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.
In a Clinical Crossroads article published in the Journal of American Medical Association, Dr. Kuna discussed the epidemiology, pathophysiology, diagnosis, and treatment of obstructive sleep apnea. The wife of the patient (Mr J) noted that he sometimes stopped breathing at night. Mr J also recalled that he awoke, on occasion, in the middle of the night with palpitations. A sleep study revealed 206 obstructive events, giving an apnea-hypopnea index of 36 per hour. Mr J tried treatment with nasal continuous positive airway pressure (CPAP), with which Mr J's palpitations ceased, but after about a year he discontinued the nasal CPAP because it interfered with his ability to fall asleep and with his sex life. He did, however, lose 20 lb and weighed 205 lb (his body mass index was 28.6). He felt well and did not experience any difficulties with his sleep patterns or daytime sleepiness.
Full Article at JAMA
Full Article at JAMA