Predictors of pulmonary hypertension in obstructive sleep apnoea syndrome.
نویسنده
چکیده
I have read with much interest the paper by LAKS et al. [1] on pulmonary hypertension (PHT) in obstructive sleep apnoea (OSA), in which there is new evidence that daytime PHT can exist without daytime hypoxaemia in OSA. Finding predictors of the existence of PHT in these normoxaemic patients may have important practical consequences. However, in their general series the authors [1] find that only daytime arterial oxygen tension (Pa,O2), arterial carbon dioxide tension (Pa,CO2), and forced expiratory volume in one second (FEV1), are statistically significant predictors of PHT (however, since the coefficients of correlation have low values and, as is stated by the authors, 67% of the variability is left unexplained if these variables are considered, one may wonder whether it actually has any clinical importance). It is surprising that no index of severity of OSA is correlated with PHT, which goes against previously published studies and against what one could expect to be "logical". Perhaps it is true that, as is stated by LAKS et al. [1], the apnoea/hypopnoea index (AHI) and the respiratory disturbance index (RDI) do not accurately represent hypoxaemic exposure (and, hence, the severity of OSA). However, I think three points must be discussed: 1. Severity of OSA is defined by RDI, not by AHI. Since RDI is not defined, one cannot know if it is the same as AHI, or whether both indices can be made equal without error. Since RDI has been defined by other authors as comprising apnoeas longer than 10 s as well as other events with a shorter duration [2], perhaps it overestimates the severity of OSA (there can be desaturations associated with snoring without apnoea [3]), and so AHI should be used to define the severity of OSA. 2. Apnoeas/hypopnoeas are not described as they usually are, with a duration of at least 10 s [4–8]. The definition the authors give for apnoea and hypopnoea [1] may include situations that would not otherwise be described as apnoeas or hypopnoeas (since their duration is shorter than 10 s), thus overestimating the severity of OSA. 3. The authors stress the need for indices of exposure to hypoxaemia and hypercapnia. In this sense, several indices have been proposed that could be used as markers of hypoxaemic stress (and in fact some of them have been used for this purpose) in addition to minimal arterial oxygen saturation (Sa,O2): a) mean [4, 9] or median [7] Sa,O2 during sleep; b) mean Sa,O2 of abnormal respiratory patterns [7]; c) number of desaturations under 85%, which has been called "severity index" [10]; d) sleep time (or fraction of total sleep time (TST)) spent at each level of Sa,O2 [11]: under 60% [7], 70% [7], 80% [7], 85% [4], 90 [7, 9] or 95% [12]; e) fraction of TST spent in each 10% interval of Sa,O2 [6, 11] and cumulative distribution function of Sa,O2 [11]; f) apnoea-hypopnoea time (usually as percentage of TST) [13]; g) mean desaturation time [13]; h) desaturation index [9]; and i) nocturnal desaturation score [14]. I would like to raise one question that, in view of the thorough study LAKS et al. [1] have performed, will surely be easy to answer: Could any of the abovementioned indices (apnoeas and hypopnoeas being defined following "classical" criteria in order to assess AHI) predict the development or existence of PHT, even in normoxaemic patients?
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ورودعنوان ژورنال:
- The European respiratory journal
دوره 9 4 شماره
صفحات -
تاریخ انتشار 1996