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      Acute Effect of DDD versus VVI Pacing on Arterial Distensibility

      , ,

      Cardiology

      S. Karger AG

      Pacemaker, Pulse wave velocity, Atherosclerosis, Distensibility, Stiffness

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          Abstract

          Pulse wave velocity (PWV) is a new technique and frequently used today to determine the elastic distensibility of great arteries. Increased arterial stiffness and PWV have been proposed as possible mechanisms in the initiation and/or progression and/or complications of atherosclerosis and cardiovascular disease. We evaluated the acute effect of two frequently used pacing modes (DDD vs. VVI) on arterial distensibility using PWV. Methods: Seventeen patients (age, 56 ± 14 years) implanted with DDD pacemakers were included in the study. All patients were pacemaker dependent and continuously paced at the programmed rate. PWV was measured first in DDD mode, and then the mode was switched to VVI, and PWV was measured again at the same programmed heart rate as in the DDD mode. Results: Although systolic blood pressure significantly decreased from 129 ± 18 to 119 ± 16 mm Hg (p = 0.001) after switching the mode from DDD to VVI, diastolic blood pressure (81 ± 12 vs. 80 ± 13 mm Hg; p = 0.38) did not change. In addition, PWV significantly increased from 11 ± 2.46 m/s in DDD mode to 11.29 ± 2.43 m/s (p = 0.01) after having been programmed to VVI mode. Conclusions: Our results suggest that VVI pacing increases PWV, and therefore decreases arterial distensibility, and thus may contribute to the development and progression of atherosclerosis.

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          Most cited references 3

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          Effects of physiologic pacing versus ventricular pacing on the risk of stroke and death due to cardiovascular causes. Canadian Trial of Physiologic Pacing Investigators.

           S Yusuf,  M Sami,  M Talajic (2000)
          Evidence suggests that physiologic pacing (dual-chamber or atrial) may be superior to single-chamber (ventricular) pacing because it is associated with lower risks of atrial fibrillation, stroke, and death. These benefits have not been evaluated in a large, randomized, controlled trial. At 32 Canadian centers, patients without chronic atrial fibrillation who were scheduled for a first implantation of a pacemaker to treat symptomatic bradycardia were eligible for enrollment. We randomly assigned patients to receive either a ventricular pacemaker or a physiologic pacemaker and followed them for an average of three years. The primary outcome was stroke or death due to cardiovascular causes. Secondary outcomes were death from any cause, atrial fibrillation, and hospitalization for heart failure. A total of 1474 patients were randomly assigned to receive a ventricular pacemaker and 1094 to receive a physiologic pacemaker. The annual rate of stroke or death due to cardiovascular causes was 5.5 percent with ventricular pacing, as compared with 4.9 percent with physiologic pacing (reduction in relative risk, 9.4 percent; 95 percent confidence interval, -10.5 to 25.7 percent [the negative value indicates an increase in risk]; P=0.33). The annual rate of atrial fibrillation was significantly lower among the patients in the physiologic-pacing group (5.3 percent) than among those in the ventricular-pacing group (6.6 percent), for a reduction in relative risk of 18.0 percent (95 percent confidence interval, 0.3 to 32.6 percent; P=0.05). The effect on the rate of atrial fibrillation was not apparent until two years after implantation. The observed annual rates of death from all causes and of hospitalization for heart failure were lower among the patients with a physiologic pacemaker than among those with a ventricular pacemaker, but not significantly so (annual rates of death, 6.6 percent with ventricular pacing and 6.3 percent with physiologic pacing; annual rates of hospitalization for heart failure, 3.5 percent and 3.1 percent, respectively). There were significantly more perioperative complications with physiologic pacing than with ventricular pacing (9.0 percent vs. 3.8 percent, P<0.001). Physiologic pacing provides little benefit over ventricular pacing for the prevention of stroke or death due to cardiovascular causes.
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            Effect of Smoking on Arterial Stiffness and Pulse Pressure Amplification

             A. Mahmud,  J Feely (2003)
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              Higher sympathetic nerve activity during ventricular (VVI) than during dual-chamber (DDD) pacing.

              We determined the short-term effects of single-chamber ventricular pacing and dual-chamber atrioventricular (AV) pacing on directly measured sympathetic nerve activity. Dual-chamber AV cardiac pacing results in greater cardiac output and lower systemic vascular resistance than does single-chamber ventricular pacing. However, it is unclear whether these hemodynamic advantages result in less sympathetic nervous system outflow. In 13 patients with a dual-chamber pacemaker, we recorded the electrocardiogram, noninvasive arterial pressure (Finapres), respiration and muscle sympathetic nerve activity (microneurography) during 3 min of underlying basal heart rate and 3 min of ventricular and AV pacing at rates of 60 and 100 beats/min. Arterial pressure was lowest and muscle sympathetic nerve activity was highest at the underlying basal heart rate. Arterial pressure increased with cardiac pacing and was greater with AV than with ventricular pacing (change in mean blood pressure +/- SE: 10 +/- 3 vs. 2 +/- 2 mm Hg at 60 beats/min; 21 +/- 5 vs. 14 +/- 2 mm Hg at 100 beats/min; p < 0.05). Sympathetic nerve activity decreased with cardiac pacing and the decline was greater with AV than with ventricular pacing (60 beats/min -40 +/- 11% vs. -17 +/- 7%; 100 beats/min -60 +/- 9% vs. -48 +/- 10%; p < 0.05). Although most patients showed a strong inverse relation between arterial pressure and muscle sympathetic nerve activity, three patients with severe left ventricular dysfunction (ejection fraction < or = 30%) showed no relation between arterial pressure and sympathetic activity. Short-term AV pacing results in lower sympathetic nerve activity and higher arterial pressure than does ventricular pacing, indicating that cardiac pacing mode may influence sympathetic outflow simply through arterial baroreflex mechanisms. We speculate that the greater incidence of adverse outcomes in patients treated with single-chamber ventricular rather than dual-chamber pacing may be due in part to increased sympathetic nervous outflow.
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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
                : 89-92
                Affiliations
                Department of Cardiology, Trakya University School of Medicine, Edirne, Turkey
                Article
                77910 Cardiology 2004;102:89–92
                10.1159/000077910
                15103178
                © 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
                Tables: 1, References: 9, Pages: 4
                Categories
                Arrhythmia and Electrophysiology

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