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      The Heart Rate Response to Exercise Is Blunted in Patients with Sleep-Related Breathing Disorder

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          Abstract

          Background: This study addressed the hypothesis that cardiovascular reactivity during graded bicycle exercise is influenced by a coexisting sleep-related breathing disorder (SRBD). Methods: Blood pressure and heart rate were assessed at rest and during graded exercise (110 W and maximal load) in 1,149 patients of a Sleep Disorders Center. The degree of SRBD, and potential confounders, including blood gases and pulmonary function, were determined. Results: Maximal exercise capacity tended to decrease with SRBD activity (p = 0.07). The heart rate reactivity was blunted and reduced by –0.07 and –0.09 beats/min for every SRBD unit at 110 W (p < 0.001) and at maximal load (p < 0.001), respectively. Systolic and diastolic blood pressure reactivity at maximal load were positively associated with SRBD severity. These associations were independent of possible confounders. Conclusion: SRBD is associated with reduced physical working capacity and a modified hemodynamic response to exercise.

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          Most cited references 8

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          Prospective study of the association between sleep-disordered breathing and hypertension.

          Sleep-disordered breathing is prevalent in the general population and has been linked to chronically elevated blood pressure in cross-sectional epidemiologic studies. We performed a prospective, population-based study of the association between objectively measured sleep-disordered breathing and hypertension (defined as a laboratory-measured blood pressure of at least 140/90 mm Hg or the use of antihypertensive medications). We analyzed data on sleep-disordered breathing, blood pressure, habitus, and health history at base line and after four years of follow-up in 709 participants of the Wisconsin Sleep Cohort Study (and after eight years of follow-up in the case of 184 of these participants). Participants were assessed overnight by 18-channel polysomnography for sleep-disordered breathing, as defined by the apnea-hypopnea index (the number of episodes of apnea and hypopnea per hour of sleep). The odds ratios for the presence of hypertension at the four-year follow-up study according to the apnea-hypopnea index at base line were estimated after adjustment for base-line hypertension status, body-mass index, neck and waist circumference, age, sex, and weekly use of alcohol and cigarettes. Relative to the reference category of an apnea-hypopnea index of 0 events per hour at base line, the odds ratios for the presence of hypertension at follow-up were 1.42 (95 percent confidence interval, 1.13 to 1.78) with an apnea-hypopnea index of 0.1 to 4.9 events per hour at base line as compared with none, 2.03 (95 percent confidence interval, 1.29 to 3.17) with an apnea-hypopnea index of 5.0 to 14.9 events per hour, and 2.89 (95 percent confidence interval, 1.46 to 5.64) with an apnea-hypopnea index of 15.0 or more events per hour. We found a dose-response association between sleep-disordered breathing at base line and the presence of hypertension four years later that was independent of known confounding factors. The findings suggest that sleep-disordered breathing is likely to be a risk factor for hypertension and consequent cardiovascular morbidity in the general population.
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            Obstructive sleep apnoea syndrome as a risk factor for hypertension: population study.

             V Hoffstein,  P Lavie,  P Herer (2000)
            To assess whether sleep apnoea syndrome is an independent risk factor for hypertension. Population study. Sleep clinic in Toronto. 2,677 adults, aged 20-85 years, referred to the sleep clinic with suspected sleep apnoea syndrome. Medical history, demographic data, morning and evening blood pressure, and whole night polysomnography. Blood pressure and number of patients with hypertension increased linearly with severity of sleep apnoea, as shown by the apnoea-hypopnoea index. Multiple regression analysis of blood pressure levels of all patients not taking antihypertensives showed that apnoea was a significant predictor of both systolic and diastolic blood pressure after adjustment for age, body mass index, and sex. Multiple logistic regression showed that each additional apnoeic event per hour of sleep increased the odds of hypertension by about 1%, whereas each 10% decrease in nocturnal oxygen saturation increased the odds by 13%. Sleep apnoea syndrome is profoundly associated with hypertension independent of all relevant risk factors.
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              Ambulatory blood pressure after therapeutic and subtherapeutic nasal continuous positive airway pressure for obstructive sleep apnoea: a randomised parallel trial.

              Obstructive sleep apnoea is associated with raised blood pressure. If blood pressure can be reduced by nasal continuous positive airway pressure (nCPAP), such treatment could reduce risk of cardiovascular disease in patients with obstructive sleep apnoea. Our aim was to see whether nCPAP for sleep apnoea reduces blood pressure compared with the most robust control intervention subtherapeutic nCPAP. We did a randomised parallel trial to compare change in blood pressure in 118 men with obstructive sleep apnoea (Epworth score > 9, and a > 4% oxygen desaturation index of > 10 per h) who were assigned to either therapeutic (n=59) or subtherapeutic (59) nCPAP (about 1 cm H(2)O pressure) for 1 month. The primary outcome was the change in 24-h mean blood pressure. Secondary outcomes were changes in systolic, diastolic, sleep, and wake blood pressure, and relations between blood pressure changes, baseline blood pressure, and severity of sleep apnoea. Therapeutic nCPAP reduced mean arterial ambulatory blood pressure by 2.5 mm Hg (SE 0.8), whereas subtherapeutic nCPAP increased blood pressure by 0.8 mm Hg (0.7) (difference -3.3 [95% CI -5.3 to -1.3]; p=0.0013, unpaired t test). This benefit was seen in both systolic and diastolic blood pressure, and during both sleep and wake. The benefit was larger in patients with more severe sleep apnoea than those who had less severe apnoea, but was independent of the baseline blood pressure. The benefit was especially large in patients taking drug treatment for blood pressure. In patients with most severe sleep apnoea, nCPAP reduces blood pressure, providing significant vascular risk benefits, and substantially improving excessive daytime sleepiness and quality of life.
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                Author and article information

                Journal
                CRD
                Cardiology
                10.1159/issn.0008-6312
                Cardiology
                S. Karger AG
                0008-6312
                1421-9751
                2004
                July 2004
                09 July 2004
                : 102
                : 2
                : 93-99
                Affiliations
                aSleep Disorders Center, Pulmonary Medicine, Sahlgrenska University Hospital, Gothenburg, Sweden; bSleep Disorders Centre, Department of Internal Medicine, University of Marburg, Marburg, Germany
                Article
                77911 Cardiology 2004;102:93–99
                10.1159/000077911
                15103179
                © 2004 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 3, Tables: 2, References: 34, Pages: 7
                Categories
                Clinical Investigation

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