Hypertension The Seventh Report on Hypertension in the United States listed OSAHS as the leading cause of secondary hypertension. Data from 20 hospitals in China showed that the incidence of hypertension in OSAHS patients was 49.3%, and the incidence of hypertension increased with increasing AHI. Intermittent hypoxia in OSAHS patients stimulates carotid chemoreceptors and causes post-apnea sympathetic nervous system excitation, leading to blood pressure fluctuations. Intermittent hypoxia also directly damages the vascular endothelium, activates the renin-angiotensin-aldosterone system, initiates inflammation and oxidative stress, and accelerates target organ functional damage and apoptosis. The rapid increase in negative intrathoracic pressure during apnea increases transmural gradients in the atria, ventricles, and aorta, and causes a rapid increase in return blood volume and elevated blood pressure. Long-term chronic effects can cause hypertrophy of vascular smooth muscle, leading to increased blood pressure during sleep and after waking at night. 24-h non-arytenoid and anti-arytenoid blood pressure changes and nocturnal hypertension are very common in patients with OSAHS. The risk of coronary heart disease is 1.2 to 6.9 times higher in patients with OSAHS than in the normal population. Moderately severe (AHI ≥ 20 beats/h) OSAHS is an independent risk factor for coronary heart disease, and AHI is an independent predictor of coronary heart disease death. The 5-year mortality rate was 24.6% higher in patients with coronary artery disease combined with OSAHS than in the control group. CPAP treatment for patients with OSAHS can help reduce the morbidity and mortality of patients with coronary heart disease and improve the prognosis. Possible mechanisms of coronary artery disease in OSAHS: (1) hypoxia and hypercapnia; (2) intermittent hypoxia and ischemia-reperfusion cause oxidative stress; (3) decreased SaO2 stimulates renal secretion of erythropoietin and increases blood viscosity; (4) patients with OSAHS are in a pre-thrombotic state; (5) increased endothelin-1, a blood constrictor, and decreased nitric oxide, a diastolic substance; (6) activation of CPAP in patients with OSAHS; and (7) increased endothelin-1 and decreased nitric oxide in patients with OSAHS. (6) Activation of inflammatory factors affects lipid metabolism. Arrhythmias Almost all types of arrhythmias can be observed in patients with OSAHS, especially slow arrhythmias and sudden cardiac death are significantly more frequent. Arrhythmias tend to occur at night and correlate with the severity of OSAHS. It is believed that autonomic disorders, inflammatory responses and oxidative damage, which affect sinus node and atrioventricular conduction function, are the main causes of slow arrhythmias in patients with OSAHS. Slow arrhythmias increase blood viscosity and slow blood flow, which predispose to cardiac emergencies. Studies suggest that patients with atrial fibrillation combined with OSAHS have a recurrence rate more than two times higher after ablation than patients without sleep apnea. In addition, persistent hypoxemia, hypercapnia, sympathetic hyperexcitability and left atrial traction may create new lesions and lead to AF recurrence. OSAHS is an independent predictor of AF recurrence, and treatment with CPAP may reduce the risk of AF recurrence. Chronic heart failure In patients with chronic heart failure, sleep apnea has a high incidence and can precipitate and exacerbate chronic heart failure. Central sleep apnea is most often seen in patients with chronic heart failure. The mechanism by which OSAHS and central sleep apnea affect chronic heart failure: increased negative intrathoracic pressure causes increased left ventricular transmural pressure, which increases left ventricular afterload; increased venous return blood volume causes increased right ventricular internal diameter, left septal shift prevents left ventricular filling and decreases left ventricular compliance, which decreases preload; decreased cardiac output per beat, decreased oxygen supply, and increased myocardial ischemia, which can trigger or worsen chronic heart failure in the long term. chronic heart failure. The increased sympathetic excitability and peripheral vasoconstriction in sleep apnea patients; and the increase in cardiac output after the termination of apnea increases the peripheral vascular resistance, causing a sudden rise in blood pressure and an increase in heart rate, which increases the burden on the heart and increases myocardial oxygen consumption. Continuous sympathetic excitation promotes the release of catecholamines, accelerates myocardial remodeling, and induces arrhythmias.