elevated hs-TropT or ST-segment depression.
阻塞性睡眠呼吸暂停(OSA)与心血管并发症风险增加相关。OSA和冠状动脉疾病(CAD)具有相同的危险因素,且在许多患者中并存。在先前的研究中,已报道患有CAD的OSA患者夜间反复出现心脏缺血事件。
我们假设OSA可能会诱发心肌缺血,这可通过重度OSA合并CAD患者的ST段压低、N末端脑钠肽(NT-proBNP)升高和高敏肌钙蛋白T(hs-TropT)水平升高来证明。我们还旨在评估持续气道正压通气(CPAP)治疗是否可以逆转这些影响。
21例重度OSA(呼吸暂停低通气指数>15/小时,最低氧饱和度≤80%)且并存CAD的患者在基线时和接受CPAP治疗时进行了院内多导睡眠图检查。在睡眠前和睡眠后立即采集血样以测量hs-TropT和NT-proBNP。在睡眠期间最大氧饱和度时测量ST段压低情况。
CPAP显著降低了升高的NT-proBNP水平,从睡眠前的475±654 pg/mL降至睡眠后的353±573 pg/mL,并减轻了睡眠期间的ST段压低。hs-TropT未升高,且在基线和CPAP治疗后的夜间氧饱和度下降后无差异。
CPAP显著降低了重度OSA合并CAD患者的NT-proBNP。夜间反复心肌缺血并未导致hs-TropT升高或ST段压低所证明的心肌细胞坏死。