ABSTRACT Obstructive sleep apnea (OSA) is associated with increased cardiovascular risk and hypertension. While continuous positive airway pressure (CPAP) therapy reduces blood pressure (BP), its effect shows substantial interindividual variability. Hypoxic burden (HB) has been proposed as a potentially superior predictor of cardiovascular outcomes compared to the apnea–hypopnea index (AHI). In this retrospective study, 141 patients with OSA underwent in‐laboratory polysomnography and initiated CPAP therapy. Office BP and clinical parameters were assessed at baseline and follow‐up (median 200 days). Receiver operating characteristic (ROC), correlation, multiple linear and logistic regression analyses were performed to compare the predictive value of HB and AHI for BP reduction. CPAP therapy resulted in a modest, non‐significant reduction in systolic BP(−2.3 mmHg ±17.7,0.1237), while diastolic BP remained unchanged. Higher AHI and HB levels were associated with higher baseline systolic BP and numerically greater BP reductions, particularly in individuals with a higher than the median HB ≥57.5%min/h or median AHI ≥34.3/h. However, neither HB nor AHI predicted a systolic BP reduction ≥5 mmHg (AUC values≈0.5), and no relevant correlations between AHI, HB and blood pressure response were observed. HB is associated with OSA severity and higher baseline BP. However, it is not superior to AHI in the prediction of a CPAP‐associated reduction of BP in patients with OSA.

Objective: Sleep apnea is associated with hypertension. Metaanalyses indicate that treatment of sleep apnea by continuous positive airway pressure (CPAP) reduces blood pressure (BP) by a mean of 3 mmHg. To date, predictors of BP response to CPAP remain incompletely understood. We hypothesized that the magnitude of CPAP-induced BP reduction depends on baseline apnea hypopnea index (AHI) and the extent of daytime sleepiness. Design and method: We performed a retrospective study on the association of BP response to CPAP with polysomnographic readings, intensity of sleepiness (measured by Epworth Sleepiness Scale, ESS), and epidemiologic parameters in 2461 patients with obstructive sleep apnea. BP response was defined as the difference between office BP at polysomonography examinations before and after initiation of CPAP. Results: 555 patients fulfilled all in- and exclusion criteria and were included in the analysis. Median monthly CPAP usage was 143.7h (85.4-204.1h). BP was significantly higher at baseline than at follow-up (129.9±15.5 vs. 128.3±15.2, p=0.021) resulting in mean reduction of BP of -1.5±19.2 mmHg. Subjects with a higher than median baseline AHI (median 21) showed a more pronounced reduction of BP than those with lower AHI (AHI >21: 130.5±15.3 vs. 128.6±14.6, p=0.06; AHI <21: 129.5±15.8 vs. 127.9±15.8, p=0.18). CPAP therapy led to a significant reduction in sleepiness (8.3±4.8 vs. 6.6±4.5, p<0.0001). Those subjects with higher than median sleepiness score (ESS >8), however, did not show a significant difference in BP response compared to those with a lower sleepiness score. Receiver-operating characteristic (ROC) curve analyses investigating the accuracy of AHI and ESS to predict a BP reduction >5 mmHg revealed an AUC of 0.51 and 0.52, respectively. Conclusions: The study confirms that CPAP therapy for sleep apnea has a mild BP lowering effect. Although this effect is slightly higher in patients with above-average AHI, neither AHI nor ESS can be used to define threshold values predicting a BP decrease > 5 mmHg.

Background: Sleep apnea is associated with hypertension. Metaanalyses indicate that treatment of sleep apnea by continuous positive airway pressure (CPAP) reduces blood pressure (BP) by a mean of 3 mmHg. To date, predictors of BP response to CPAP remain incompletely understood. We hypothesized that the magnitude of CPAP-induced BP reduction depends on baseline apnea–hypopnea index (AHI) and the extent of daytime sleepiness Methods: We performed a retrospective study on the association of BP response to CPAP with polysomnographic readings, intensity of sleepiness (measured by Epworth Sleepiness Scale, ESS), and epidemiologic parameters in 2461 patients with obstructive sleep apnea. BP response was defined as the difference between office BP at polysomonography examinations before and after initiation of CPAP. Results: Five hundred and fifty-five patients fulfilled all inclusion and exclusion criteria and were included in the analysis. Median monthly CPAP usage was 143.7 h (85.4–204.1 h). BP was significantly higher at baseline than at follow-up (129.9 ± 15.5 vs. 128.3 ± 15.2, P = 0.021) resulting in mean reduction of BP of −1.5 ± 19.2 mmHg. patients with a higher than median baseline AHI (median 21) showed a more pronounced reduction of BP than those with lower AHI (AHI ≥21: 130.5 ± 15.3 vs. 128.6 ± 14.6, P = 0.06; AHI <21: 129.5 ± 15.8 vs. 127.9 ± 15.8, P = 0.18). CPAP therapy led to a significant reduction in sleepiness (8.3 ± 4.8 vs. 6.6 ± 4.5, P < 0.0001). Those subjects with higher than median sleepiness score (ESS ≥8), however, did not show a significant difference in BP response compared with those with a lower sleepiness score. Receiver-operating characteristic (ROC) curve analyses investigating the accuracy of AHI and ESS to predict a BP reduction at least 5 mmHg revealed an AUC of 0.51 and 0.52, respectively. Conclusion: The study confirms that CPAP therapy for sleep apnea has a mild BP lowering effect. Although this effect is slightly higher in patients with above-average AHI, neither AHI nor ESS can be used to define threshold values predicting a BP decrease at least 5 mmHg.

Improving sleep quality in patients with obstructive sleep apnea (OSA) by positive airway pressure therapy is associated with a decrease of blood pressure (BP). It remains elusive, whether treatment of sleep disturbances due to restless legs syndrome with symptomatic periodic limb movements in sleep (PLMS) affects BP as well. The present study provides first data on this issue. Retrospective study on patients undergoing polysomnography in a German University Hospital. Inclusion criteria were first diagnosis of restless legs syndrome with PLMS (PLM index ≥ 15/h and PLM arousal index ≥ 5/h) with subsequent initiation of levodopa/benserazide or dopamine agonists. Exclusion criterion was an initiation or change of preexisting positive airway pressure therapy between baseline and follow-up. BP and Epworth sleepiness scale were assessed at two consecutive polysomnographies. After screening of 953 PLMS data sets, 114 patients (mean age 62.1 ± 12.1 years) were included. 100 patients (87.7%) were started on levodopa/benserazide, 14 patients (12.2%) on dopamine agonists. Treatment was associated with significant reductions of PLM index (81.2 ± 65.0 vs. 39.8 ± 51.2, p < 0.001) and ESS (6 [interquartile range, IQR, 3–10.5] vs. 5 [IQR 3–10], p = 0.013). Systolic BP decreased from 132.9 ± 17.1 to 128.0 ± 15.8 mmHg (p = 0.006), whereas there was no significant change of diastolic BP (76.7 ± 10.9 vs. 75.1 ± 9.2 mmHg, p = 0.15) and heart rate (71.5 ± 11.9 vs. 71.3 ± 12.7, p = 0.84). The number of antihypertensive drugs remained unchanged with a median of 2 (IQR 1–3, p = 0.27). Dopaminergic treatment of PLMS is associated with an improvement of sleep quality and a decrease of systolic BP comparable to treatment OSA.

BACKGROUND:Developing therapeutic strategies for a SARS-CoV-2 infection is challenging, but first the correct diagnosis has to be made. Unspecific upper and lower respiratory tract symptoms can be misleading; hence, a nasopharyngeal swab test with a real-time reverse-transcription-polymerase chain reaction is of great importance. However, early viral clearing jeopardizes a sound diagnosis of COVID-19.CASE PRESENTATION:We report on two Caucasian patients who had negative pharyngeal swab tests at the onset of SARS-CoV-2 pneumonia. In one patient, the virus was not even detectable in bronchoalveolar lavage despite typical radiomorphologic changes.CONCLUSIONS:Negative PCR findings in both the pharynx and bronchoalveolar lavage do not exclude COVID-19 pneumonia. Computed tomography is a crucial diagnostic prerequisite in this context.