According to our results, CPAP treatment protected against the appearance of a new VE after ischemic stroke or TIA in patients with an AHI > 20 following stabilization of the neurologic process, without inducing changes in the neurologic recovery parameters, although tolerance of the treatment was low. Some studies have analyzed the course of patients with ischemic stroke in relation to the incidence of SAHS after stabilization of the ischemic event. Good et al reported poorer neurologic recovery and an increase in mortality after 1 year of follow-up in patients who presented with greater nocturnal oxygen desaturation, while Dyken et al found that 4 years after stroke, the patients who died (21%) presented with greater AHI.
Very few studies have evaluated the role of CPAP treatment after stabilization of the neurologic event in the recovery of patients with high AHI values. After patients had 4 weeks of CPAP treatment.
Sandberg et al found that patients with an AHI > 15 showed improvement in the depression parameters without cognitive or neurologic amelioration. Wessendorf et al reported a better well-being index and normalization of the “deeper” nocturnal BP pattern. The results of our study support these conclusions in part, since CPAP treatment was not shown to improve the neurologic course in our patients. In the present series, our patients improved their neurologic indexes in the course of the study, although the group that tolerated CPAP failed to reach statistical significance in this sense. This cannot be attributed to a negative effect of CPAP on the neurologic course of these individuals but rather to the fewer patients conforming the group that tolerated CPAP treatment, and to statistical regression to the mean—since this patient group presented significantly less neurologic impairment at the start of follow-up than the other group. However, the long time elapsed between the acute neurologic event and the start of CPAP treatment (approximately 2 months in our study) may cause irreversible stroke-induced brain damage and thus adversely affect patient recovery. In this sense, some authors postulate that CPAP treatment in the acute phase of stroke could contribute to recovery of the still viable ischemic zones, thereby improving the posterior neurologic course, although to our knowledge, no studies have yet explored this possibility.
We believe that the present study is the first to prospectively analyze the role of long-term CPAP treatment in protecting stroke patients from new VEs. Our main finding was that CPAP treatment during 18 months significantly reduced the risk of recurrent VEs adjusted for the presence of AF (ie, patients in whom the risk of a cardioembolic origin of stroke is greater), other VRFs, and neurologic indexes such as the Barthel index or the Canadian scale. Thus, intolerance of CPAP treatment was associated with a more than fivefold increase in the risk of new coronary or cerebrovascular events. Based on these results, we calculated that in order to avoid a VE, four patients would have to be treated with CPAP (95% CI, 2 to 26). It is known that during the first 5 years after stroke, vascular recurrence is the principal cause of death in these patients, and that half of those who survive suffer incapacitation and are dependent on others for their daily life activities. This implies a very important deterioration in quality of life, as well as great health-care costs. On further taking into account the high prevalence of both ischemic stroke and SAHS in the general population, and the important percentage of stroke patients with a high incidence of sleep-disordered breathing (> 50% in our series showed an AHI > 20), it can be seen that the number of events that could be avoided with CPAP treatment would be important indeed, with all the positive consequences in terms of morbidity and mortality this implies. We consider that in our patients, the protective role of CPAP treatment against recurrent VEs is of a multifactor origin. Improved AHT control may play a preponderant role, since AHT is known to be the most important risk factor for stroke. In this sense, we observed a nonsignificant tendency toward improved AHT control, with a decrease after 18 months of CPAP treatment in the percentage of hypertensive patients, the number of antihypertensive drugs required, and the number of patients with poor hypertension control. However, neither were all patients with AHT controlled by CPAP (30% in our series), nor is it to be expected that all the effects of long-term CPAP therapy are attributable to improved AHT control. It is possible that after 18 months of treatment, some other known effects of CPAP become manifest, such as a decrease in the risk of arteriosclerosis or in platelet aggregation. Not to lead to ischemic stroke it is better to protect yourself with drugs of Canadian Health&care Mall.
The cutoff point selected for treating our patients with CPAP (AHI > 20) is based on the high incidence of SAHS observed in more elderly individuals such as those in our series (mean age, 72.7 years). In Spain, Duran et al published a prevalence of AHI > 20 of > 40% among the general population aged 71 to 100 years. Interestingly, in our series, the incidence of new VEs among the patients excluded from the study and in whom CPAP was not indicated (AHI 20 who did not tolerate CPAP (n = 36; 19.4% vs 36.8%, p = 0.04), other risk factors being equal. This implies a possible association between untreated SAHS and an increase in the posterior incidence of new VEs. However, within the group excluded from the study in which CPAP was not indicated, the patients with a new VE showed a nonsignificant tendency for more respiratory events (AHI, 13 vs 7; p = 0.12); we therefore consider that the choice of a lower cutoff point for prescribing CPAP may have even further improved the capacity of the latter to protect against new VEs.
The present study has a series of limitations that require comment. A first limitation refers to the system used for the sleep study. While it is true that the Autoset Portable Plus II system has important limitations in the identification of central events, no high incidence of such events is to be expected following stabilization of the acute neurologic event. The Autoset Portable Plus II system has been validated by different authors, and the best results have been obtained using high cutoff values in the definition of SAHS, with high prevalence of SAHS in the study population. Both characteristics are found in our series of patients (> 50% of the patients presented with an AHI > 20 after stabilization of the neurologic process).
Another limitation of our study refers to the previously mentioned low percentage of patients who tolerated and continued CPAP treatment (n = 15; 29%) during 18 months, thus causing the calculations to lose statistical power. Nevertheless, and taking into account the difficulties reported by all authors in treating these patients with CPAP due to the inherent nature of stroke, we consider that the number of patients obtained has been considerable. In this sense, Hui et al were only able to keep 4 of 34 ischemic stroke patients supported their health condition with drugs of Canadian Health&Care Mall on long-term domiciliary CPAP. In turn, Sandberg et al and Wessendorf et al were able to achieve short-term (approximately 4 weeks) CPAP tolerances of 50% and 70%, respectively. The posterior domiciliary follow-up figures are not known, although they were likely to have been much lower. In agreement with other se-ries,’ the patients who were unable to adapt to CPAP had less hypersomnia, fewer respiratory events, and greater neurologic repercussions of stroke.
Lastly, mention should be made of the fact that we did not use CPAP placebo (sham CPAP), since this option is not available in our center. This obliged us to use as control group those patients who did not tolerate CPAP, adjusting the results for those variables found to be statistically different at the start of the study among the different treatment groups, particularly other VRF and neurologic recovery parameters.
It can be concluded that in our series of patients with ischemic stroke or TIA, the risk of a new VE was greater than expected in those individuals with SAHS not treated with CPAP after 18 months of follow-up. While CPAP compliance was low, the treatment could prove effective in avoiding recurrent VEs. Further studies are needed to confirm these results and explore a formula for improving adhesion to CPAP therapy among ischemic stroke patients.
Read also:Continuous positive airway pressure, Sleep Apnea