Gupta MA. Effect of varying definitions of hypopnea on the calculation of the apnea-hypopnea index may depend upon the level of sympathetic activation: results from a patient with posttraumatic stress disorder. J Clin Sleep Med. 2019;15(10):1555.
The review by Mansukhani and colleagues1 of the effect of different hypopnea definitions on calculations of the apnea-hypopnea index (AHI) is highly clinically relevant. They included studies that used polysomnography or home sleep apnea testing (HSAT).1 They further carried out a meta-analysis of studies that compared the 2007 Recommended or IA criteria of ≥ 30% airflow reduction and ≥ 4% oxyhemoglobin desaturation (4%OD) for hypopnea diagnosis,1 against the reference standard of the 2012 Recommended or IA criteria requiring an airflow reduction of ≥ 30% with ≥ 3% oxyhemoglobin desaturation or an arousal (3%ODA).1 Against the 3%ODA rule, the 4%OD rule demonstrated a sensitivity of 82.7% (95% CI 0.72–0.90) and specificity of 93.2% (95% CI 0.82–0.98).1 The differences in AHI using the 2 criteria diminished with increasing OSA severity,1 suggesting that with increasing OSA severity the majority of respiratory events are associated with ≥ 4% oxyhemoglobin desaturation.
In the same issue I have reported a patient with posttraumatic stress disorder (PTSD),2 a disorder associated with sympathetic activation, who underwent serial HSAT2 (data from 22 HSAT are reported in this communication; results of first 10 HSAT were reported earlier2) and demonstrated a marked variation in her AHI.2 The AHI in this patient2 was recalculated using both the 3%ODA and 4%OD criteria. As expected, the 3%ODA criteria (which includes a lower oxyhemoglobin desaturation cutoff and arousals) yielded a higher AHI score with a mean ± standard deviation difference (AHI3%ODA−AHI4%OD) in AHI scores of 4.56 ± 1.54 events/h (range 2–7.10 events/h). The difference score (AHI3%ODA−AHI4%OD) did not correlate significantly with OSA severity however correlated inversely with both the number of wakenings per hour (Pearson r = −.460, P = .031) and mean pulse rate during sleep (Pearson r = −.436, P = .043),2 which are measures of sympathetic activation and resultant sleep fragmentation, and likely represent the culmination of several factors including bilateral interactions between OSA severity and underlying level of autonomic activation in the patient. It is conceivable that the underlying state of sympathetic activation which contributed to the variation of AHI was also associated with more arousals which further contributed to a higher AHI with the 3%ODA versus the 4%OD rule; however, above a certain level of sympathetic activation there was greater (≥ 4%) oxyhemoglobin desaturation with most apneas, resulting in a lower discrepancy in the AHI calculation using the 3%ODA versus 4%OD rules. This could be a factor in other disorders (eg, cardiovascular disease) that are associated with OSA and sympathetic activation. A lower discrepancy in AHI scores obtained with the 3%ODA versus 4%OD criteria, may therefore indicate greater underlying sympathetic activation in the patient, which can have additional treatment implications.
The author reports no conflicts of interest.