Abstract Title

Hypertension and Obstructive Sleep Apnea are Associated with Abnormal Pressor Responses to Apnea

Presenter Name

Noah Jouett

Abstract

Background: Cardiovascular diseases are commonly associated with elevated sympathetic nerve activity (SNA). Previously, we have shown that the blood pressure response to a voluntary apnea is closely correlated with the SNA response in patients with sleep disordered breathing (SDB) and thus may serve as an index of SNA responsiveness. In the current study, we hypothesized that the pressor response to apnea is 1) reduced with effective treatment of SDB in SDB patients, and 2) that it is exaggerated in hypertensive patients (HTN) when compared to healthy control subjects.

Methods: 22 OSA patients (14 treated and 8 untreated), 19 treated hypertensive patients and 23 healthy normotensive control subjects were recruited from the UNTHSC Primary Care Center and Sleep Consultants of Texas. Subjects completed a medical history questionnaire and Epworth Sleepiness survey. Blood pressure was measured by standard auscultatory assessment in the seated position. Baseline blood pressure was obtained in triplicate during quiet rest. Then after practicing a voluntary breath hold, subjects repeated three voluntary 20-second breath holds each beginning at end-expiration. Comparisons were made 1) between treated and untreated SDB patients, and 2) between HTN patients and healthy control subjects using a Student t test.

Results:Importantly, as in prior studies the pressor response to apnea was not different from zero in the healthy control subjects (-1.0 ± 4.2 mmHg, p>0.05). In the SDB patients, the pressor response was significantly greater than zero in both treated (11.4 ± 3.9 mm Hg) and untreated (24.5 ± 9.8 mm Hg) SDB patients (p

Conclusions: These data support our hypotheses that the pressor response to voluntary apnea is exaggerated in both untreated SDB and treated HTN patients and that effective treatment of SDB reduces this response, but does not normalize the response. These data suggest that the pressor response to apnea may be a simple physiologic index of exaggerated sympathetic responsiveness.

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Hypertension and Obstructive Sleep Apnea are Associated with Abnormal Pressor Responses to Apnea

Background: Cardiovascular diseases are commonly associated with elevated sympathetic nerve activity (SNA). Previously, we have shown that the blood pressure response to a voluntary apnea is closely correlated with the SNA response in patients with sleep disordered breathing (SDB) and thus may serve as an index of SNA responsiveness. In the current study, we hypothesized that the pressor response to apnea is 1) reduced with effective treatment of SDB in SDB patients, and 2) that it is exaggerated in hypertensive patients (HTN) when compared to healthy control subjects.

Methods: 22 OSA patients (14 treated and 8 untreated), 19 treated hypertensive patients and 23 healthy normotensive control subjects were recruited from the UNTHSC Primary Care Center and Sleep Consultants of Texas. Subjects completed a medical history questionnaire and Epworth Sleepiness survey. Blood pressure was measured by standard auscultatory assessment in the seated position. Baseline blood pressure was obtained in triplicate during quiet rest. Then after practicing a voluntary breath hold, subjects repeated three voluntary 20-second breath holds each beginning at end-expiration. Comparisons were made 1) between treated and untreated SDB patients, and 2) between HTN patients and healthy control subjects using a Student t test.

Results:Importantly, as in prior studies the pressor response to apnea was not different from zero in the healthy control subjects (-1.0 ± 4.2 mmHg, p>0.05). In the SDB patients, the pressor response was significantly greater than zero in both treated (11.4 ± 3.9 mm Hg) and untreated (24.5 ± 9.8 mm Hg) SDB patients (p

Conclusions: These data support our hypotheses that the pressor response to voluntary apnea is exaggerated in both untreated SDB and treated HTN patients and that effective treatment of SDB reduces this response, but does not normalize the response. These data suggest that the pressor response to apnea may be a simple physiologic index of exaggerated sympathetic responsiveness.