Matthew N Bartels1, G J Gates, J A Downey, H F Armstrong, R E De Meersman. 1. Department of Rehabilitation and Regenerative Medicine, Columbia College of Physicians and Surgeons, Columbia University, 180 Fort Washington Ave., HP 1-169b, New York, NY 10032, USA. mnb4@columbia.edu
Abstract
PURPOSE: Reduced baroreceptor sensitivity (BRS) results in changes in autonomic modulation. Patients with chronic obstructive pulmonary disease (COPD) may have altered BRS. Therefore, we compared BRS between COPD patients and normal controls. METHODS: We compared 14 COPD patients [mean (±SD) age, 62 ± 8 years] to 14 healthy controls [mean (±SD) age, 59 ± 6 years] for the loss of BRS. All patients received β(2)-agonist therapy but were free from any other type of medication that would interfere with autonomic responses, all controls were free from cardiopulmonary disease, and none was taking medications. All participants were female, post-menopausal, had no known cardiac disease and were ex-smokers. Reduced baroreceptor sensitivity was determined using the slope of the magnitude of R-R widening over the increase in systolic blood pressure following Valsalva maneuver. RESULTS: The mean BRS in controls versus COPD patients showed a mean value of 6.15 ± 2.26 versus 1.91 ± 2.92 ms/mmHg (p < 0.001). CONCLUSIONS: These findings are consistent with other abnormalities of autonomic disruption as previously reported, and demonstrate a severe blunting of the baroreceptor response in individuals with COPD. The cause of this altered BRS response in COPD is not fully clear, we postulate that air trapping with persistent elevation of intrathoracic pressure may lead to a subsequent blunting of the sensitivity of the baroreceptors.
PURPOSE: Reduced baroreceptor sensitivity (BRS) results in changes in autonomic modulation. Patients with chronic obstructive pulmonary disease (COPD) may have altered BRS. Therefore, we compared BRS between COPDpatients and normal controls. METHODS: We compared 14 COPDpatients [mean (±SD) age, 62 ± 8 years] to 14 healthy controls [mean (±SD) age, 59 ± 6 years] for the loss of BRS. All patients received β(2)-agonist therapy but were free from any other type of medication that would interfere with autonomic responses, all controls were free from cardiopulmonary disease, and none was taking medications. All participants were female, post-menopausal, had no known cardiac disease and were ex-smokers. Reduced baroreceptor sensitivity was determined using the slope of the magnitude of R-R widening over the increase in systolic blood pressure following Valsalva maneuver. RESULTS: The mean BRS in controls versus COPDpatients showed a mean value of 6.15 ± 2.26 versus 1.91 ± 2.92 ms/mmHg (p < 0.001). CONCLUSIONS: These findings are consistent with other abnormalities of autonomic disruption as previously reported, and demonstrate a severe blunting of the baroreceptor response in individuals with COPD. The cause of this altered BRS response in COPD is not fully clear, we postulate that air trapping with persistent elevation of intrathoracic pressure may lead to a subsequent blunting of the sensitivity of the baroreceptors.
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