It is primarily over the past 2 to 3 decades that the implications of OSA for cardiovascular disease have become recognized. Nevertheless, the general cardiovascular community has been slow in assimilating OSA into the cardiovascular diagnostic and therapeutic paradigms. This lag between information and intervention can be attributed to a number of factors, including the considerable expense and wait time required for sleep studies, and the variable and sometimes unsuccessful responses to initiation of CPAP therapy. Furthermore, the cardiovascular community is accustomed to management strategies driven by evidence from large-scale randomized trials and has come to regard smaller studies with appropriate caution, even those that show substantial benefit. While the evidence for activation of a broad spectrum of cardiovascular disease mechanisms in patients with OSA is compelling, there are very few longitudinal studies of the effects of OSA on cardiovascular outcomes, and no large-scale, randomized, double-blind trials of the cardiovascular effects of therapeutic intervention.
Such studies are constrained by the numerous comorbid conditions that accompany OSA, as well as by the technical problems associated with double-blind studies of CPAP treatment. Furthermore, there is reasonable evidence that CPAP will reduce daytime sleepiness, favorably affecting the likelihood of motor vehicle crashes. Thus, any long-term outcome study focused on the effects of CPAP therapy on cardiovascular end points would be limited by the proven benefit of CPAP on daytime somnolence. Possible solutions to this limitation would be to ensure that participants in any such study understand the known benefits they could derive from CPAP, or alternatively limiting such an outcomes study to patients without significant daytime sleepiness.
Even should OSA be conclusively implicated in adverse cardiovascular outcomes, it is important that cost-effectiveness issues be addressed, given the expense of current diagnostic and therapeutic strategies. For example, should all obese patients with hypertension, heart failure, or atrial fibrillation be evaluated for OSA? Even if significant OSA is identified and effectively treated in these patients, what is the likelihood that this approach would improve cardiovascular outcomes? Mechanistic and technical advances that would enable more economical and effective diagnostic and therapeutic approaches would greatly enhance resolution of these questions.
What is known is that OSA is common, readily diagnosed, usually treatable, frequently coexists undiagnosed in patients with cardiovascular disease, activates disease mechanisms known to elicit cardiac and vascular damage, and may be implicated in progression of cardiovascular disease and resistance to conventional therapeutic strategies. The epidemic of obesity speaks to the likelihood of a dramatic increase in the prevalence of OSA. Further investigation of the implications of OSA and its treatment is an important priority in the study of cardiovascular disease. In the absence of definitive evidence from large-scale trials and a better understanding of potential cost-effectiveness, the likely benefits of diagnosis and treatment of OSA are presently best appraised on an individual patient basis.
Full Article at JAMA
Such studies are constrained by the numerous comorbid conditions that accompany OSA, as well as by the technical problems associated with double-blind studies of CPAP treatment. Furthermore, there is reasonable evidence that CPAP will reduce daytime sleepiness, favorably affecting the likelihood of motor vehicle crashes. Thus, any long-term outcome study focused on the effects of CPAP therapy on cardiovascular end points would be limited by the proven benefit of CPAP on daytime somnolence. Possible solutions to this limitation would be to ensure that participants in any such study understand the known benefits they could derive from CPAP, or alternatively limiting such an outcomes study to patients without significant daytime sleepiness.
Even should OSA be conclusively implicated in adverse cardiovascular outcomes, it is important that cost-effectiveness issues be addressed, given the expense of current diagnostic and therapeutic strategies. For example, should all obese patients with hypertension, heart failure, or atrial fibrillation be evaluated for OSA? Even if significant OSA is identified and effectively treated in these patients, what is the likelihood that this approach would improve cardiovascular outcomes? Mechanistic and technical advances that would enable more economical and effective diagnostic and therapeutic approaches would greatly enhance resolution of these questions.
What is known is that OSA is common, readily diagnosed, usually treatable, frequently coexists undiagnosed in patients with cardiovascular disease, activates disease mechanisms known to elicit cardiac and vascular damage, and may be implicated in progression of cardiovascular disease and resistance to conventional therapeutic strategies. The epidemic of obesity speaks to the likelihood of a dramatic increase in the prevalence of OSA. Further investigation of the implications of OSA and its treatment is an important priority in the study of cardiovascular disease. In the absence of definitive evidence from large-scale trials and a better understanding of potential cost-effectiveness, the likely benefits of diagnosis and treatment of OSA are presently best appraised on an individual patient basis.
Full Article at JAMA
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