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Acetazolamide Decreases Susceptibility to Hypocapnic Central Apnea in Chronic SCI
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A3986 - Acetazolamide Decreases Susceptibility to Hypocapnic Central Apnea in Chronic SCI
Author Block: G. M. Ginter, S. E. Vaughan, S. W. Carroll, M. Eshraghi, W. H. Ayesh, E. A. Kruppe, A. E. Caruso, A. Alquadan, A. Salloum, S. Chowdhuri, A. Sankari, M. Badr; John D. Dingell VA Medical Center/Wayne State University, Detroit, MI, United States.
Background: Spinal cord injury (SCI) is a risk factor for central sleep apnea (CSA). Acetazolamide (ACZ) increases CO2 reserve by inhibiting luminal carbonic anhydrase, leading to excretion of bicarbonate culminating in metabolic acidosis and stabilization of breathing. We hypothesized that ACZ would decrease the propensity to develop hypocapnic central apnea and the apneic threshold.
Methods: We studied 9 participants with sleep-disordered breathing (SDB) (4 SCI and 5 able-bodied controls, mean age 55.44±12.78, BMI 25.45±3.52, 7 men, AHI 15.82±7.97). Participants were randomized to receive ACZ (500 mg bid x 3 days) or placebo with one week washout before crossing over to the other arm of the study. Study nights included polysomnography and induction of central hypopnea and apnea with non-invasive ventilation protocol during sleep. CO2 reserve was calculated by subtracting the maximum PETCO2 that resulted in an apnea from eupneic PETCO2. Steady-state plant gain (PG) was calculated from PETCO2 and minute ventilation (VE) ratio during stable sleep. Controller gain (CG) was defined as the ratio of change in VE between control and hypopnea or apnea to the ΔPETCO2. Results are reported as mean ± standard deviation.
Results: Seven participants completed both ACZ and placebo, and two participants only completed one arm of the study. Serum bicarbonate levels were 23.18±2.72 mEq/L on ACZ vs 28.15 mEq/L±3.15 on placebo (p=0.009). CO2 reserve increased significantly on ACZ compared to placebo (-3.63±0.64 and -2.65±0.75 respectively; p=0.028). ACZ significantly improved sleep efficiency compared to placebo (86.54±8.59% vs. 75.96±10.96%, respectively; p=0.048). For the 7 participants who completed both arms of the study, AHI was 16.74±12.62 versus 25.43±22.23 events/h (p=0.65), plant gain was 4.94±1.41 versus 6.12±2.36 mmHg/L/min (p=0.44) and controller gain was 2.00±0.71 versus 2.01±0.59 L/min/mmHg (p=0.96) for ACZ and placebo, respectively).
Conclusion: Based on our preliminary data, treatment with ACZ decreases the susceptibility to induced hypocapnic central apnea and improves sleep efficiency. However, the severity of SDB and other sleep parameters are not significantly changed. The clinical utility of ACZ in the treatment of SDB requires further investigation in a larger sample of patients.
Author Block: G. M. Ginter, S. E. Vaughan, S. W. Carroll, M. Eshraghi, W. H. Ayesh, E. A. Kruppe, A. E. Caruso, A. Alquadan, A. Salloum, S. Chowdhuri, A. Sankari, M. Badr; John D. Dingell VA Medical Center/Wayne State University, Detroit, MI, United States.
Background: Spinal cord injury (SCI) is a risk factor for central sleep apnea (CSA). Acetazolamide (ACZ) increases CO2 reserve by inhibiting luminal carbonic anhydrase, leading to excretion of bicarbonate culminating in metabolic acidosis and stabilization of breathing. We hypothesized that ACZ would decrease the propensity to develop hypocapnic central apnea and the apneic threshold.
Methods: We studied 9 participants with sleep-disordered breathing (SDB) (4 SCI and 5 able-bodied controls, mean age 55.44±12.78, BMI 25.45±3.52, 7 men, AHI 15.82±7.97). Participants were randomized to receive ACZ (500 mg bid x 3 days) or placebo with one week washout before crossing over to the other arm of the study. Study nights included polysomnography and induction of central hypopnea and apnea with non-invasive ventilation protocol during sleep. CO2 reserve was calculated by subtracting the maximum PETCO2 that resulted in an apnea from eupneic PETCO2. Steady-state plant gain (PG) was calculated from PETCO2 and minute ventilation (VE) ratio during stable sleep. Controller gain (CG) was defined as the ratio of change in VE between control and hypopnea or apnea to the ΔPETCO2. Results are reported as mean ± standard deviation.
Results: Seven participants completed both ACZ and placebo, and two participants only completed one arm of the study. Serum bicarbonate levels were 23.18±2.72 mEq/L on ACZ vs 28.15 mEq/L±3.15 on placebo (p=0.009). CO2 reserve increased significantly on ACZ compared to placebo (-3.63±0.64 and -2.65±0.75 respectively; p=0.028). ACZ significantly improved sleep efficiency compared to placebo (86.54±8.59% vs. 75.96±10.96%, respectively; p=0.048). For the 7 participants who completed both arms of the study, AHI was 16.74±12.62 versus 25.43±22.23 events/h (p=0.65), plant gain was 4.94±1.41 versus 6.12±2.36 mmHg/L/min (p=0.44) and controller gain was 2.00±0.71 versus 2.01±0.59 L/min/mmHg (p=0.96) for ACZ and placebo, respectively).
Conclusion: Based on our preliminary data, treatment with ACZ decreases the susceptibility to induced hypocapnic central apnea and improves sleep efficiency. However, the severity of SDB and other sleep parameters are not significantly changed. The clinical utility of ACZ in the treatment of SDB requires further investigation in a larger sample of patients.
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