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      Impact of All-Day Physical Activity on Ventilatory Perfusion Coupling in Patients Undergoing Cardiac Resynchronization Therapy

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          Abstract

          Objectives: There is still little information about the cardiorespiratory effects of cardiac resynchronization therapy (CRT) in patients undergoing all-day physical activity. This study aimed to assess the effects of CRT on ventilatory perfusion coupling during submaximal exercise. Methods: Metabolic and hemodynamic parameters were obtained during treadmill exercise testing as well as during rest for each single-right (RV), -left (LV) and biventricular (BiV) pacing mode as well as during intrinsic conduction (VVI 30) in 37 patients. Only responders to CRT (>10% increase in cardiac output (CO) during BiV pacing; n = 27) were included into the evaluation. Results: LV and BiV pacing increased systolic (144 ± 25 and 142 ± 28 vs. 118 ± 29 mm Hg, p < 0.05) and mean blood pressure (108 ± 19 and 109 ± 19 vs. 94 ± 25 mm Hg, p < 0.05) as well as CO (7.0 ± 0.6 and 7.2 ± 0.8 vs. 6.0 ± 0.6 l/min, p < 0.05 and p < 0.01) during exercise as compared to VVI 30. Simultaneously, LV and BiV pacing decreased dead space ventilation (18 ± 3 and 17 ± 3 vs. 20 ± 4, p < 0.01) and the ventilatory equivalent for oxygen (31 ± 4 and 31 ± 5 vs. 36 ± 6; p < 0.05) compared to intrinsic conduction. Conclusion: The improvement in ventilatory efficacy during CRT, which is demonstrated by the decrease in the ventilatory equivalent for oxygen, results from an increase in CO and thus from a reduction in the ventilatory perfusion mismatch.

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          Most cited references 23

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          Prevalence of heart failure and left ventricular dysfunction in the general population; The Rotterdam Study.

          To determine the prevalence of heart failure and symptomatic as well as asymptomatic left ventricular systolic dysfunction in the general population. In 5540 participants of the Rotterdam Study (age 68.9+/-8.7 years, 2251 men) aged 55-95 years, the presence of heart failure was determined by assessment of symptoms and signs (shortness of breath. ankle oedema and pulmonary crepitations) and use of heart failure medication. In 2267 subjects (age 65.7+/-7.4 years, 1028 men) fractional shortening was measured. The overall prevalence of heart failure was 3.9% (95% CI 3.0+/-4.7) and did not differ between men and women. The prevalence increased with age, with the exception of the highest age group in men. Fractional shortening was higher in women and did not decrease appreciably with age. The prevalence of left ventricular systolic dysfunction (fractional shortening <=25%) was approximately 2.5 times higher in men (5.5%, 95% CI 4.1-7.0) than in women (2.2%, 95% CI 1.4-3.2). Sixty percent of persons with left ventricular systolic dysfunction had no symptoms or signs of heart failure at all. The prevalence of heart failure is appreciable and does not differ between men and women. The majority of persons with left ventricular systolic dysfunction can be regarded as having asymptomatic left ventricular systolic dysfunction.
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            Skeletal muscle function and its relation to exercise tolerance in chronic heart failure.

            This study sought to define the relation between muscle function and bulk in chronic heart failure (HF) and to explore the association between muscle function and bulk and exercise capacity. Skeletal muscle abnormalities have been postulated as determinants of exercise capacity in chronic HF. Previously, muscle function in chronic HF has been evaluated in relatively small numbers of patients and with variable results, with little account being taken of the effects of muscle wasting. One hundred male patients with chronic HF and 31 healthy male control subjects were studied. They were matched for age (59.0 +/- 1.0 vs. 58.7 +/- 1.7 years [mean +/- SEM]) and body mass index (26.6 +/- 0.4 vs. 26.3 +/- 0.7 kg/m2). We assessed maximal treadmill oxygen consumption (VO2), quadriceps maximal isometric strength, fatigue (20-min protocol, expressed in baseline maximal strength) and computed tomographic cross-sectional area (CSA) at midthigh. Peak VO2 was lower in patients (18.0 +/- 0.6 vs. 33.3 +/- 1.4 ml/min per kg, p < 0.0001), although both groups achieved a similar respiratory exchange ratio at peak exercise (1.15 +/- 0.01 vs. 1.19 +/- 0.03, p = 0.13). Quadriceps (582 vs. 652 cm2, p < 0.05) and total leg muscle CSA (1,153 vs. 1,304 cm2, p < 0.005) were lower in patients with chronic HF. Patients were weaker than control subjects (357 +/- 12 vs. 434 +/- 18 N, p < 0.005) and also exhibited greater fatigue at 20 min (79.1% vs. 92.1% of baseline value, p < 0.0001). After correcting strength for quadriceps CSA, significant differences persisted (5.9 +/- 0.2 vs. 7.0 +/- 0.3 N/cm2, p < 0.005), indicating reduced strength per unit muscle. In patients, but not control subjects, muscle CSA significantly correlated with peak absolute VO2 (R = 0.66, p < 0.0001) and is an independent predictor of peak absolute VO2. Patients with chronic HF have reduced quadriceps maximal isometric strength. This weakness occurs as a result of both quantitative and qualitative abnormalities of the muscle. With increasing exercise limitation there is increasing muscle weakness. This progressive weakness occurs predominantly as a result of loss of quadriceps bulk. In patients, this muscular atrophy becomes a major determinant of exercise capacity.
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              Effect of losartan compared with captopril on mortality in patients with symptomatic heart failure: randomised trial—the Losartan Heart Failure Survival Study ELITE II

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                Author and article information

                Journal
                CRD
                Cardiology
                10.1159/issn.0008-6312
                Cardiology
                S. Karger AG
                0008-6312
                1421-9751
                2008
                July 2008
                01 February 2008
                : 111
                : 1
                : 68-74
                Affiliations
                Departments of aCardiology, and bSports Medicine and Cardiovascular Medicine, Innsbruck Medical University, Innsbruck, and cDepartment of Respiratory and Critical Care Medicine, Otto Wagner Hospital, Vienna, Austria
                Article
                113431 Cardiology 2008;111:68–74
                10.1159/000113431
                18239396
                © 2008 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: 29, Pages: 7
                Categories
                Original Research

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