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J Am Coll Cardiol. Author manuscript; available in PMC 2017 August 21. Published in final edited form as: J Am Coll Cardiol. 2017 February 21; 69(7): 841–858. doi:10.1016/j.jacc.2016.11.069.
Types, Mechanisms, and Clinical Cardiovascular Consequences Shahrokh Javaheri, MDa, Ferran Barbe, MDb, Francisco Campos-Rodriguez, MDc, Jerome A. Dempsey, PHDd, Rami Khayat, MDe, Sogol Javaheri, MDf, Atul Malhotra, MDg, Miguel A. Martinez-Garcia, MDh, Reena Mehra, MDi, Allan I. Pack, MBChB, PhDj, Vsevolod Y. Polotsky, MDk, Susan Redline, MDf,l, and Virend K. Somers, MD, PhDm
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aPulmonary
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and Sleep Division, Bethesda North Hospital, Cincinnati, Ohio bRespiratory Department, Institut Ricerca Biomèdica de Lleida, Hospital Universitari Arnau de Vilanova, Lleida, Spain cRespiratory Department, Hospital Universitario de Valme, Sevilla, Spain dDepartment of Population Health Sciences and John Rankin Laboratory of Pulmonary Medicine, University of Wisconsin-Madison, Madison, Wisconsin eSleep Heart Program, the Ohio State University, Columbus, Ohio fHarvard Medical School, Brigham and Women’s Hospital, Boston, Massachusetts gPulmonary, Critical Care and Sleep Medicine, University of California, San Diego, California hRespiratory Department, Hospital Universitario de Politecnico La Fe, Valencia, Spain iCleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, Ohio jDivision of Sleep Medicine/Department of Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania kDivision of Pulmonary and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland lBeth Israel Deaconess Medical Center, Boston, Massachusetts mDepartment of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota
Abstract
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Sleep apnea is highly prevalent in patients with cardiovascular disease. These disordered breathing events are associated with a profile of perturbations that include intermittent hypoxia, oxidative stress, sympathetic activation, and endothelial dysfunction, all of which are critical mediators of cardiovascular disease. Evidence supports a causal association of sleep apnea with the incidence and morbidity of hypertension, coronary heart disease, arrhythmia, heart failure, and stroke. Several discoveries in the pathogenesis, along with developments in the treatment of sleep apnea, have accumulated in recent years. In this review, we discuss the mechanisms of sleep apnea, the evidence that addresses the links between sleep apnea and cardiovascular disease, and research that has addressed the effect of sleep apnea treatment on cardiovascular disease and clinical endpoints. Finally, we review the recent development in sleep apnea treatment options, with special consideration of treating patients with heart disease. Future directions for selective areas are suggested.
ADDRESS FOR CORRESPONDENCE: Dr. Shahrokh Javaheri, Pulmonary and Sleep Division, Bethesda Sleep Laboratory, Bethesda North Hospital, 10535 Montgomery Road, Suite 200, Cincinnati, Ohio 45242. [email protected]. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
Javaheri et al.
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Author Manuscript
Keywords central sleep apnea; hypertension; obstructive sleep apnea Cardiovascular disease (CVD) accounted for >800,000 deaths (31% of all deaths) in 2013 in the United States, with an estimated 155,000 deaths in Americans
J Am Coll Cardiol. Author manuscript; available in PMC 2017 August 21. Published in final edited form as: J Am Coll Cardiol. 2017 February 21; 69(7): 841–858. doi:10.1016/j.jacc.2016.11.069.
Types, Mechanisms, and Clinical Cardiovascular Consequences Shahrokh Javaheri, MDa, Ferran Barbe, MDb, Francisco Campos-Rodriguez, MDc, Jerome A. Dempsey, PHDd, Rami Khayat, MDe, Sogol Javaheri, MDf, Atul Malhotra, MDg, Miguel A. Martinez-Garcia, MDh, Reena Mehra, MDi, Allan I. Pack, MBChB, PhDj, Vsevolod Y. Polotsky, MDk, Susan Redline, MDf,l, and Virend K. Somers, MD, PhDm
Author Manuscript
aPulmonary
Author Manuscript
and Sleep Division, Bethesda North Hospital, Cincinnati, Ohio bRespiratory Department, Institut Ricerca Biomèdica de Lleida, Hospital Universitari Arnau de Vilanova, Lleida, Spain cRespiratory Department, Hospital Universitario de Valme, Sevilla, Spain dDepartment of Population Health Sciences and John Rankin Laboratory of Pulmonary Medicine, University of Wisconsin-Madison, Madison, Wisconsin eSleep Heart Program, the Ohio State University, Columbus, Ohio fHarvard Medical School, Brigham and Women’s Hospital, Boston, Massachusetts gPulmonary, Critical Care and Sleep Medicine, University of California, San Diego, California hRespiratory Department, Hospital Universitario de Politecnico La Fe, Valencia, Spain iCleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, Ohio jDivision of Sleep Medicine/Department of Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania kDivision of Pulmonary and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland lBeth Israel Deaconess Medical Center, Boston, Massachusetts mDepartment of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota
Abstract
Author Manuscript
Sleep apnea is highly prevalent in patients with cardiovascular disease. These disordered breathing events are associated with a profile of perturbations that include intermittent hypoxia, oxidative stress, sympathetic activation, and endothelial dysfunction, all of which are critical mediators of cardiovascular disease. Evidence supports a causal association of sleep apnea with the incidence and morbidity of hypertension, coronary heart disease, arrhythmia, heart failure, and stroke. Several discoveries in the pathogenesis, along with developments in the treatment of sleep apnea, have accumulated in recent years. In this review, we discuss the mechanisms of sleep apnea, the evidence that addresses the links between sleep apnea and cardiovascular disease, and research that has addressed the effect of sleep apnea treatment on cardiovascular disease and clinical endpoints. Finally, we review the recent development in sleep apnea treatment options, with special consideration of treating patients with heart disease. Future directions for selective areas are suggested.
ADDRESS FOR CORRESPONDENCE: Dr. Shahrokh Javaheri, Pulmonary and Sleep Division, Bethesda Sleep Laboratory, Bethesda North Hospital, 10535 Montgomery Road, Suite 200, Cincinnati, Ohio 45242. [email protected]. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
Javaheri et al.
Page 2
Author Manuscript
Keywords central sleep apnea; hypertension; obstructive sleep apnea Cardiovascular disease (CVD) accounted for >800,000 deaths (31% of all deaths) in 2013 in the United States, with an estimated 155,000 deaths in Americans
