Abstract

IntroductionObstructive sleep apnea (OSA) has been associated with non-dipping blood pressure (BP). The precise mechanism is still under investigation, but repetitive oxygen desaturation and arousal induced sleep fragmentation are considered the main contributors.MethodsWe analyzed beat-to-beat measurements of hemodynamic parameters (HPs) during a 25-min period of wake–sleep transition. Differences in the mean HP values for heart rate (HR), systolic BP (SBP), and stroke volume (SV) during wake and sleep and their standard deviations (SDs) were compared between 34 controls (C) and 22 OSA patients. The Student’s t-test for independent samples and the effect size by Cohen’s d (d) were calculated. HP evolution was investigated by plotting the measured HP values against each consecutive pulse wave. After a simple regression analysis, the calculated coefficient beta (SCB) was used to indicate the HP evolution. We furthermore explored by a hierarchical block regression which variables increased the prediction for the SCB: model 1 BMI and age, model 2 + apnea/hypopnea index (AHI), and model 3 + arousal index (AI).ResultsBetween the two groups, the SBP increased in OSA and decreased in C resulting in a significant difference (p = 0.001; d = 0.92). The SV demonstrated a similar development (p = 0.047; d = 0.56). The wake/sleep variation of the HP measured by the SD was higher in the OSA group—HR: p < 0.001; d = 1.2; SBP: p = 0.001; d = 0.94; and SV: p = 0.005; d = 0.82. The hierarchical regression analysis of the SCB demonstrated in SBP that the addition of AI to AHI resulted in ΔR2: +0.163 and ΔF + 13.257 (p = 0.001) and for SV ΔR2: +0.07 and ΔF 4.83 (p = 0.003). The AI but not the AHI remained statistically significant in the regression analysis model 3—SBP: β = 0.717, p = 0.001; SV: β = 0.469, p = 0.033.ConclusionIn this study, we demonstrated that in OSA, the physiological dipping in SBP and SV decreased, and the variation of all investigated parameters increased. Hierarchical regression analysis indicates that the addition of the AI to BMI, age, and AHI increases the prediction of the HP evolution following sleep onset for both SBP and SV and may be the most important variable.

Highlights

  • Obstructive sleep apnea (OSA) has been associated with non-dipping blood pressure (BP)

  • We investigated in a detailed beat-to-beat analysis the influence of either OSAs or sleep fragmentation on the evolution of hemodynamic parameters (HPs) including heart rate (HR), systolic BP, and stroke volume (SV)

  • We investigated in patients with OSA the evolution of three HPs: systolic blood pressure (SBP), SV, and HR during sleep onset

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Summary

Introduction

Obstructive sleep apnea (OSA) has been associated with non-dipping blood pressure (BP). The relationship between obstructive sleep apnea (OSA) and cardiovascular diseases (CVDs) has been intensively investigated by both basic science and clinical researchers (Floras, 2018). The assembled scientific evidence indicates a relevant negative impact of OSA on several components of the cardiovascular system, including an increased risk for arterial hypertension (AHT) (Javaheri et al, 2017). The precise mechanism of this interaction remains unclear, and the effect of OSA therapy on AHT is inconsistent. Several longitudinal studies confirmed OSA as a risk factor for AHT and a benefit from therapy with continuous positive airway pressure (CPAP) (Peppard et al, 2000; Marin et al, 2012; Mokhlesi et al, 2014), others were inconclusive (McEvoy et al, 2016). The importance to use the correct methods for OSA diagnostic to avoid false-negative results has been recently underlined (Parati et al, 2019)

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