Abstract
Sleep-disordered breathing (SDB) is highly prevalent in patients with cardiovascular disease. We have recently shown that an elevation of the electrocardiographic (ECG) parameter P wave terminal force in lead V1 (PTFV1) is linked to atrial proarrhythmic activity by stimulation of reactive oxygen species (ROS)-dependent pathways. Since SDB leads to increased ROS generation, we aimed to investigate the relationship between SDB-related hypoxia and PTFV1 in patients with first-time acute myocardial infarction (AMI). We examined 56 patients with first-time AMI. PTFV1 was analyzed in 12-lead ECGs and defined as abnormal when ≥4000 µV*ms. Polysomnography (PSG) to assess SDB was performed within 3–5 days after AMI. SDB was defined by an apnea-hypopnea-index (AHI) >15/h. The multivariable regression analysis showed a significant association between SDB-related hypoxia and the magnitude of PTFV1 independent from other relevant clinical co-factors. Interestingly, this association was mainly driven by central but not obstructive apnea events. Additionally, abnormal PTFV1 was associated with SDB severity (as measured by AHI, B 21.495; CI [10.872 to 32.118]; p < 0.001), suggesting that ECG may help identify patients suitable for SDB screening. Hypoxia as a consequence of central sleep apnea may result in atrial electrical remodeling measured by abnormal PTFV1 in patients with first-time AMI independent of ventricular function. The PTFV1 may be used as a clinical marker for increased SDB risk in cardiovascular patients.
Highlights
Sleep-disordered breathing (SDB) is a common co-morbidity in patients with cardiovascular disease [1,2,3]
We investigated the relationship between SDB and SDB-related hypoxia with P wave terminal force in lead V1 (PTFV1) in patients presenting with acute myocardial infarction
We show here that nocturnal oxygen desaturation in SDB was associated with atrial electrical remodeling measured by abnormal PTFV1 in patients with first-time acute myocardial infarction (AMI) independent of ventricular function
Summary
Sleep-disordered breathing (SDB) is a common co-morbidity in patients with cardiovascular disease [1,2,3]. Obstructive sleep apnea (OSA) is characterized by the presence of repetitive episodes of upper airway collapse. Central sleep apnea (CSA) is caused by an intermittent lack of centrally controlled respiratory drive, which often manifests as Cheyne–Stokes respiration and leads to significant oxygen desaturation. The most commonly used treatment is continuous positive airway pressure (CPAP), which can alleviate the clinical symptoms of SDB. The adherence to this therapy is generally poor and no significant benefit has been shown regarding cardiovascular outcome in patients with OSA [7,8].
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
