SUMMARY

The authors consider that the data to date have left it unclear whether or not OSA is a progressive disease. In retrospective accounts, patients with OSA report that initially they snored, more and more loudly with time, until they developed respiratory pauses at night that gradually became more frequent. In Upper Airway Resistance Syndrome, snorers without apneas still show sleep disruption and daytime sleepiness, suggesting a precursor of OSA.One study using oximetry repeated after six months found 62% of patients increased their desaturation indices by 50% in six months. But another study with 32 patients given polysomnography five years apart showed no change in Apnea Hypopnea Index. As the authors point out, if OSA does progress there are important consequences: mildly ill apneics must continue in follow-up because of the risk of varied complications such as hypertension as the disease persists and worsens. Also, this would underscore the need for sticking with treatment despites side-effects of CPAP. Finally, it would argue for treating even the mildly ill apneics in hope or preventing progression. This was a “retrospective case note study,” meaning that the authors collected their data by looking back through the records of their selected subjects: 55 patients with mild to moderate OSA who had polysomnography twice at least four months apart without intervening treatment for OSA. It happened that additional data was available from upper airway imaging by computerized tomography in 43 patients, and cephalometry in 32. The rationale behind the delay of treatment was one of instructing mildly ill patients to make lifestyle changes first, before embarking on more “invasive” treatment (e.g., CPAP). The severely ill subjects were those who initially refused CPAP. At initial evaluation subjects averaged 56 years of age (SD=+/-10, range 19-72). Their BMIs (see Glossary) averaged 30 (SD=+/-5), their AHIs (see Glossary), their minimum oxygen saturation 78 (SD=+/-10), their total sleep time 410 minutes (SD=+/-98), their proportion of REM sleep low at10% (SD=+/-7), proportion of stages 1 & 2 sleep high at 86% (SD=+/-22), and proportion of stages 3 & 4 sleep very low at 2% (SD=+/-4). Pulmonary function test, cephalometrics, and airway imaging will be described more in relation to the follow-up testing, but in general the patients began with normal arterial blood gas tensions, normal respiratory function, and upper airway dimensions similar to those found in other studies of patients with OSA. Follow-up testing occurrred an average of 77 (SD=+/-50, range=17-229) weeks after the initial testing.To make these figures a little clearer, on average the patients were retested about a year and a half later, but with wide variability where many patients were tested a year later or two years later, while some patients were tested 4 months later and some 4 years later. Over this variable interval, patients averaged a significant increase in AHI, from 22 (SD=+/-12) to 33 (SD=+/-21), an average increase of about 50%. Total sleep time was reduced by about 8% (28 minutes). Proportion of REM sleep increased slightly, from 10% to 13%. Other sleep measures showed no significant change. BMI remained unchanged. Alcohol and cigarette consumption remained stable.The increase in AHI was less marked, actually non-significant, in women, contrasted to men. Using criteria of 25% increase or decrease in AHI to indicate worsening or improvement, with any change less than that “remaining stable,” the authors found that 30 (54%) of patients worsened. Only 9 (16%) improved, while 16 (29%) remained much the same. Thie outcome could not be predicted from age, BMI, interval of time between testing, upper airway anatomy, blood gas tensions, or respiratory function. Patients denied any change in snoring or daytime sleepiness between the two evaluations, but morbidity for the group as a whole was considerable: hypertension in 46%, heart arrhythmias in 33%, anginal chest pain in 23%, myocardial infarction in 19%, and stroke in 19%. Patients with such events were a little older on the average (57 years vs. 53 years) than those who didn’t. Nine patients developed cardiovascular disease during the follow-up period. In fact, six patients (11%) suffered heart attacks or strokes. After the follow-up, 29 patients (52%) were prescribed CPAP, of whom three went on to have surgery; 26 patients (47%) were considered stable enough to require no treatment. The authors considered that, since the majority of patients showed significant increases in AHI over an average of 17 months, without any relationship to weight gain, age, upper airway anatomy, respiratory function, smoking, or drinking, the predominant trend toward worsening over time was attributable to the natural, untreated course of the illness itself. They found their results similar to one other study showing deterioration in oximetry results in 62% over the course of six months. They explained the discrepant results of a study which found no change over five years to the very high initial AHIs (averaging 52) which may have set a limit to the deterioration possible. They suggested possible mechanisms of deterioration to include sensory nerve damage in the pharynx due to snoring trauma, loss of reflexes in the airway musculature, and muscular lesions increasing airway collapsibility. They mentioned that their failure to find increased snoring or sleepiness despite the increase in AHI may relate to the poor correlation between disease and symptom severity in OSA, and the lack of a standardized scale to measure sleepiness in a retrospective study. They concluded by pointing out that their findings would lead towards greater use of CPAP in patients who had heretofore been considered “stable” without treatment.

COMMENTS

I consider this quite an important study despite its shortcomings, such as the retrospective nature, the use of only clinical case records, and the extremely variable time interval of follow-up. It is important because it has data from a substantial number of subjects left untreated for mild to severe OSA over a considerable period of time, which show a statistically and clinically significant worsening of apnea in the majority of patients over a period best thought of as “a year or two.” The fact that the authors were able to demonstrate this worsening was unrelated to weight gain, smoking, drinking, is especially important as these are the sort of factors commonly used to “blame the victim” for their illness. It is also of interest that there was no relation of this worsening to anatomical measures of the upper airway of pulmonary function. All this combines to make the worsening seem an inherent part of the disease process of Obstructive Sleep Apnea, not an incidental result of other factors. Their report of severe medical complications in this relatively young group of patients should help reinforce the need for treatment of the OSA which may well contribute to these cardiovascular and other diseases. The authors are remarkably judicious in noting that, contrary to the practice of their own centers, their data indicate that even “mild” sleep apneics must be carefully followed, and probably treated, in hope of stemming the process of deterioration. It is a great mistake to “let such patients go” as if they were likely to remain the same; doctors who treat “mild” apneics, or even snorers with Upper Airway Obstruction Syndromne, may later find themselves sued for the consequences of strokes, heart attacks, emphysema, kidney failure, hypertension, brain dysfunction, auto and other accidents, and the probably many more effects of untreated OSA in its process of worsening. Nor should any patient who has been told he has “only mild” OSA comfort himself that nothing more need be done about that!





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