Evaluation of an OSA risk stratifying and treatment protocol during inpatient rehabilitation of post-stroke patients.

PURPOSE: To evaluate outcomes, outside of a clinical trial setting, of a protocol utilizing overnight oximetry (NOx) to risk stratify post-stroke patients for obstructive sleep apnea (OSA) followed by autoadjusting continuous positive airway pressure (APAP) treatment in patients considered high risk for OSA. METHODS: Retrospective observational study of post-stroke patients at an academic inpatient stroke rehabilitation facility. Patients underwent NOx, and those at high risk for OSA (oxygen desaturation index 3% > 10 per hour) were attempted on a trial of APAP, and further stratified into high risk adherent with treatment (HRAT) or high-risk failed treatment (HRFT). Change in functional independence measure (FIM) was used to assess recovery. RESULTS: Two hundred twenty-four post-stroke patients underwent NOx, with 120 (53%) considered high risk for OSA. Twelve (10%) were compliant with APAP treatment (> 4 h/night on > 70% of nights). No difference in change in FIM scores was observed for HRAT versus HRFT [total FIM change - 5.8, 95% CI (- 13.9, 2.2); motor FIM change - 4.5, 95% CI (- 11.5, 2.4); cognitive FIM change - 1.3, 95% CI (-3.8, 1.2)]. A subgroup analysis matched 14 HRAT patients (using adherence criterion of APAP usage > 50% of nights) to 35 HRFT patients. A statistically significant, but clinically irrelevant, difference in total FIM change was observed (HRAT vs HRFT, difference between means - 5.2, p = 0.03). CONCLUSIONS: The use of APAP in high-risk patients was poorly tolerated and did not improve post-stroke recovery. Further studies with larger sample sizes are needed to determine the effect of APAP treatment on short-term recovery.

A sleeping beast: Obstructive sleep apnea and stroke.

Up to two-thirds of patients who have had a stroke have obstructive sleep apnea (OSA) afterward. These patients have worse outcomes than those without OSA in terms of short-term morbidity, functional and cognitive recovery, and mortality rates over the long term. Following a stroke, identifying OSA and treating it with positive airway pressure, if possible, are important clinical goals.

Anti-cytomegalovirus activity of the anthraquinone atanyl blue PRL.

Human cytomegalovirus (CMV) causes significant disease in immunocompromised patients and serious birth defects if acquired in utero. Available CMV antivirals target the viral DNA polymerase, have significant toxicities, and suffer from resistance. New drugs targeting different pathways would be beneficial. The anthraquinone emodin is proposed to inhibit herpes simplex virus by blocking the viral nuclease. Emodin and related anthraquinones are also reported to inhibit CMV. In the present study, emodin reduced CMV infectious yield with an EC50 of 4.9µM but was cytotoxic at concentrations only twofold higher. Related anthraquinones acid blue 40 and alizarin violet R inhibited CMV at only high concentrations (238-265µM) that were also cytotoxic. However, atanyl blue PRL inhibited infectious yield of CMV with an EC50 of 6.3µM, significantly below its 50% cytotoxic concentration of 216µM. Atanyl blue PRL reduced CMV infectivity and inhibited spread. When added up to 1h after infection, it dramatically reduced CMV immediate early protein expression and blocked viral DNA synthesis. However, it had no antiviral activity when added 24h after infection. Interestingly, atanyl blue PRL inhibited nuclease activities of purified CMV UL98 protein with IC50 of 4.5 and 9.3µM. These results indicate that atanyl blue PRL targets very early post-entry events in CMV replication and suggest it may act through inhibition of UL98, making it a novel CMV inhibitor. This compound may provide valuable insights into molecular events that occur at the earliest times post-infection and serve as a lead structure for antiviral development.