Recent studies have found that people with obstructive sleep apnea syndrome have a significantly higher incidence of atrial fibrillation (AF) than the general population.
Sleep apnea can lead to AF; it can not only cause changes in heart structure but also affect the regulatory function of the cardiac autonomic nervous system, causing neural imbalance and thus promoting the occurrence of AF.
Furthermore, sleep apnea syndrome is also an important factor in predicting whether atrial fibrillation patients will relapse after electrical cardioversion.
Treating sleep apnea with positive airway pressure (PEP) helps reduce the risk of atrial fibrillation recurrence after PEP.
Therefore, early diagnosis and treatment of obstructive sleep apnea are crucial for the initial prevention and recurrence control of atrial fibrillation.
Definition and Diagnosis of Sleep Apnea
Sleep apnea is one of the most common sleep disorders. Statistics show that approximately 24% of middle-aged men and 9% of middle-aged women suffer from obstructive sleep apnea.
Common symptoms include snoring at night, sleep apnea or waking up gasping for air, daytime fatigue and sleepiness, abnormal movements during sleep, memory loss, possible hallucinations, morning headaches and dizziness, personality changes, as well as increased nocturia, bedwetting, decreased libido, and impotence.
Sleep apnea is generally classified into three types: obstructive, central, and mixed.
Obstructive sleep apnea: The brain can send breathing commands, but due to upper airway obstruction, air cannot pass smoothly through the mouth and nose, while breathing movements still occur in the chest and abdomen.
Central sleep apnea: Because the respiratory center temporarily stops sending respiratory signals, there is no airflow through the mouth and nose, and no respiratory movements can be seen in the chest and abdomen.
Mixed sleep apnea: refers to a condition in which both obstructive and central sleep apnea occur on the same night.
Sleep apnea is defined as the complete cessation of airflow through the mouth and nose for more than 10 seconds during sleep.
Hypopnea is defined as a decrease in airflow intensity of more than 50% compared to normal levels during sleep, accompanied by a reduction in blood oxygen saturation of more than 4%.
Polysomnography (PSG) is the most authoritative method for diagnosing sleep apnea-hypopnea syndrome. Diagnosis is primarily based on the Apnea-Hypopnea Index (AHI).
It is calculated as: (the total number of apneas and hypopneas during the entire sleep period) divided by the total sleep time (in hours). Generally, an AHI index greater than or equal to 5 is sufficient for a diagnosis of sleep apnea.
OSA Is One of The Most Important Factors In AFIB
A study found that among 312 patients with atrial fibrillation, 49% had obstructive sleep apnea, compared to 32% in an equivalent number of patients with ordinary heart disease—a statistically significant difference.
Further multivariate analysis showed that high body mass index, hypertension, and the presence of obstructive sleep apnea were all significantly associated with the occurrence of atrial fibrillation.
A retrospective study followed 3,452 patients who underwent sleep apnea monitoring for an average of 4.7 years. The results showed that the incidence of atrial fibrillation was 4.3% in the group with obstructive sleep apnea (OSA), compared to only 2.1% in the group without OSA, a statistically significant difference.
Further multivariate analysis showed that obstructive sleep apnea and its resulting nocturnal oxygen saturation were independent predictors of new-onset atrial fibrillation in people under 65 years of age.
Another study found that when using an AHI > 15 as the diagnostic criterion, the proportion of obstructive sleep apnea in patients with isolated atrial fibrillation (32%) was not significantly different from that in the control group (29%), but this criterion may underestimate the proportion of patients.
A study analyzed 121 patients who developed atrial fibrillation after coronary artery bypass grafting (CABG). The results showed that even after excluding other factors, sleep apnea itself significantly increases the risk of atrial fibrillation after CABG.
How OSA Affects AFIB
Obstructive sleep apnea and atrial fibrillation share several of the same risk factors, such as male sex, obesity, hypertension, heart failure, and coronary artery disease.
These shared risk factors provide the pathological basis for sleep apnea to induce atrial fibrillation.
On the other hand, even if a patient does not have other organic heart disease, sleep apnea itself can independently cause abnormal changes in the structure and function of the heart, thereby directly leading to an increased risk of atrial fibrillation.
1.Effects of OSA on Cardiac Structure
A cardiac ultrasound study compared 43 patients with sleep apnea without severe heart disease with an age-matched obese control group and found significant differences between the two groups in several cardiac parameters:
Indicators significantly higher than the control group: right ventricular diameter, pulmonary artery pressure, and interventricular septum thickness.
Indicators significantly lower than the control group: stroke volume, left ventricular ejection fraction, mitral valve velocity, and tricuspid valve velocity.
The main mechanisms by which obstructive sleep apnea causes changes in cardiac structure include the following two aspects:
(1) Changes in cardiac load trigger structural remodeling: During respiratory arrest, the increased negative pressure within the thoracic cavity leads to both increased afterload in the left ventricle and increased venous return, increasing preload in the right ventricle and consequently decreasing preload in the left ventricle.
This long-term alteration of preload and afterload ultimately promotes structural remodeling of the heart.
(2) Enlarged left atrium increases the risk of AFIB: Sleep apnea reduces left ventricular diastolic function, leading to increased left atrial filling pressure and thus causing left atrial enlargement.
Left atrial enlargement is closely related to the occurrence of atrial fibrillation.
2.Effects of OSA on Cardiac Electrophysiology
When obstructive sleep apnea occurs, the oxygen content in the patient’s blood decreases while the carbon dioxide content increases.
This state of hypoxia and hypercarbonation directly affects the normal function of sodium, potassium, and calcium ion channels on myocardial cells.
However, current research primarily focuses on ventricular myocytes; the specific effects of hypoxia and hypercapnia on atrial myocytes remain to be further explored.
Furthermore, the dramatic fluctuations in intrathoracic pressure during sleep apnea alter the electrophysiological properties of pressure-sensitive ion channels.
In particular, changes in the properties of ion channels around the pulmonary vein ostium are considered a potential electrophysiological mechanism by which obstructive sleep apnea induces atrial fibrillation.
3.Effects of OSA on The Autonomic Nervous System
When obstructive sleep apnea occurs, increased negative pressure in the thoracic cavity is accompanied by lung expansion and hypoxemia. This process triggers two neural reflexes in sequence.
First, lung expansion stimulates airway receptors, increasing afferent signals to the vagus nerve; then, the hypoxic state further stimulates carotid chemoreceptors, leading to abnormal excitation of the cardiac sympathetic nervous system.
This imbalance between the sympathetic and vagal nerves is key to triggering atrial fibrillation (especially nocturnal atrial fibrillation).
Increased vagal tone shortens the effective refractory period of the atria, making atrial fibrillation more likely to persist; while sympathetic nerve excitation facilitates the generation of ectopic impulses (abnormal electrical signals).
Furthermore, some patients experience bradycardia when vagal tone is increased at night, and atrial fibrillation may be a compensatory tachycardia occurring on this basis.
4.OSA and Inflammation
Patients with sleep apnea often exhibit a significant inflammatory state. Studies have found that these patients have significantly higher levels of C-reactive protein (CRP) and interleukin-6 (IL-6) in their blood than healthy individuals, and these two inflammatory markers can significantly decrease after receiving positive airway pressure (PEP) therapy.
During atrial fibrillation, excessive calcium accumulation in cardiomyocytes can trigger apoptosis. CRP can participate in clearing these apoptotic cells, and subsequently, fibrous tissue replaces the original myocardium, forming fibrosis.
Fibrotic tissue disrupts normal electrical conduction in the myocardium, easily forming reentry circuits, thereby inducing arrhythmias.
In recent years, the role of inflammation in the development and progression of atrial fibrillation (AF) has received increasing attention.
Studies have shown that C-reactive protein (CRP) levels in AF patients are not only significantly higher than in the general population but also an independent predictor of AF risk; furthermore, CRP levels in patients with persistent AF are typically higher than in those with paroxysmal AF.
A large-scale clinical study called the “Cardiovascular Health Study” included 5,806 participants with an average follow-up of approximately 7 years, further confirming that higher baseline CRP levels are associated with a greater risk of developing AF in the future.
Another inflammatory marker, serum amyloid A, is also significantly elevated in patients with moderate to severe obstructive sleep apnea.
If it is deposited in atrial tissue, it may affect myocardial contraction and electrical conduction, which may be another important mechanism by which such patients are prone to atrial fibrillation.
Treatment of OSA with AFIB
There is currently no consensus in the medical community regarding whether patients with sleep apnea without obvious symptoms should receive treatment.
For patients who already have related symptoms or other comorbidities, the treatment plan must be determined comprehensively based on the specific type and severity of sleep apnea.
Patients with mild sleep apnea can improve their condition by adjusting their lifestyle, such as losing weight, quitting smoking, and limiting alcohol consumption, cultivating good sleep hygiene habits, and avoiding the use of sedative-hypnotic drugs as much as possible.
For moderate to severe cases, the preferred treatment is generally continuous positive airway pressure (CPAP). This method is suitable for all types of sleep apnea, effectively reducing the number of awakenings at night, improving sleep structure, and thus improving sleep quality.
Obstructive sleep apnea is closely related to the development and progression of atrial fibrillation (AF). Studies have shown that actively treating sleep apnea (such as through weight loss) can help prevent or reduce AF recurrence.
For example, a study of 10 patients with nocturnal paroxysmal AF and sleep apnea found that after undergoing ENT surgery, none of the patients experienced AF recurrence after a 3-6 month follow-up period.
Furthermore, as mentioned earlier, continuous positive airway pressure (CPAP) therapy for sleep apnea patients has also been shown to effectively reduce the risk of AF recurrence after electrical cardioversion.
Obstructive sleep apnea not only increases the risk of atrial fibrillation recurrence but also affects the ventricular rate during atrial fibrillation episodes.
The heart rate during atrial fibrillation is regulated by both neural pathways and the atrioventricular node. Some patients with concurrent obstructive sleep apnea (OSA) experience prolonged pauses in their heartbeat at night.
This is mostly a “functional” phenomenon caused by the apnea disrupting neural regulation and does not necessarily indicate that the heart’s conduction system is actually “damaged.”
Some of these patients have undergone permanent pacemaker implantation due to excessively slow nighttime heart rates. If sleep apnea monitoring is performed before pacemaker implantation and existing apneas are actively addressed, it may be possible to avoid unnecessary pacemaker implantation for some patients.
Currently, there is a lack of strong evidence from trials regarding the optimal treatment strategy for atrial fibrillation patients with obstructive sleep apnea.
However, given that obstructive sleep apnea is not only a significant contributing factor to atrial fibrillation but also causes damage to multiple systems throughout the body, the primary step is to actively treat sleep apnea to control its overall health risks.
If atrial fibrillation persists after effective control of sleep apnea, it should be combined with standard atrial fibrillation treatment.
Conclusion
Atrial fibrillation (AF) is currently a hot research topic in the field of cardiac arrhythmias, and obstructive sleep apnea is a common and important comorbid condition.
Therefore, proactively screening for and monitoring for related symptoms of obstructive sleep apnea is a crucial step in the diagnosis and treatment of AF. This strategy has positive value for both the initial prevention and recurrence prevention of AF.
