School of Medicine and Health Sciences Poster Presentations

Title

Continuous Positive Airway Pressure Improves Arterial Stiffness and Endothelial Progenitor Cells (CD34+ cells)

Document Type

Poster

Keywords

Obstructive Sleep Apnea (OSA); endothelial progenitor cells (EPCs); Continuous positive airway pressure (CPAP); arterial stiffness (AS); Pulse Wave Velocity (PWV)

Publication Date

Spring 2017

Abstract

Overview: Obstructive sleep apnea (OSA) is a common condition characterized by intermittent breathing pauses during sleep. OSA is an independent risk factor for cardiovascular disorders (CVDs) with endothelial dysfunction playing a role in its pathogenesis. OSA patients are known to have endothelial damage due to oxidative stress and decreased ability to repair via endothelial progenitor cells (EPCs). Arterial stiffness (AS) is a known indicator of endothelial health, and hence cardiovascular risk. Continuous positive airway pressure (CPAP) is the gold standard when it comes to treating patients with OSA, and has shown to decrease cardiovascular risk in OSA patients. We studied the effect of CPAP on the EPCs and arterial stiffness in OSA patients.

Methods: 8 patients diagnosed with OSA, but without prior CPAP treatment, were recruited. Pulse Wave Velocity (PWV), a measure of AS, and EPC number and function were assessed at baseline (prior to starting CPAP treatment) and post-12 week CPAP treatment. The Wilcoxon Signed Rank Test was used to test changes in measurements per day of CPAP > 4hr (median of 48 days).

Results: Arterial stiffness, measured by PWV, was improved with CPAP treatment (p = 0.008). Although no statistically significant change was noted in EPC colony forming units, the percent of CD34+ cells (relative to total mononuclear cells) increased after treatment (p = 0.05). Additionally, in targeted gene expression analysis, a trend towards increased gene expression was noted for eNOS (endothelial nitric oxide synthase) and CXCR4 (a receptor for SDF1A, a known chemotactic factor for EPCs).

Conclusions: An improvement in arterial stiffness, along with an increase in CD34+ cell numbers most likely explains the cardiovascular risk reduction post CPAP therapy. While a larger cohort is needed to elucidate the specific molecular mechanisms involved in this process, this pilot study serves to introduce potential key players.

Creative Commons License

Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 4.0 License.

Open Access

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Comments

Poster to be presented at GW Annual Research Days 2017.

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Continuous Positive Airway Pressure Improves Arterial Stiffness and Endothelial Progenitor Cells (CD34+ cells)

Overview: Obstructive sleep apnea (OSA) is a common condition characterized by intermittent breathing pauses during sleep. OSA is an independent risk factor for cardiovascular disorders (CVDs) with endothelial dysfunction playing a role in its pathogenesis. OSA patients are known to have endothelial damage due to oxidative stress and decreased ability to repair via endothelial progenitor cells (EPCs). Arterial stiffness (AS) is a known indicator of endothelial health, and hence cardiovascular risk. Continuous positive airway pressure (CPAP) is the gold standard when it comes to treating patients with OSA, and has shown to decrease cardiovascular risk in OSA patients. We studied the effect of CPAP on the EPCs and arterial stiffness in OSA patients.

Methods: 8 patients diagnosed with OSA, but without prior CPAP treatment, were recruited. Pulse Wave Velocity (PWV), a measure of AS, and EPC number and function were assessed at baseline (prior to starting CPAP treatment) and post-12 week CPAP treatment. The Wilcoxon Signed Rank Test was used to test changes in measurements per day of CPAP > 4hr (median of 48 days).

Results: Arterial stiffness, measured by PWV, was improved with CPAP treatment (p = 0.008). Although no statistically significant change was noted in EPC colony forming units, the percent of CD34+ cells (relative to total mononuclear cells) increased after treatment (p = 0.05). Additionally, in targeted gene expression analysis, a trend towards increased gene expression was noted for eNOS (endothelial nitric oxide synthase) and CXCR4 (a receptor for SDF1A, a known chemotactic factor for EPCs).

Conclusions: An improvement in arterial stiffness, along with an increase in CD34+ cell numbers most likely explains the cardiovascular risk reduction post CPAP therapy. While a larger cohort is needed to elucidate the specific molecular mechanisms involved in this process, this pilot study serves to introduce potential key players.