Getting the Most Out of Nocturnal Pulse Oximetry

stroke and is, as mentioned previously, associated with a bad prognosis. However, idiopathic CSA is observed in those without any comorbidities and is not necessarily periodic in nature. Moreover, there are no data indicating that the presence of idiopathic or postarousal CSA by itself is a poor prognostic marker for patients, and no consensus on when and how it should be treated. In view of these differences, there is a definite need to develop a more precise definition of CSR-CSA to better define the relevance of CSR-CSA in CHF, and to foster comparisons of data across studies. We believe that studies examining CSR-CSA should, as a minimum, report on the cycle length, magnitude of oxyhemoglobin desaturation, the timing of arousals relative to the respiratory events, and frequency and duration of apneas and hypopneas of their study patients to distinguish classic CSR-CSA from idiopathic CSA. Second, the data by Mansfield and colleagues indicate that sympathetic nervous activity, which is overexpressed in those with CSR-CSA, can be markedly attenuated by cardiac transplantation. Indeed, in the posttransplant setting, those with classic CSRCSA before transplantation had urinary norepinephrine levels remarkably similar to those without CSRCSA following surgery. Some may argue that these data support the contention that CSR-CSA is responsible for the excess sympathetic nervous stimulation (beyond that observed in patients with CHF and no CSR-CSA) and that its abolition “caused” the fall in the excess sympathetic nervous activity in the posttransplant setting. This statement, however, largely ignores the fact that 20% of patients with CSR-CSA in the study by Mansfield and colleagues had “residual” CSA on posttransplant polysomnography. If CSR-CSA, indeed, contributes to the downward spiral of patients with CHF by perturbing the autonomic nervous system, one might have expected to see a higher urinary norepinephrine level in the CSR-CSA group than in the control group following transplantation (since none in the control group acquired CSR-CSA posttransplant). An alternative explanation of the data of Mansfield and colleagues on urinary norepinephrine is that CSR-CSA by itself is not the primary cause of the sympathetic overactivity and that their expression is an epiphenomenon. Treatment of the “broken” heart is, therefore, the only relevant clinical issue. The study of Mansfield and colleagues was not designed to address this critically important question. Well-designed, larger prospective studies are needed to determine whether posttransplant CSA is associated with elevations in the sympathetic nervous activity and, more importantly, whether their presence leads to worse clinical outcomes in cardiac patients.