TY - JOUR
T1 - Sleep Apnea and Cardiovascular Disease. An American Heart Association/American College of Cardiology Foundation Scientific Statement From the American Heart Association Council for High Blood Pressure Research Professional Education Committee, Council on Clinical Cardiology, Stroke Council, and Council on Cardiovascular Nursing In Collaboration With the National Heart, Lung
AU - Somers, Virend K.
AU - White, David P.
AU - Amin, Raouf
AU - Abraham, William T.
AU - Costa, Fernando
AU - Culebras, Antonio
AU - Daniels, Stephen
AU - Floras, John S.
AU - Hunt, Carl E.
AU - Olson, Lyle J.
AU - Pickering, Thomas G.
AU - Russell, Richard
AU - Woo, Mary
AU - Young, Terry
PY - 2008/8/19
Y1 - 2008/8/19
N2 - In the context of the current epidemics of obesity, hypertension, atrial fibrillation, and heart failure, the prevalence and consequences of both OSA and CSA are likely to increase. Numerous hurdles face the cardiovascular community in the development of consensus regarding best practice. One objective of this document is to help develop the platform from which, in collaboration with specialists in sleep medicine and related disciplines, such consensus may emerge. Challenges to be met include 1) the general absence of any structured sleep medicine education in cardiovascular training programs; 2) the logistic and economic obstacles to diagnosing and treating sleep apnea; 3) widespread comorbidities, including obesity, that obscure clearer understanding of any independent cardiovascular consequence of sleep apnea per se; 4) treatment options that are varied, predominantly device based, and not easily tolerated, particularly in patients with CSA; and 5) the absence of robust longitudinal interventional studies addressing whether treating sleep apnea confers any tangible benefit in terms of cardiovascular events. We also remain uncertain about what in the apneic patient facilitates cardiovascular disease and its progression. There is no clear evidence as to the best measurement for quantifying the severity of sleep apnea. Is it the frequency of apneas, the severity of desaturation, the overall burden of nocturnal hypoxemia, the arousals, sleep deprivation, or a combination of these and perhaps other characteristics that are key in promoting heart and blood vessel damage? In addition, we do not know the threshold of severity of apnea that we should treat and whether the thresholds for therapy are different in people with cardiovascular disease compared with those who are otherwise healthy. Recognition that a multidisciplinary strategy is critical to appropriate evaluation of sleep-related disease (416) and heightened interaction between specialists in cardiovascular and sleep medicine hold promise for future improved and integrated patient care. In the meantime, the relative lack of definitive outcomes data to guide clinical practice necessitates a highly individualized approach to evaluation and management of those patients with comorbid cardiovascular disease and sleep apnea. There will likely be continued rapid evolution in interpretation, dissemination, and implementation of mechanistic, prognostic, and therapeutic data. Evidence of activation of cardiovascular disease mechanisms by sleep apnea and evidence of sleep apnea as an independent etiologic factor in cardiovascular disease should serve as catalysts for definitive intervention studies. Important next steps in understanding and treating SDB as a means of preventing and mitigating cardiac and vascular disease should include further characterizing fundamental disease mechanisms, identifying economical and better-tolerated therapeutic options, confirming whether therapy attenuates cardiovascular morbidity and mortality, and defining appropriate therapeutic targets and cost-effective benefits of such therapy.
AB - In the context of the current epidemics of obesity, hypertension, atrial fibrillation, and heart failure, the prevalence and consequences of both OSA and CSA are likely to increase. Numerous hurdles face the cardiovascular community in the development of consensus regarding best practice. One objective of this document is to help develop the platform from which, in collaboration with specialists in sleep medicine and related disciplines, such consensus may emerge. Challenges to be met include 1) the general absence of any structured sleep medicine education in cardiovascular training programs; 2) the logistic and economic obstacles to diagnosing and treating sleep apnea; 3) widespread comorbidities, including obesity, that obscure clearer understanding of any independent cardiovascular consequence of sleep apnea per se; 4) treatment options that are varied, predominantly device based, and not easily tolerated, particularly in patients with CSA; and 5) the absence of robust longitudinal interventional studies addressing whether treating sleep apnea confers any tangible benefit in terms of cardiovascular events. We also remain uncertain about what in the apneic patient facilitates cardiovascular disease and its progression. There is no clear evidence as to the best measurement for quantifying the severity of sleep apnea. Is it the frequency of apneas, the severity of desaturation, the overall burden of nocturnal hypoxemia, the arousals, sleep deprivation, or a combination of these and perhaps other characteristics that are key in promoting heart and blood vessel damage? In addition, we do not know the threshold of severity of apnea that we should treat and whether the thresholds for therapy are different in people with cardiovascular disease compared with those who are otherwise healthy. Recognition that a multidisciplinary strategy is critical to appropriate evaluation of sleep-related disease (416) and heightened interaction between specialists in cardiovascular and sleep medicine hold promise for future improved and integrated patient care. In the meantime, the relative lack of definitive outcomes data to guide clinical practice necessitates a highly individualized approach to evaluation and management of those patients with comorbid cardiovascular disease and sleep apnea. There will likely be continued rapid evolution in interpretation, dissemination, and implementation of mechanistic, prognostic, and therapeutic data. Evidence of activation of cardiovascular disease mechanisms by sleep apnea and evidence of sleep apnea as an independent etiologic factor in cardiovascular disease should serve as catalysts for definitive intervention studies. Important next steps in understanding and treating SDB as a means of preventing and mitigating cardiac and vascular disease should include further characterizing fundamental disease mechanisms, identifying economical and better-tolerated therapeutic options, confirming whether therapy attenuates cardiovascular morbidity and mortality, and defining appropriate therapeutic targets and cost-effective benefits of such therapy.
KW - ACCF Expert Consensus Document
KW - apnea
KW - arrhythmia
KW - blood pressure
KW - cerebrovascular disorders
KW - death, sudden
KW - sleep
UR - http://www.scopus.com/inward/record.url?scp=48949085757&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=48949085757&partnerID=8YFLogxK
U2 - 10.1016/j.jacc.2008.05.002
DO - 10.1016/j.jacc.2008.05.002
M3 - Review article
C2 - 18702977
AN - SCOPUS:48949085757
SN - 0735-1097
VL - 52
SP - 686
EP - 717
JO - Journal of the American College of Cardiology
JF - Journal of the American College of Cardiology
IS - 8
ER -