Obstructive sleep apnea is associated with a variety of cardiovascular diseases such as hypertension, ischemic heart disease, heart failure, stroke, arrhythmias, and pulmonary hypertension. In most cases, there is only indirect evidence to confirm the association of OSA with the development of cardiovascular disease, including the fact that the detection of OSA is time-consuming in many epidemiological studies and, to some extent, the diagnosis of OSA in large samples is a result of financial considerations. In addition, patients with obstructive sleep apnea often already have comorbidities such as obesity, hypertension, and hypoglycemia, and the independent effects of OSA on cardiovascular disease risk factors may be obscured by these comorbidities. In any case, longitudinal studies of smaller samples predisposed to cardiovascular disease and studies of the interventional effects of CPAP therapy have strongly confirmed a causal relationship between obstructive sleep apnea and multiple cardiovascular diseases. (i) Hypertension The prevalence of hypertension in adults is about 20%, and usually patients with obstructive sleep apnea have higher blood pressure than age- and sex-matched controls. About 40% of patients with obstructive sleep apnea have combined hypertension in the waking state according to the criteria, while 40% of patients with persistent hypertension have detectable obstructive sleep apnea. The most compelling data confirming the association of obstructive sleep apnea with the onset and progression of hypertension comes from the findings of the Wisconsin Sleep Population Study. Four years after the study began, the risk of developing new hypertension was three times higher in the study population with an AHI greater than or equal to 15, and this association was independent of other known risk factors such as high basal blood pressure, body mass index, age, sex, and alcohol intake and smoking, suggesting that a proportion of what is commonly thought of as essential hypertension is actually secondary to undiagnosed obstructive sleep apnea. The incidence of obstructive sleep apnea is particularly high in drug-resistant hypertension. In one study, the prevalence of obstructive sleep apnea was found to be as high as 83% in patients whose hypertension was not controlled even though they were taking two or three antihypertensive medications. Consensus guidelines for the management of hypertension have responded to the growing body of evidence suggesting a relationship between obstructive sleep apnea and hypertension. The sixth report of the 1997 Joint National Conference on the Prevention, Diagnosis, Evaluation, and Treatment of Hypertension in the United States recommended eliminating obstructive sleep apnea as a cause of intractable hypertension and specifying the importance of sleep apnea for the first time; the 2003 recommendations ranked obstructive sleep apnea as the first identifiable cause of hypertension. Patients with hypertension without a corresponding reduction in nocturnal blood pressure or “non-dippers” are at risk for cardiovascular compromise. blood pressure in patients with SDB increases repeatedly with apnea events and may exhibit a typical non-dipper pattern. The risk factors for hypertension are multifaceted, and hypertension can lead to increased incidence of cardiovascular disease and mortality. Similarly, the risk factors for OSAHS are multifaceted. An increased risk of hypertension is associated with an increased risk of sleep apnea. Moreover, even at levels of AHI where obstructive sleep apnea cannot be diagnosed at present, it is possible that this may lead to an increased incidence of hypertension, and studies have confirmed that snoring alone is associated with an increased risk of hypertension. The mechanisms by which obstructive sleep apnea causes hypertension are multifaceted. Chemoreceptor activation, subsequent sympathetic nervous system activation and elevated blood pressure due to nocturnal hypoxemia and hypercapnia may lead to excessive sympathetic nervous system activation and high blood pressure during the day. It is possible that chemoreceptor resetting and tonic chemoreceptor activation may also lead to daytime sympathetic activity and elevated blood pressure. Patients with obstructive sleep apnea also have endothelial dysfunction, elevated endothelin levels, and low nitric oxide levels, all of which may enhance the vasoconstrictive effect. Conventional treatments are more difficult to control hypertension in patients with obstructive sleep apnea than non-obstructive sleep apnea hypertension. And obstructive sleep apnea is very common in patients with intractable hypertension (up to 40%). If hypertensive patients do not respond to maximal drug therapy, 87% of them have obstructive sleep apnea, so those with obstructive sleep apnea combined with hypertension respond relatively poorly to antihypertensive drugs. A study at Peking Union Medical College Hospital confirmed that even if the daytime blood pressure of patients with obstructive sleep apnea combined with hypertension could be controlled to normal when treated with combined antihypertensive drugs, their nighttime blood pressure would still rise repeatedly if the obstructive sleep apnea was not effectively treated. Effective treatment of obstructive sleep apnea has a significant effect on daytime blood pressure in both persistent hypertension and relatively mild hypertension. Studies have shown that CPAP treatment can reduce blood pressure by approximately 10 mm Hg in hypertensive patients with obstructive sleep apnea, and this effect occurs rapidly within 4-8 weeks, with effects on both nocturnal and daytime blood pressure, but the reduction is most pronounced in the early morning. Blood pressure was more likely to fall in patients with more severe nocturnal hypoxemia prior to treatment and who used CPAP for at least 4-5 hours per night, whereas a 50% reduction in AHI alone (subtherapeutic level CPAP) did not lower blood pressure, even though it improved hypoxia and daytime sleepiness. Logan showed that even in hypertensive patients with uncontrolled blood pressure despite two or three therapeutic doses of antihypertensive drugs, there was a reduction in blood pressure after CPAP treatment, with a rapid reduction in systolic blood pressure at night and a sustained reduction in daytime and nighttime blood pressure after two months. Compared with daytime blood pressure or diastolic blood pressure, nighttime systolic blood pressure is more difficult to control and is a better indicator of cardiovascular morbidity and mortality, so CPAP therapy is particularly important for nighttime systolic blood pressure. (ii) Ischemic heart disease Controlled studies have demonstrated a correlation between sleep apnea and increased risk of myocardial infarction. In 62 patients with known coronary artery disease, the 5-year odds of death from heart disease after controlling for important risk factors such as age, weight, and smoking history were much higher for AHI >10/hour than for AHI <10/hour (37.5 and 9.3%, respectively). ODI >5 predicted a 70% relative increase in death, cerebrovascular events, and myocardial infarction, and the same results were found in patients with AHI >10/hour, with the strongest correlation being with cerebrovascular events. The Sleep Heart Health Study (SHHS) confirmed a very linear correlation between AHI and the risk of coronary heart disease, including myocardial infarction, and that any degree of SDB with AHI >1/hour was associated with most cardiovascular outcomes, and that the risk of cardiovascular disease increased progressively with the severity of SDB. The clinical significance of obstructive sleep apnea in ischemic heart disease is twofold. First, epidemiological evidence supports the notion that obstructive sleep apnea is etiologically correlated with the development of atherosclerosis. The prevalence of obstructive sleep apnea in coronary artery disease is very high, and several controlled and prospective studies have suggested that obstructive sleep apnea is an independent risk predictor of coronary artery disease. Although the exact mechanism by which obstructive sleep apnea leads to atheromatous plaque formation is unclear, a strong possibility is the involvement of inflammatory processes.CRP, a biomarker of systemic inflammation, is a risk factor for an increased incidence of coronary events and may likewise have a direct role in atheromatous plaque formation. Elevated CRP levels in obstructive sleep apnea suggest inflammation as a mechanism for OSA-associated atheromatous plaque formation. And elevated oxidative stress has been similarly noted in obstructive sleep apnea. Second, there is evidence that obstructive sleep apnea can promote acute nocturnal acute myocardial ischemia with acute ST-segment depression with or without a history of coronary artery disease, and usually does not respond to conventional therapy. Multiple OSA-related mechanisms such as hypoxemia, hypersympathetic activity, increased cardiac oxygen demand (due to tachycardia and increased systemic vascular resistance), and procoagulant state can contribute to these ischemic events. Whether these same mechanisms contribute to coronary plaque rupture and the occurrence of acute coronary events is unclear. Obstructive sleep apnea can produce acute and chronic stresses that trigger myocardial ischemia during sleep. On the acute side, significant hypoxemia, CO2 retention, sympathetic activation, and blood pressure surge can cause myocardial ischemia. On the chronic side, the development of daytime hypertension, vasoactive and nutrient production such as endothelin, and activation of inflammatory and procoagulant mechanisms can all contribute to the development and progression of ischemic heart disease. In the Sleep Heart Health Study, obstructive sleep apnea has been shown to be an independent risk factor for coronary artery disease (CAD). Nocturnal ST-segment changes consistent with myocardial ischemia are evident in patients with obstructive sleep apnea without clinically significant CAD, and ST-segment depression is more common in patients with more severe obstructive sleep apnea or a history of nocturnal angina episodes, which is clearly associated with hypoxia. CPAP therapy significantly reduces the total duration of ST-segment depression in patients with obstructive sleep apnea. The association between obstructive sleep apnea or snoring and myocardial infarction (MI) is further supported by epidemiological studies. Obstructive sleep apnea is very common in patients who have had an MI. Post-MI changes in cardiac function may predict the development of obstructive sleep apnea or may influence the severity of obstructive sleep apnea. Obstructive sleep apnea can also be used as a prognostic indicator in patients with CAD. A 5-year follow-up of 62 patients with a definite diagnosis of CAD showed a significantly higher mortality rate (38%) in patients with obstructive sleep apnea compared to patients without obstructive sleep apnea (9%), after correcting for confounding factors. In a prospective study of the effect of CPAP in patients with known coronary artery disease (coronary stenosis >70%), Milleron et al. demonstrated a significant reduction in cardiovascular mortality, acute coronary syndrome, hospitalization for heart failure, or the need for coronary revascularization in 25 treated patients with SDB compared to matched untreated patients with SDB. (iii) Cerebrovascular disease Studies have confirmed the prevalence of sleep apnea in patients with moderate to moderate rehabilitation up to 80%, and in a controlled study of newly diagnosed strokes more than 71% of these were PSG-confirmed sleep apnea, most of which were obstructive sleep apnea. There is a correlation between AHI and risk of stroke, especially at AHI <10/hour. Several studies have also demonstrated a correlation between snoring and increased risk of stroke after correcting for important confounders. In a rigorous prospective study of 161 patients with a first transient ischemic attack (TIA) or stroke, Parra et al. found that the severity of SDB did not vary with the type or site of stroke and did not change from the immediate post-stroke hospitalization until 3 months later. The presence of Chen-Schi breathing (central sleep apnea) in 26% of patients at the initial evaluation and only 7% after 3 months, and the same incidence of obstructive sleep apnea in both evaluations, led to the conclusion that obstructive sleep apnea preceded the cerebrovascular event and could possibly be its risk factor, while central sleep apnea could be its consequence. Patients with combined sleep apnea and stroke tend to have early neurological degeneration, depression, cognitive impairment, and a longer hospital recovery time. There are no prospective studies on the treatment of sleep apnea to prevent stroke, and one early study confirmed that tracheotomy reduces the risk of stroke in sleep apnea patients. In patients with combined sleep apnea and stroke, CPAP treatment appears to help lower blood pressure and improve mood, but no improvement in cognition has been shown Factors contributing to the increased risk of stroke in patients with obstructive sleep apnea include decreased blood flow with each apnea event (due to negative intrathoracic pressure and increased intracranial pressure), prethrombotic state, atherosclerosis, and hypertension. (iv) Congestive heart failure Obstructive sleep apnea is very common in patients with congestive heart failure (CHF). Central sleep apnea (CSA), another form of SDB, is also commonly seen in patients with HF. Epidemiological findings suggest a relationship between both OSA and CSA and congestive heart failure, with patients with congestive heart failure and impaired diastolic function being particularly susceptible to combined OSA - approximately half of patients with impaired diastolic function in a small sample study had an AHI greater than 10. The incidence of obstructive sleep apnea combined with CHF was as high as 11%. Soft tissue edema (exacerbated by supine sleep) and the consequent increase in upper airway resistance can lead to increased inspiratory force and upper airway collapse, thereby increasing the risk of new-onset obstructive sleep apnea. In contrast, epidemiological data suggest that, independent of other risk factors, obstructive sleep apnea is also associated with an increased risk of CHF. OSA may contribute to CHF through its effects on sympathetic drive, endothelin, endothelial function, hypertension, and ischemic heart disease, which are known to be important risk factors for CHF. In addition, OSA may enhance acute ventricular dysfunction by increasing transmural pressure and ventricular wall stress. . The combined presence of OSA and CHF thus creates a vicious cycle leading to progressive CHF, with OSA worsening cardiac function and the latter subsequently exacerbating OSA. A sleep apnea prevalence study confirmed that SDB is common in patients with heart failure, and the Sleep Heart Health Study confirmed a strong correlation between OSA severity and CHF in patients with obstructive sleep apnea with an AHI >11. Risk factors for comorbid OSA in patients with HF include obesity in men and women older than 60 years. CSA is also common in reduced left ventricular function, even in the absence of significant heart failure. The incidence of CSA in CHF is 40-63%, and in most of the current literature, CSA in CHF refers to Cheyne-Stokes Respiration, which is characterized by augmented-decompensated breathing that can be spaced by central apnea. CSA in CHF can increase mortality. As in patients with obstructive sleep apnea, CPAP therapy is beneficial for CSA, improving left ventricular ejection fraction, reducing mortality, and increasing non-transplant survival. OSA may directly contribute to the development of systolic and diastolic dysfunction in patients. Hypoxemia during sleep, spikes in adrenaline levels, elevated blood pressure, and daytime hypertension together may predispose them to the development of hypertensive heart failure. This can manifest as both systolic and diastolic dysfunction. Systolic dysfunction can also be caused by inflammatory cytokines that affect myocardial contractility, as well as afterload and myocardial wall stress due to rapid changes in transmural pressure differentials caused by negative intrathoracic pressure during OSA events. Hypertension and endothelin together with myocardial nutrients such as epinephrine can lead to structural changes in the heart that affect diastolic function. Congestive heart failure itself can also affect the development of OSA. Patients with congestive heart failure are prone to periodic respiration. During periodic breathing, respiratory drive and drive to the pharyngeal dilator muscles is reduced, and collapse of the upper airway results. Edema in patients with congestive heart failure can also involve the soft tissues of the cervicopharynx, especially in the supine position, which can also further lead to narrowing of the upper airway, increased resistance of the upper airway, and therefore make the upper airway more prone to collapse. Sympathetic system and inflammatory activation during sleep apnea and other mechanisms can worsen the prognosis of patients with heart failure and obstructive sleep apnea. Treatment of patients with OSA or CSA in combination with heart failure can be of significant benefit. In a small study of patients with heart failure combined with obstructive sleep apnea, there was indeed a very definite improvement in ejection fraction and cardiac function class after CPAP treatment. In some of these patients, these indicators worsened again after discontinuation of treatment. In patients with combined obstructive sleep apnea and heart failure, CPAP improved left ventricular ejection fraction and quality of life, and reduced blood pressure and sympathetic activity. In an Australian study, the mean CPAP pressure was 8.8 cmH2O and the mean duration of nighttime use was 5.6 hours. In the Kaneko study the mean CPAP use time was 6.2 hours per night. It is not clear what the effect of CPAP is on very mild OSA or diastolic function. roebuck et al. reported that although OSA is often combined and may even lead to heart failure, there is no increase in long-term mortality (>4 years), although there is an increase in short-term mortality in those with OSA combined with SDB. In contrast, patients with OSA combined with heart failure are mostly not drowsy as evaluated by traditional methods (e.g., Epworth score), which may also contribute to their lower compliance to CPAP therapy. Unlike OSA, CSA is more a consequence than a cause of the development of HF, which is caused by fluctuations in PaCO2 up and down in the apnea domain, and HF combined with CSA is more likely to be hypocapnic, as HF is more likely to have pulmonary stasis, which stimulates vagal excitatory receptors, increases central and peripheral chemosensitivity, and increases microarousals during sleep. And CSA has the same effect on deteriorating cardiac function as OSA except that it does not produce negative intrathoracic pressure during apnea. Although CSA is mostly a non-HF cause, treatment for CSA is also beneficial, and HF patients with combined CSA improve their left ventricular ejection fraction and mortality when treated with CPAP. results from studies of the effects of CPAP on patients with combined heart failure with CSA suggest that treatment of CSA also appears to improve non-transplant survival. (v) Arrhythmias The likelihood of arrhythmias is reduced in normal sleep because of reduced sympathetic nerve activity. Atrial and ventricular premature beats are very common, but the most common arrhythmias are severe sinus bradycardia, sinus block and atrioventricular block. Other tachyarrhythmias such as sustained supraventricular tachycardia, atrial fibrillation or atrial flutter, and ventricular arrhythmias, especially sustained or unsustained ventricular tachycardia, occur more frequently in patients with preexisting structural heart disease. Guilleminault demonstrated that the prevalence of arrhythmias during single-night sleep in patients with obstructive sleep apnea was 48%, including persistent ventricular tachycardia in 2%, sinus arrest in 11%, second-degree AV block in 8%, and frequent premature ventricular contractions in 19%. The rate of arrhythmias during sleep in patients with obstructive sleep apnea was found to be as high as 58%, and nocturnal hypoxemia was more severe in patients with arrhythmias. Significant sinus arrhythmias are very common in significant sleep apnea and have been shown to be a strong indication for positive findings on PSG monitoring. Studies have also confirmed that OSA can also be associated with supraventricular and ventricular tachycardia, although the latter is more likely to occur in other heart conditions such as ischemic heart disease or heart failure. The Peking Union Medical College Hospital also demonstrated a significantly higher incidence of arrhythmias in patients with obstructive sleep apnea compared to those with non-obstructive sleep apnea (56.2% vs. 36.4%), with 82 of 146 patients with obstructive sleep apnea having arrhythmias (56.2%), including premature beats or tachycardia, conduction block, or both. Nineteen of these patients with severe obstructive sleep apnea combined with arrhythmias were treated with nasal continuous positive airway pressure (nCPAP) for 7 hours, and 14 of them (73.7%) had complete resolution of arrhythmias after treatment. The study confirmed that the incidence of arrhythmia was positively correlated with the severity of hypoxia and nocturnal apnea. nCPAP was effective in treating OSA while reversing or improving arrhythmias. Nocturnal bradyarrhythmias in patients with obstructive sleep apnea are usually the result of a “dive reflex” in response to apnea and hypoventilation, i.e., an increased vagal tone reflex. Bradyarrhythmias often occur even in the absence of any cardiac conduction system abnormalities and disappear after effective obstructive sleep apnea treatment. Gami et al. found that 49% of AF patients with elective electrical resuscitation had significant SDB, a higher incidence than in the general cardiac population (32%), and that sinus rhythm was maintained in these patients if they were treated with CPAP after electrical resuscitation. Hypoxemia, sympathetic activation, blood pressure surge, and cardiac distortion during an obstructive apnea event can predispose to the development of atrial fibrillation. In patients with previous AF, those with untreated sleep apnea were twice as likely to have a recurrence of AF within 12 months as those with obstructive sleep apnea treated with CPAP. Therefore, any treatment that includes long-term atrial pacing needs to clarify the potential relationship between obstructive sleep apnea and atrial fibrillation, and CPAP should be tried first if the patient has obstructive sleep apnea. Because patients with obstructive sleep apnea sometimes fall asleep during the day, daytime bradycardia may also originate from obstructive sleep apnea. Arrhythmias are significantly reduced after CPAP treatment and disappear completely after four months of treatment.