Obstructive sleep apnea (OSA) is a common disorder characterized by complete or partial airway obstruction during sleep, resulting in hypoxia, arousal, autonomic fluctuations, and sleep fragmentation. The Wisconsin Sleep Cohort study defined OSA as having an apnea-hypopnea index (AHI) of more than 5/hour and reported a prevalence rate of 24% in men and 9% in women between 30 and 60 years of age [1]. Undiagnosed or untreated OSA has significant public health implications, as it increases the risk of motor vehicle accidents, occupational injuries, daytime sleepiness, hypertension, diabetes, stroke, mood disorders, cognitive impairment, and cardiovascular diseases, such as arrhythmia, heart failure, and coronary artery disease [2]. The association between OSA and cardiac arrhythmias has been consistently reported. Studies investigating this association have shown that the prevalence of arrhythmias in patients with OSA is 48% [3]. A study comparing the prevalence of arrhythmias between individuals with OSA and those with simple snoring reported rates of 8.0% and 4.8%, respectively, demonstrating a significantly higher prevalence of cardiac arrhythmias in the OSA group [4]. Sinus tachycardia has been reported to be more prevalent in patients with OSA than in the simple snoring and control groups [5]. Although this association is well established, the connection between OSA and arrhythmia is often overlooked in clinical practice. This report highlights the connection between OSA and nocturnal sinus tachycardia, indicating that sleep-breathing disorders can trigger nocturnal cardiac symptoms.

A 58-year-old woman presented with snoring and difficulty maintaining sleep. Considering the possibility of OSA, a STOP questionnaire was administered, and the patient reported snoring and daytime fatigue. Furthermore, she had experienced nocturnal tachycardia episodes for the past 4 years and underwent a 24-hour Holter monitor test for further evaluation. The test confirmed sinus tachycardia during nocturnal tachycardia episodes, for which she was prescribed a beta-blocker (propranolol, 10 mg/day) and anxiolytic agent (alprazolam, 0.375 mg/day). The patient had diabetes and had a body mass index of 24.0 kg/m². The serum hemoglobin and thyroid hormone levels before polysomnography (PSG) were within normal ranges: hemoglobin was 11.8 g/dL (reference range: 11.2–15.0 g/dL), thyroid-stimulating hormone was 0.57 µIU/mL (reference range: 0.3–5.0 µIU/mL), and free T4 was 1.25 ng/dL (reference range: 0.75–2.00 ng/dL). In the PSG, the total sleep time was 315.5 minutes, and sleep efficiency was 66.2%. Heavy snoring was observed, and the AHI was 36.1/hour. A total of 22 apnea episodes and 168 hypopnea episodes were recorded, with hypopnea accounting for the highest proportion. The periodic limb movement index was 20.2/hour, and the arousal index was 52.9/hour. During the PSG, the mean heart rate was 71.5 beats/minutes, with a maximum rate of 148 beats/minutes. PSG revealed frequent episodes of apnea and hypopnea, leading to arousal and eventual awakening with sinus tachycardia (Fig. 1A). Moreover, the patient reported experiencing tachycardia, awakening from sleep, and anxiety during the study. OSA was suspected to be a potential cause of the nocturnal tachycardia and associated anxiety symptoms that she had been experiencing over the past 4 years (Fig. 2). Continuous positive airway pressure (CPAP) titration was performed to investigate the association between OSA and nocturnal tachycardia and determine the optimal positive airway pressure for treatment. Moreover, CPAP titration was performed, and the optimal CPAP pressure was determined to be 7 cm H₂O. During titration, tachycardia was not observed, and the frequency of apnea and hypopnea decreased significantly. (Fig. 1B). At the 3-month follow-up after CPAP therapy, the patient reported resolution of sleep maintenance difficulties and nocturnal tachycardia. Additionally, she consulted her prescribing physicians for propranolol and alprazolam, who reported that she was tapering the medication and planning to discontinue it over time.

In this study, we emphasized that despite the well-established association between OSA and arrhythmia, including nocturnal sinus tachycardia, OSA is often overlooked as a potential cause of arrhythmia in clinical practice. In our patient, several factors likely contributed to the oversight, which included a non-obese patient with a body mass index of 24.0 kg/m²; a predominance of hypopneas over apneas, masking the typical OSA symptoms; and the patient’s female gender, which is often associated with a lower clinical suspicion for OSA [6]. Thus, this study provides valuable insights into OSA-induced sinus tachycardia and emphasizes the importance of timely diagnosis and appropriate intervention.

The case report demonstrates a direct correlation between nocturnal sinus tachycardia and sleep disturbances, particularly OSA, as evidenced using PSG. The patient exhibited repetitive episodes of apnea and hypopnea, which led to arousal, awakening, autonomic fluctuations, and nocturnal tachycardia. The resolution of tachycardia after CPAP therapy further confirms the causal relationship between OSA and nocturnal sinus tachycardia. Previous studies reported that CPAP therapy reduced cardiac arrhythmias. This effect has been observed in patients with OSA presenting with atrial fibrillation (AF), and the potential of CPAP therapy to reduce AF occurrence or reverse the electrical or structural remodeling associated with OSA has been reported [7]. Moreover, this study highlights the potential for misdiagnosis and unnecessary pharmacological intervention when OSA is not considered in patients with nocturnal tachycardia.

The exact mechanism by which OSA induces cardiac arrhythmias has not been fully elucidated. However, factors such as airway collapse during sleep, hypoxia, and hypercapnia are thought to contribute to its pathogenesis [8,9]. OSA induces recurrent episodes of oxygen desaturation and increased arterial carbon dioxide levels due to dysfunction of both the baroreflex and chemoreflex. This leads to activation of the sympathetic nervous system, which contributes to abnormal atrial electrical remodeling and promotes supraventricular arrhythmias, particularly AF. Electrical remodeling disrupts interatrial conduction and facilitates atrial arrhythmogenesis. Increased sympathetic activity associated with hypoxia and arousal during respiratory events is thought to trigger action potentials in cardiac cells, thereby promoting cardiac automaticity. Furthermore, OSA causes abrupt increases in the intrathoracic negative pressure, leading to excessive cardiac stretching in the atrial and ventricular free walls, which may further predispose patients to arrhythmias. The sinus tachycardia observed in our patient was attributed to sympathetic activation induced by sleep apnea, which led to rapid activation of the sinoatrial node [10].

In conclusion, this study highlights the importance of considering OSA in patients with unexplained nocturnal tachycardia. Early recognition and treatment with CPAP may resolve tachycardia and prevent unnecessary pharmacological interventions.