Relationship Between Vascular Endothelial Dysfunction and Beat-to-beat Blood Pressure Variability in Patients With OSAS

Relationship Between Vascular Endothelial Dysfunction and Beat-to-beat Blood Pressure Variability in Patients With Obstructive Sleep Apnea Syndrome

It is thought that intermittent hypoxia, poor tissue oxygenation, and perfusion in OSA can lead to eNOS uncoupling. Uncoupled eNOS can reduce nitric oxide (NO), which will result in an imbalance of contraction and diastole. Furthermore, OSA may increase beat-to-to BPV via the characteristic acute blood pressure peaks that follow the end of obstructive apnoeas. Therefore, the aim is to discuss the relationship between vascular endothelial dysfunction and beat-to-beat blood pressure variability in patients with OSAS (Obstructive sleep apnea syndrome).

Obstructive sleep apnea (OSA) is characterized by recurrent airway collapse that causes chronic intermittent hypoxia(CIH). OSA is associated with systemic inflammation and oxidative stress resulting in endothelial dysfunction and cardiovascular disease (CVD). Under physiological conditions, eNOS is activated by shear stress and Ach. L-arginine and O2 are catalyzed by BH4, FMN, FAD, NADPH, and eNOS to produce nitric oxide (NO)， which has an important vasodilating effect， and L-citrulline. During the episode of OSA, intermittent hypoxia leads to oxidative stress resulting in the production of superoxide anions. The reaction between O2- and NO occurs rapidly, resulting in ONOO-. ONOO- and H2O2 oxidize BH4 to dihydrobiotrexate (BH2), which is a competitive inhibitor with BH4, thus limiting the availability of eNOS substrates and preventing NO production, resulting in an imbalance between contraction and diastolic. It has been documented that beat-to-beat blood pressure variability in OSAS patients is much higher than that in healthy adults. In some patients, intermittent hypoxia was observed with the episode of OSA, and blood pressure fluctuated with the episode of hypoxia. However, this was not found in the other patients, whose blood pressure did not change significantly during the hypoxia episode. Therefore, the investigators considered that the endothelial function of patients with high sensitivity to hypoxia was healthy or in the early stage, while the endothelial function of those patients with low sensitivity to hypoxia was at a relatively high level of impairment. Endothelial dysfunction can be measured indirectly by brachial artery flow-mediated dilation (FMD), beat-to-beat blood pressure variability can be measured by Polysomnography (PSG), and biological examinations can be performed by blood sampling. Thus, the purpose is to explore the specific relationship between OSAS beat-to-beat blood pressure variability and endothelial dysfunction.

Inclusion Criteria:

1. ≥18 years old;
2. Moderate to severe OSA(AHI≥15 times/hour);
3. Hypertension (systolic blood pressure ≥140mmHg and/or diastolic blood pressure ≥90mmHg);

Exclusion Criteria:

1. Malignant tumor, severe arrhythmia and heart disease, moderate and severe renal dysfunction, peripheral vascular disease, diabetes
2. Systolic blood pressure ≤140mmHg and diastolic blood pressure ≤90mmHg
3. Vigorous exercise 24 hours before the experiment;
4. Vasoactive drugs (ACEI, ARB, CCB, β blockers, nitrates) were used 48 hours before the experiment;
5. Smoking, drinking and consuming caffeinated beverages 12 hours before the experiment