Influence of sleep apnea on autonomic nervous activity and QT dispersion in patients with essential hypertension and old myocardial infarction

• Published in: Journal of electrocardiology Vol. 37; no. 1; pp. 31 - 40
• Main Authors: Yamashita, Jyunji, Nomura, Masahiro, Uehara, Kohzou, Nakaya, Yutaka, Uemura, Eiko, Iga, Akiko, Sawa, Yuko, Nishikado, Akiyoshi, Saito, Ken, Ito, Susumu
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 2004; Elsevier Science Ltd
• Subjects: autonomic nervous activity; Autonomic Nervous System - physiopathology; cardiac events; Electrocardiography, Ambulatory; Female; Heart Rate - physiology; Humans; Hypertension - complications; Hypertension - physiopathology; Male; Middle Aged; Myocardial Infarction - complications; Myocardial Infarction - physiopathology; QT dispersion; Retrospective Studies; SAS; Sleep Apnea Syndromes - complications; Sleep Apnea Syndromes - physiopathology; autonomic nervous activity; cardiac events; SAS; QT dispersion
• DOI: 10.1016/j.jelectrocard.2003.10.009
• ISSN: 0022-0736

Sleep apnea syndrome (SAS) is an important cardiovascular risk factor in patients with hypertension or myocardial infarction (MI). We evaluated the influence of SAS on autonomic nervous activity and QT dispersion in patients with hypertension or coronary artery disease with old MI. A portable sleep polygraph was attached to 30 healthy volunteers (N group), 30 patients with essential hypertension (HT group), and 30 patients with old myocardial infarction (MI group) to serially record oronasal respiration, tracheal sound, thoracic respiratory movement, and percutaneous arterial oxygen saturation. In addition, a digital Holter ECG was used to examine heart rate variability during nighttime sleep. Heart rate variability was analyzed by obtaining low-frequency (LF) power, high-frequency (HF) power, the LF/HF ratio, and very low-frequency (VLF) power. Dispersion of QT intervals was obtained by CM5 and CM1 leads. VLF and LF powers were significantly higher in the HT-SAS group (hypertensive patients with SAS) than the N and HT-NSAS groups (hypertensive patients without SAS). The HF power was significantly lower in the HT-NSAS group than the N group, but the decrease in HF power in hypertension was not observed in the HT-SAS group. The LF/HF ratio was significantly higher in the HT-NSAS group than the N group, and this value was further increased in the HT-NSAS group. Percutaneous arterial oxygen saturation was decreased, and QT dispersion was significantly increased in the MI group during sleep apnea episodes. More severe autonomic nervous dysfunction and increased QTc dispersion were observed in hypertensive patients with SAS during episodes of apneas and hypopneas compared to those without SAS. These findings suggest that SAS may be associated with the future development of cardiac events.