OSAHS is characterized by recurrent episodes of breathing cessation during sleep, each lasting more than 10 s and occurring over 30 times within a 7-h sleep period, or by an apnea-hypopnea index (AHI) of five or more events per hour (1, 2). This disorder, primarily resulting from the collapse of the upper airway, triggers physiological changes such as elevated heart rate, increased blood pressure, and negative intrathoracic pressure, ultimately leading to hypoxemia, hypercapnia, and disrupted sleep architecture (3). These pathophysiological effects manifest in excessive daytime sleepiness, heightened cardiovascular risk, and progressive damage to multiple organs, thereby decreasing both life expectancy and overall quality of life (4). Globally, OSAHS is a prevalent condition, particularly among individuals who are overweight, obese, or elderly, with an estimated prevalence ranging from 3% to 7% in men and 2% to 5% in women (5).

Recent studies have established a strong association between OSAHS and cardiac arrhythmias, particularly AF. Patients with OSAHS experience cyclical fluctuations in heart rhythm and elevated catecholamine levels, which significantly heighten the risk of tachyarrhythmias and heart failure (6). Evidence indicates that adults with OSAHS are two to four times more likely to develop AF, with approximately 39% of individuals diagnosed with atrial fibrillation (AF also exhibiting OSAHS (5). Proposed mechanisms underlying this relationship include increased negative intrathoracic pressure, as well as enhanced vagal and sympathetic nervous system activity, both of which may contribute to atrial structural and electrical remodeling, thereby amplifying the risk of AF (7, 8).

We hypothesized that simple indicators in patients with sleep disorders could predict serious arrhythmias for early identification. The 12-lead electrocardiogram (ECG) stands out as a widely utilized, cost-effective, and patient-friendly diagnostic tool (9). The P-wave on the ECG, which reflects atrial depolarization, provides valuable insights into atrial health across a range of pathological conditions. Specifically, PWPs are instrumental in identifying atrial enlargement and conduction abnormalities. A comprehensive review has affirmed that alterations in PWPs are significantly associated with adverse clinical outcomes, including atrial fibrillation, ischemic stroke, sudden cardiac death, heart failure, and cognitive impairment, underscoring their critical relevance in clinical practice (10).

In this study, we are examining a range of PWPs that reflect atrial structural and electrical activity, including P-wave duration (PWD) and P-wave area (PWA) (10). To further assess atrial electromechanical dysfunction, we analyzed two well-established electrocardiographic markers. The Macruz Index (11), calculated as the ratio of PWD to the PR segment, serves as an indicator of interatrial conduction heterogeneity and is known to increase significantly in the presence of structural atrial remodeling. Another marker, P-terminal force in lead V1 (PtfV1) (12), quantified as the product of negative P-wave duration and voltage (ms mV), reflects left atrial enlargement and delayed conduction, with abnormal values (typically ≥0.04 mm s) predicting AF risk. Notably, patients with persistent atrial fibrillation or atrial flutter were excluded from this study due to the absence of a sinus P wave, which is essential for accurate P-wave analysis. Additionally, we applied the Kleiger grading system in an innovative manner by redefining the outcome endpoint as the occurrence of complex atrial, arrhythmias, a category previously identified as having a higher likelihood of progressing to AF (13, 14).

This study aimed to identify non-invasive predictors of complex atrial arrhythmias in patients with OSAHS using standard electrocardiographic tools. A total of 187 patients presenting with difficulty falling asleep were analyzed, with comparisons made between those in the control group (AHI < 5) and those with varying degrees of OSAHS severity. Our findings underscore the clinical utility of PWPs, particularly PtfV₁ and the Macruz Index, as effective indicators for identifying patients at elevated risk of developing complex atrial arrhythmias. The four data points collected (ECG, PSG, echocardiogram, and Holter monitoring) are non-invasive, affordable, and feasible. Additionally, we accounted for variables affecting the OSAHS severity and atrial arrhythmias, boosting the reliability of the results.

According to the American Heart Association, OSAHS arises from the interaction between upper airway anatomical characteristics and sleep-related changes in airway function, and is closely linked to cardiovascular conditions such as hypertension and heart failure (20). The significant health and economic burden posed by OSAHS and its associated comorbidities highlights the urgent need for early risk stratification. ECG changes can serve as physiological markers of respiratory events, aiding not only in the detection of OSAHS but also in assessing its severity (21). Recent advances have demonstrated the effectiveness of deep learning models using single-lead ECG signals to classify OSAHS severity with high accuracy (22). In alignment with these technological developments, our study utilizes the more widely available 12-lead ECG to investigate electrophysiological markers predictive of arrhythmic risk in patients with OSAHS.

Apnea-induced hypoxemia and hypercapnia activate the sympathetic nervous system, leading to elevated heart rate and peripheral vasoconstriction (23). This recurrent autonomic stress, coupled with intrathoracic pressure fluctuations during apneic episodes, contributes to myocardial remodeling and dysfunction (24). These pathophysiological changes specifically increase left atrial (LA) afterload, promote structural alterations such as fibrosis, and prolong atrial conduction time, reflected electrophysiologically through changes in P-wave alterations (25). The resulting increase in sympathetic tone and atrial structural remodeling associated with OSAHS facilitates the onset of atrial arrhythmias, particularly AF. Our findings are consistent with this mechanism: patients with OSAHS who developed complex atrial arrhythmias exhibited significantly prolonged PWD and enlarged left atrial diameter (LAD). Multivariable logistic regression analysis confirmed both LAD (OR = 1.15, p < 0.05) and PWD as significant risk factors, supporting the hypothesis that OSAHS-induced atrial stretch and conduction delay contribute to arrhythmogenesis. This is further corroborated by follow-up observations in which several patients with severe OSAHS progressed to AF. Notably, continuous positive airway pressure (CPAP) therapy has been shown to reduce AF recurrence in this patient population (26).

An international consensus document endorsed by the International Society for Holter and Noninvasive Electrocardiology (ISHNE) has acknowledged the predictive value of PWPs in certain cardiovascular conditions (10), suggesting a future direction in which alterations in P-wave characteristics may serve not only as reflections of atrial structural and electrical activity but also as indicators of underlying pathophysiological changes during disease progression. Our findings reinforce this potential within the context of OSAHS-associated arrhythmias. To ensure measurement accuracy, we utilized advanced ECG analysis software capable of automatic PWP calculation, which enhanced waveform magnification for precise boundary detection. Given the limitations and variability associated with manual P-wave measurements, the use of such software significantly improved reliability by clearly identifying the onset and offset of the P-wave and PR segment (27). In the domain of cardiac electrophysiology, excitation initiated by the sinoatrial node produces the P-wave, with its first half representing right atrial depolarization and the latter half corresponding to left atrial depolarization. Anatomical changes such as right atrial enlargement can increase P-wave amplitude, while left atrial enlargement often results in prolonged PWD. Ultimately, the morphology of the P-wave during sinus rhythm is shaped by complex interactions between anatomical structures, electrophysiological properties, and geometric orientations (28).

PWD serves as a direct and reliable measure of atrial conduction time, with numerous studies demonstrating a positive correlation between both the presence and severity of OSAHS and P-wave prolongation observed on a 12-lead ECG. This prolongation, coupled with uneven sinus node excitation, may predispose patients to atrial arrhythmias (29). Apneic episodes impose increased mechanical and pressure load on the left atrium, leading to structural remodeling and prolonged PWD, and have been identified as independent predictors of atrial scar formation (30). Histopathological investigations further link P-wave morphology changes to conduction disturbances and fibrofatty infiltration of atrial tissue. Specifically, delayed conduction through Bachmann's bundle, referred to as interatrial block, can result in atrial remodeling and asynchronous atrial contraction (31). In our study, 98 out of 187 patients developed complex atrial arrhythmias, with this group demonstrating a significantly higher incidence of PWD prolongation compared to those with simple arrhythmias. The observed prolongation reflects a delay in atrial conduction likely associated with hypoxia-induced fibrotic changes, supporting prior research findings. Moreover, structural remodeling of atrial tissue and electrical conduction abnormalities appear to be key contributors to the complexity and persistence of these arrhythmias (Figure 4).

PtfV₁ demonstrates a moderate correlation with left atrial size and has been associated with a range of cardiovascular conditions, including sudden cardiac death. It represents left atrial activation via Bachmann's bundle, typically producing a negative deflection in lead V₁ on the ECG (24, 32). Increasingly, researchers are investigating PtfV₁ to explore the pathophysiological link between OSAHS and AF. Elevated PtfV₁ values in OSAHS patients are indicative of abnormal left atrial electrophysiological activity, which may explain the association between OSAHS and adverse cardiovascular outcomes such as AF and stroke (17). Importantly, PtfV₁ has also been shown to predict ischemic stroke independently of AF, highlighting the clinical significance of left atrial abnormalities in thromboembolic risk (33). AF, one of the most common arrhythmias in adults, is closely associated with increased risks of stroke, heart failure, cardiovascular mortality, and sudden cardiac death (34). In our study, patients with moderate and severe OSAHS exhibited significantly higher PtfV₁ levels than those in the control and mild OSAHS groups (Figure 5). Furthermore, logistic regression analysis confirmed PtfV₁ as an independent and significant predictor of complex atrial arrhythmias. (OR = 1.61, 95% CI: 1.17–2.21, p < 0.01), reinforcing its diagnostic and prognostic value in identifying OSAHS patients at increased arrhythmic risk.

In this study, we investigated the novel application of the Macruz Index, defined as the ratio of PWD to the PR segment, in patients with OSAHS. First introduced by Macruz and Perloff in 1958, this ECG-derived index was originally proposed as a simple method for detecting atrial enlargement (35). The Macruz Index has since attracted growing clinical interest for its diagnostic value. In cases of right atrial enlargement, the PWD typically remains stable, while the PR segment increases, resulting in a lower Macruz Index. Conversely, left atrial enlargement is characterized by prolonged PWD relative to the PR segment, which leads to an elevated index value, often exceeding the normal upper limit of 1.6 (11). This physiological basis underscores the index's sensitivity to left atrial conduction disturbances. Previous research has demonstrated significantly higher Macruz Index values in patients with multiple sclerosis compared to healthy controls, further indicating its utility in detecting subclinical atrial abnormalities. Moreover, a marked reduction in the Macruz Index has been reported following successful percutaneous mitral balloon valvuloplasty, suggesting its responsiveness to structural and functional cardiac changes (36). Recent studies have also established a strong association between elevated Macruz Index values and AF recurrence following radiofrequency ablation, highlighting its potential as a cost-effective and practical predictor for post-ablation AF recurrence (37).

In our study, compared with Group I, patients in Group II exhibited higher levels of several clinical indicators, including BMI, AHI, LAD, PWD, PtfV1, and the Macruz index, particularly among male patients, while the minimum SpO2 value was notably lower. These disparities suggest that chronic intermittent hypoxia and fluctuating intrathoracic pressure in OSAHS patients contribute to left atrial dilation and fibrosis, pathological changes that prolong PWD, elevate PtfV1, and amplify the Macruz index. An elevated PtfV1 typically reflects increased left atrial pressure, whereas a heightened Macruz index is more indicative of prolonged atrial conduction time. Enlargement of the left atrial anterior-posterior diameter offers a structural substrate conducive to the development of atrial arrhythmias, underscoring the mechanisms of atrial remodeling in OSAHS. The box plot analysis further illustrates that median PtfV1 in Group II was significantly elevated (median = 2.055 ms mV, IQR = 3.17) with greater variability compared to Group I (median = 1.05 ms mV, IQR = 1.89). Similarly, the Macruz index in Group II demonstrated higher mean and median values (2.38/2.24 vs. 1.82/1.79) and a broader interquartile range (1.07 vs. 0.57), indicating increased central tendency and dispersion. ROC curve analysis revealed that both PtfV1 and the Macruz index possess clinical utility in predicting complex arrhythmias in OSAHS patients: PtfV1 showed the highest specificity (80.9%), while the Macruz index, despite a lower AUC value (0.681), maintained good specificity (77.5%) and moderate sensitivity (59.2%). While PtfV1 demonstrates moderate predictive capacity, the Macruz index offers superior positive predictive value but is slightly less effective in ruling out negative cases, suggesting its greater suitability for identifying high-risk individuals, whereas PtfV1 is better suited for excluding those at lower risk. Collectively, these findings support the use of PtfV1 and the Macruz index in tandem as robust indicators for stratifying the risk of complex atrial arrhythmias in patients with OSAHS.

This study demonstrates that PWPs derived from 12-lead ECG, particularly PtfV1 and the Macruz index, possess significant predictive value for identifying patients with OSAHS who are at elevated risk for developing complex atrial arrhythmias. While the study has certain limitations, the findings lay a valuable foundation for enhancing risk stratification and guiding early clinical interventions in this high-risk population.