Kidney Week

Abstract: FR-PO209

CPAP Therapy Improves Central Arterial Stiffness and Decreases Arterial Renin Angiotensin System Activity in Humans with Obstructive Sleep Apnea

Session Information

• Vascular Biology and Dysfunction
  November 03, 2017 | Location: Hall H, Morial Convention Center
  Abstract Time: 10:00 AM - 10:00 AM

Category: Hypertension

• 1103 Vascular Biology and Dysfunction

Authors

• Nicholl, David Donald McTavish, University of Calgary, Calgary, Alberta, Canada

David Donald McTavish Nicholl,

• Hanly, Patrick, University of Calgary, Calgary, Alberta, Canada

Patrick Hanly,

• Zalucky, Ann A., University of Calgary, Calgary, Alberta, Canada

Ann A. Zalucky,

• Mann, Michelle C., University of Calgary, Calgary, Alberta, Canada

Michelle C. Mann,

• MacRae, Jennifer M., University of Calgary, Calgary, Alberta, Canada

Jennifer M. MacRae,

• Poulin, Marc, University of Calgary, Calgary, Alberta, Canada

Marc Poulin,

• Handley, George, Healthy Heart Sleep Company, Calgary, Alberta, Canada

George Handley,

• Sola, Darlene Y., University of Calgary, Calgary, Alberta, Canada

Darlene Y. Sola,

• Ahmed, Sofia B., University of Calgary, Calgary, Alberta, Canada

Sofia B. Ahmed,

Background

Chronic kidney disease (CKD) is associated with increased arterial stiffness, a marker of cardiovascular risk. Treatment of obstructive sleep apnea (OSA), common in CKD, reduces arterial stiffness, though the mechanism is not clear. Limited studies suggest a prominent role for the renin angiotensin system (RAS), activation of which is deleterious to kidney and cardiovascular function. We sought to determine the effect of CPAP therapy on arterial stiffness at baseline and in response to the physiological stressor, Angiotensin II (AngII), in humans with OSA.

Methods

Newly diagnosed OSA subjects (respiratory disturbance index [RDI]>15h^-1) with nocturnal hypoxia (oxyhemoglobin saturation [SaO₂] <90% for >12% of night) who were otherwise healthy were studied in high-salt balance, at state of maximal RAS suppression, pre-CPAP and then after 4 weeks of effective CPAP therapy (>4h/night) in a second identical study day. Central (aortic augmentation index [AIx]) and peripheral (carotid-femoral pulse-wave velocity [PWV_cf]) arterial stiffness were measured by applanation tonometry. Arterial stiffness was measured at baseline and in response to a graded AngII infusion (3ng/kg/min x 30min, 6ng/kg/min x 30min, Recovery x 30min). The primary outcome was the effect of CPAP on the arterial stiffness responses to AngII.

Results

Twenty-six subjects (18 men, 8 women; 49±2y) completed the study. CPAP corrected OSA (RDI: 44.2±4.1 vs 3.5±0.5hr^-1, p<0.001; duration SaO₂<90%: 45.4±5.6 vs 6.7±2.1%, p<0.001; all values pre- vs post-CPAP). Treatment with CPAP was associated with increased sensitivity in central arterial stiffness (ΔAIx: AngII, 8.7±1.4 vs 11.6±1.6%, p=0.038; Recovery, 1.7±1.4 vs 1.0±2.0%, p=0.8), while no change in peripheral arterial stiffness (ΔPWV_cf: AngII, 1.0±0.3 vs 0.9±0.2 m/s, p=0.8; Recovery, 1.0±0.3 vs 0.2±0.4 m/s, p=0.13) was observed.

Conclusion

CPAP therapy was associated with increased central, but not peripheral, arterial stiffness sensitivity to AngII, consistent with downregulation of the vascular RAS. These findings may have important implications in mitigating cardiovascular risk in CKD patients with OSA.