Obesity or sleeping in the wrong position can cause snoring, a small thing that can happen every night. However, snoring may mean more than just noise, as “snoring rhythm” may serve as indirect evidence that you are at a higher cardiovascular risk. If you have snoring at night with irregular snoring, disturbance of breathing and sleep rhythm, recurrent apnea and awakening, or conscious breath-holding, increased nocturnal urination, morning headache, dry mouth, significant daytime drowsiness, memory loss, or even arrhythmia, especially slow-fast arrhythmia, then be careful, it may be obstructive sleep apnea syndrome (OSA). OSA.) Obstructive sleep apnea is a rarely diagnosed clinical condition characterized by recurrent episodes of upper airway obstruction leading to sleep fragmentation and intermittent hypoxia during sleep. The absence of oral and nasal airflow during episodes and the persistence of thoracoabdominal breathing: the apnea occurs due to upper airway obstruction, but the respiratory drive of the central nervous system is normal and continues to send respiratory motor commands to excite the respiratory muscles, so thoracoabdominal breathing movements persist. Patients with OSA are able to compensate for upper airway narrowing by increasing upper airway muscle activity, thereby maintaining airway patency during wakefulness. In contrast, when the muscles relax during sleep the upper airway becomes obstructed and this protective effect is lost during sleep. Obesity is a major risk factor for OSA because it promotes the enlargement of soft tissue structures in and around the airway, which significantly contributes to pharyngeal airway narrowing. Excessive fat deposition is also observed under the mandible and tongue, soft palate and uvula in obese patients. The combination of increased abdominal fat mass and recumbent posture resulted in a significant reduction in lung volume. Reduced lung volume may decrease longitudinal tracheal traction and pharyngeal wall tension, which can narrow the airway and make it more prone to obstruction. In addition, obesity-related leptin resistance may impair neuroanatomical interactions leading to airway constriction. Additional risk factors include aging, anatomical abnormalities of the upper airway (nasal obstruction, tonsillar hypertrophy, soft palate laxity, etc.), family history, use of hypnotic or muscle relaxant drugs, and chronic smoking. The prevalence of OSA is increasing worldwide due to the ongoing obesity epidemic and the susceptibility of obese individuals to develop OSA. Recent research evidence suggests that obese patients with OSA have significantly increased proxies for cardiovascular risk, including sympathetic activation, systemic inflammation, and endothelial dysfunction, compared to obese patients without OSA, suggesting that OSA is not merely incidental to obesity. In addition, findings in animal models and patients with OSA suggest that intermittent hypoxia exacerbates the metabolic dysfunction of obesity, thereby exacerbating insulin resistance and NAFLD. The relationship between OSA and hypertension is supported by substantial clinical trial evidence that elevated blood pressure in OSA is multifactorial and may depend on sympathetic overactivity, systemic inflammation, oxidative stress, endogenous vasoactive factors, and endothelial dysfunction. The diagnosis of OSA relies on polysomnography testing, and formal monitoring generally requires no less than 7 h of sleep throughout the night, with the criterion of ≥5 sleep apnea indices per hour. For the treatment of OSA, continuous positive airway pressure ventilation therapy is preferred. A randomized controlled crossover study showed that 3 months of effective treatment of OSA with continuous positive airway pressure ventilation (CPAP) significantly reduced several components of the metabolic syndrome, including blood pressure, triglycerides, and visceral fat. Finally, several cohort studies have consistently shown that OSA is associated with increased cardiovascular mortality, independent of obesity. In conclusion, these results support the concept that OSA exacerbates cardiometabolic risk due to obesity and the metabolic syndrome. In addition to this general treatment needs to be addressed: weight loss, diet and weight control, appropriate exercise alcohol cessation, smoking cessation, caution with sedative-hypnotic drugs and other drugs that can cause or aggravate OSA; sleep in the lateral position; appropriate bed elevation; and avoid overexertion during the first day.