This is an obvious violation of the following "Instructions to Authors": Submission of a manuscript to the Circulation Journal implies that the article is original and that no portion (including figures or tables) is under consideration elsewhere or has been previously published in any form other than as an abstract. Previous publication includes publishing as a component of symposia, proceedings, transactions, books (or chapters), articles published by invitations or reports of any kind, as well as in electronic data bases of a public nature.Therefore, we have decided to retract the paper from Circulation Journal.As Editor-in-Chief, I regret the time that peer reviewers and others spent evaluating this paper.I sincerely hope and trust that there will be no repetition of this kind in the future.
Hiroaki Shimokawa, MD, PhDEditor-in-Chief Circulation Journal (Released online August 3, 2010)
R E T R A C T I O Nbstructive sleep apnea (OSA) is characterized by periodic complete or partial upper airway obstruction during sleep, causing intermittent cessation of breathing (apnea) or reduction in airflow (hypopnea) despite ongoing respiratory effort. This disorder has been described for decades, but its recognition has remained a problem. OSA appears to be an independent cardiovascular risk factor; several epidemiologic studies have identified OSA syndrome as an independent risk for systemic hypertension, coronary artery disease, stroke, and cardiac arrhythmias. [1][2][3][4] There are conflicting data in the literature on the association between OSA and left ventricular (LV) hypertrophy. Although some investigators have reported that patients with OSA develop LV hypertrophy independently of hypertension, 5 others have found no difference between patients with OSA and control subjects in LV mass (LVM). 6,7 LV Circulation Journal Vol.70, June 2006 diastolic dysfunction is regarded as an early sign of myocardial disease and an important determinant of symptoms and clinical outcome in patients with cardiovascular disease. 8 It has been shown recently that impaired LV diastolic filling occurs in OSA patients with no other active pulmonary or cardiac disease. 9 Clearly, it is important to know whether OSA alone constitutes an independent risk factor for the development of LV dysfunction and hypertrophy, and thus for increased cardiovascular morbidity and mortality.Aortic elastic properties are important determinants of blood pressure (BP) and LV function. The aorta functions not only as a conduit delivering blood to the tissues but also as an important modulator of the entire cardiovascular system, buffering the intermittent pulsatile output from the heart to provide steady flow to the capillary beds. By virtue of its elastic properties, the aorta influences LV function, structure and coronary blood flow. 10 Consequently, we hypothesized that OSA affects the functional and structural properties of large arteries, contributing to impaired LV function and changes in the LV geometry.