Author + information
- Received January 24, 2013
- Revision received April 7, 2013
- Accepted April 7, 2013
- Published online August 13, 2013.
- Apoor S. Gami, MD, MSc∗,†,‡,
- Eric J. Olson, MD‡,§⋮,
- Win K. Shen, MD†,‡,
- R. Scott Wright, MD†,‡,
- Karla V. Ballman, PhD¶,
- Dave O. Hodge, MS¶,
- Regina M. Herges, BS¶,
- Daniel E. Howard, MD, MPH‡ and
- Virend K. Somers, MD, PhD†,‡∗ ()
- ∗Section of Electrophysiology and Pacing, Midwest Heart Specialists–Advocate Medical Group, Elmhurst, Illinois
- †Division of Cardiovascular Diseases, Mayo Clinic College of Medicine, Rochester, Minnesota
- ‡Department of Medicine, Mayo Clinic College of Medicine, Rochester, Minnesota
- §Sleep Disorders Center, Mayo Clinic College of Medicine, Rochester, Minnesota
- ¶Division of Pulmonary and Critical Care Medicine, Mayo Clinic College of Medicine, Rochester, Minnesota
- ⋮Department of Biostatistics, Mayo Clinic College of Medicine, Rochester, Minnesota
- ↵∗Reprint requests and correspondence:
Dr. Virend K. Somers, Mayo Clinic College of Medicine, Division of Cardiovascular Diseases, 200 First Street, SW, Rochester, Minnesota 55905.
Objectives This study sought to identify the risk of sudden cardiac death (SCD) associated with obstructive sleep apnea (OSA).
Background Risk stratification for SCD, a major cause of mortality, is difficult. OSA is linked to cardiovascular disease and arrhythmias and has been shown to increase the risk of nocturnal SCD. It is unknown if OSA independently increases the risk of SCD.
Methods We included 10,701 consecutive adults undergoing their first diagnostic polysomnogram between July 1987 and July 2003. During follow-up up to 15 years, we assessed incident resuscitated or fatal SCD in relation to the presence of OSA, physiological data including the apnea-hypopnea index (AHI), and nocturnal oxygen saturation (O2sat) parameters, and relevant comorbidities.
Results During an average follow-up of 5.3 years, 142 patients had resuscitated or fatal SCD (annual rate 0.27%). In multivariate analysis, independent risk factors for SCD were age, hypertension, coronary artery disease, cardiomyopathy or heart failure, ventricular ectopy or nonsustained ventricular tachycardia, and lowest nocturnal O2sat (per 10% decrease, hazard ratio [HR]: 1.14; p = 0.029). SCD was best predicted by age >60 years (HR: 5.53), apnea-hypopnea index >20 (HR: 1.60), mean nocturnal O2sat <93% (HR: 2.93), and lowest nocturnal O2sat <78% (HR: 2.60; all p < 0.0001).
Conclusions In a population of 10,701 adults referred for polysomnography, OSA predicted incident SCD, and the magnitude of risk was predicted by multiple parameters characterizing OSA severity. Nocturnal hypoxemia, an important pathophysiological feature of OSA, strongly predicted SCD independently of well-established risk factors. These findings implicate OSA, a prevalent condition, as a novel risk factor for SCD.
This research was supported by grants #HL65176 and #NIH 1 UL1 RR024150 from the National Institutes of Health. Dr. Gami has served as a consultant for Medtronic, Boston Scientific, and St. Jude Medical. Dr. Wright has received consulting fees from Roche/Genentech, Sanofi Regeneron, and 3M. Dr. Somers has served as a consultant for ResMed, Medtronic, Apnex Medical, Sova Pharmaceuticals, Deshum, and NeuPro; has received support from a gift from the Phillips-Respironics Foundation to the Mayo Foundation; and is working on intellectual property related to sleep and heart disease with Mayo Health Solutions and Mayo Medical Ventures and Industry Partners. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received January 24, 2013.
- Revision received April 7, 2013.
- Accepted April 7, 2013.
- American College of Cardiology Foundation