(A) Correlation between OSAHS and the development of hypertension OSAHS and hypertension are both common clinical conditions. OSAHS is an independent risk factor for hypertension, and hypertension is a major complication of OSAHS, and several studies have shown that 60% to 90% of OSAHS patients have hypertension, and about 30% of hypertensive patients have OSAHS in combination.
(i) Most patients often have OSAHS first, and hypertension occurs gradually later.
②After correction of sleep apnea, blood pressure decreases or returns to normal. Although epidemiological studies have demonstrated that OSAHS is an independent factor in hypertension, not all patients with OSAHS develop hypertension. Some patients with hypertension do not return to normal blood pressure even after complete correction of sleep apnea, and still require a certain dose of antihypertensive medication to maintain blood pressure to normal, indicating that hypertensive patients with combined sleep apnea can worsen the degree of hypertension, while OSAHS may be more likely to induce hypertension in people at high risk for hypertension, and more severe sleep breathing disorders with marked fluctuations Patients with hypoxemia are more likely to induce hypertension. Pepperd et al. observed the risk of developing hypertension in 709 patients with sleep breathing disorder for 4-8 years, using AHI of 0 as the baseline, and showed that the risk of developing hypertension after 4 years was 1,42 in snoring patients with AHI of 0,1 to 4,9 beats/hour and 5,0 to 14,9 beats/hour in AHI The risk of hypertension in OSAHS patients was 2,03, while the risk of hypertension in patients with AHI greater than 15 beats/hour increased to 2,89, indicating that OSAHS is a risk factor for the development of hypertension and can increase the incidence of cardiovascular disease.
(B) Clinical features of OSAHS combined with hypertension Compared with primary hypertension, patients with OSAHS-related hypertension have the following clinical features in addition to sleep breathing disorder.
1. higher blood pressure in the early morning when waking up from sleep and lower blood pressure during the day and at bedtime in the evening, while patients with essential hypertension have normal or slightly higher blood pressure in the early morning when waking up from sleep and higher blood pressure after daytime activities or at bedtime in the evening.
2, the effect of simple anti-hypertensive drug treatment is poor, it is difficult to maintain within the normal range, blood pressure volatility is large. 24-hour ambulatory blood pressure monitoring shows no physiological drop in blood pressure during sleep at night, that is, “non-spoon type”, the rate of blood pressure drop at night <10%.
3. Periodic increase in blood pressure accompanied by apnea, which is manifested by recurrent episodes of transient hypertension at night. Peak hypertension occurs at the end of apnea, just after resumption of ventilation. The sleep phase, degree of hypoxia, and duration of apnea correlate with changes in blood pressure, and the increase in blood pressure is more pronounced in the REM phase than in the NREM phase. Factors that cause periodic increases in blood pressure include.
(i) The wide range of fluctuations in intrathoracic pressure formed during forceful breathing in OSA, which increases cardiac transmural pressure; with the end of apnea, the right ventricular preload, left ventricular afterload and heart rate recover, and a large amount of blood flow perfuses the constricted peripheral vascular bed, causing a transient increase in blood pressure after apnea.
(ii) Intermittent hypoxemia and elevated partial pressure of carbon dioxide stimulate peripheral chemoreceptors.
(iii) frequent awakenings and disruption of sleep architecture caused by repeated apnea during sleep.
4. frequent coexistence of metabolic disorders such as obesity, hyperlipidemia, low glucose tolerance and diabetes mellitus.
5. morning headache, dry mouth, fatigue, excessive daytime drowsiness, uneven snoring, limb agitation, breath-holding, and in severe cases, frequent awakening.
6, may be accompanied by secondary erythrocytosis.
7. Correct the sleep breathing disorder, blood pressure tends to fall, and antihypertensive drugs can be reduced or discontinued.
(iii) Pathogenesis of OSAHS combined with hypertension Several studies have shown that the altered nocturnal blood pressure profile and hypertension in OSAHS may be related to long-term recurrent nocturnal episodes of hypoxemia and hypercapnia, significant intra-thoracic pressure changes, frequent arousal responses and sleep structural disorders, and imbalance of autonomic functional status. In the combination of chronic intermittent hypoxemia, increased sympathetic activity, increased secretion of certain humoral factors, carotid body malfunction, increased vascular reactivity, genetics and age, patients with OSAHS gradually develop persistent elevated daytime blood pressure.
The association with microarousal and sleep structure disorder is significantly higher in OSAHS patients due to apnea, and repeated arousals can lead to changes in sleep structure, sleep quality and sleep deprivation. microarousals are significantly higher in OSAHS than in snoring patients alone, and the microarousal index with breathing disorder is significantly higher in OSAHS patients with combined hypertension than in OSAHS patients with normal blood pressure. Those with normal blood pressure. Acute nighttime sleep deprivation in healthy individuals also causes an increase in blood pressure in the early morning; repeated awakenings during sleep in OSAHS patients are significantly associated with an increase in blood pressure at night and during the day; long-term changes in sleep structure and decreased sleep quality cause daytime fatigue, drowsiness and reduced physical activity, leading to obesity, which is also a risk factor for the development of hypertension. risk factors for the development of hypertension. Respiratory disorders related to microarousals may have an important role in the development of hypertension in OSAHS by interfering with the sleep process and affecting sleep quality.
2. Association with sympathetic tone Sympathetic hyperfunction is one of the important pathogenic mechanisms of essential hypertension. Hedner believes that in OSAHS patients, factors such as hypoxia stimulate central and peripheral chemoreceptors and excite the sympathetic nervous system causing increased heart rate, increased myocardial contractility and systemic This leads to an increase in blood pressure at night and in the morning. The increased sympathetic nerve activity and abnormal vascular response in OSAHS patients are possible factors for the elevation of nocturnal blood pressure and daytime hypertension, and CPAP treatment can lower blood pressure by reducing sympathetic nerve activity and vascular responsiveness. It is suggested that the enhanced sympathetic tone induced by intermittent hypoxia may play an important role in the development of hypertension in patients with OSAHS.
3, Association with the renin-angiotensin-aldosterone system Studies have found that serum levels of angiotensin II are significantly higher in patients with OSAHS combined with hypertension and normal blood pressure in OSAHS, with statistically significant differences compared with normal controls, indicating that angiotensin II levels are elevated in patients with OSAHS, and that there is also a hyperactive renin-angiotensin system. The application of angiotensin-converting enzyme inhibitors for the treatment of essential hypertension and OSAHS combined with hypertension also achieved good results, and ACE inhibitors lowered blood pressure while also improving sleep apnea in patients, suggesting that elevated ACE activity may play a role in the pathogenesis of cardiovascular disease in OSAHS, indicating that the renin-angiotensin system as well as angiotensin-II play a role in OSAHS play a role in the development of hypertension.
4. Association with cell adhesion molecules and cytokines OSAHS-induced hypoxemia causes cardiovascular damage by promoting an increase in inflammatory mediators in the circulatory system. Several studies have confirmed that ICAM-1 is significantly elevated in the serum of patients with OSAHS. ICAM-1 as a major cell adhesion molecule is the main inflammatory mediator produced by a certain degree of damage to vascular endothelial cells stimulated by OSAHS-induced hypoxemia, and ICAM-1 levels are significantly correlated with AHI. OSAHS-induced hypoxemia may enhance the activity of these cell The persistent elevation of ICAM-1 and VCAM-1 levels reflects the persistence of vascular endothelial cell damage in OSAHS patients due to repeated episodes of intermittent hypoxemia, which is an important risk factor for cardiovascular disease.
5, association with endothelin and other endogenous vasoactive peptides endothelin is one of the important endogenous vasoactive peptides, its acute effect is vasoconstriction, chronic effect can make smooth muscle hypertrophy, resulting in a more persistent hypertensive state. the mechanism of elevated circulating ET-1 levels in OSAHS patients may be that intermittent hypoxemia increases the pressure of blood vessels, which increases the secretion of vascular endothelial cells, and sleep deprivation can further increase plasma endothelin levels. The decrease in endothelium-dependent vasodilatory function was significantly associated with the duration and extent of nocturnal hypoxia in patients with OSAHS. the mechanism of endothelium-dependent vasodilatory insufficiency due to OSAHS may be related to prolonged nocturnal intermittent hypoxia and changes in vascular shear stress affecting nitric oxide synthase (NOS) expression and activity and changes in vascular shear stress affecting nitric oxide synthase (NOS) expression and activity. OSAHS patients have reduced plasma NO levels and their plasma NO levels can be significantly restored. In addition, the vasoconstrictive reactivity of blood vessels is significantly increased in patients with OSAHS, which may be related to early structural changes in small arterial vessel walls; increased sensitivity of vessel walls to AT and decreased endothelin NO activity. OSAHS may contribute to the development of hypertension by causing changes in vascular tone and reactivity.