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      Anxiety and P Wave Dispersion in a Healthy Young Population

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          Abstract

          Background: P wave dispersion (P<sub>d</sub>), defined as the difference between the maximum (P<sub>max</sub>) and the minimum P wave duration (P<sub>min</sub>), and P<sub>max</sub> are electrocardiographic (ECG) markers that have been used to evaluate the discontinuous propagation of sinus impulses and the prolongation of atrial conduction time. P<sub>d</sub> in normal subjects has been reported to be influenced by the autonomic tone, which induces changes in atrial size and the velocity of impulse propagation. However, the association between P<sub>d</sub> and anxiety has not been studied in normal subjects. Methods and Results: P<sub>max</sub>, P<sub>min</sub> and P<sub>d</sub> were measured in 726 physically and mentally healthy young male volunteers, aged 21.23 ± 1.25 years (range 20–26). The Spielberger State-Trait Anxiety Inventory (STAI) was scored concomitantly. Blinded intra- and interobserver reproducibility of the P wave duration and P<sub>d</sub> measurement were evaluated, and comparison revealed a Pearson correlation coefficient of 0.87 and 0.89 for the P wave duration, and 0.93 and 0.90 for P<sub>d</sub>, respectively (p < 0.001). P<sub>max</sub> and P<sub>d</sub> were significantly correlated with the state anxiety (STAI-1) subscale (r = 0.662, p < 0.001, and r = 0.540, p < 0.001, respectively) and the trait anxiety (STAI-2) subscale (r = 0.583, p < 0.001, and r = 0.479, p < 0.001, respectively). P<sub>min</sub> did not show any significant correlation with anxiety. Across 3 variables included in a multiple linear regression analysis, STAI-1 and STAI-2 were the significant independent determinants of P<sub>max</sub> and P<sub>d</sub>. Beta coefficients indicated that the contribution of STAI-1 to P<sub>max</sub> (66.3 and 33.7%) and P<sub>d</sub> (65 and 35%) was much greater than that of STAI-2. Conclusions: STAI-1 and STAI-2are associated with an increase in P<sub>max</sub> and P<sub>d</sub>. The association of P<sub>d</sub> resulted from an augmentation of P<sub>max</sub>. This is the first study to show the relation between P<sub>max</sub>, P<sub>d</sub> and anxiety.

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          Most cited references 13

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          Autonomic characteristics of generalized anxiety disorder and worry.

          Autonomic characteristics of generalized anxiety disorder (GAD) and worry were examined using measures of heart period variability. The cardiorespiratory responses of 34 GAD clients and 32 nonanxious control subjects were recorded during resting baseline, relaxation, and worry periods. Results indicated differences between GAD subjects and controls as well as among baseline, relaxation, and worry periods. GAD clients exhibited shorter cardiac interbeat intervals (IBIs) and lower high frequency spectral power across all task conditions. Relative to baseline and relaxation conditions, worry was associated with (1) shorter IBIs, (2) smaller mean successive differences (MSD) of the cardiac IBIs, and (3) lower high frequency spectral power. These findings suggest that GAD and its cardinal feature (worry), are associated with lower cardiac vagal control. The findings of the present study provide evidence for the utility of further exploration of the role of autonomic nervous system activity in GAD.
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            Role of serotonergic and noradrenergic systems in the pathophysiology of depression and anxiety disorders.

            There is abundant evidence for abnormalities of the norepinephrine (NE) and serotonin (5HT) neurotransmitter systems in depression and anxiety disorders. The majority of evidence supports underactivation of serotonergic function and complex dysregulation of noradrenergic function, most consistent with overactivation of this system. Treatment for these disorders requires perturbation of these systems. Reproducible increases in serotonergic function and decreases in noradrenergic function accompany treatment with antidepressants, and these alterations may be necessary for antidepressant efficacy. Dysregulation of these systems clearly mediates many symptoms of depression and anxiety. The underlying causes of these disorders, however, are less likely to be found within the NE and 5HT systems, per se. Rather their dysfunction is likely due to their role in modulating, and being modulated by, other neurobiologic systems that together mediate the symptoms of affective illness. Clarification of noradrenergic and serotonergic modulation of various brain regions may yield a greater understanding of specific symptomatology, as well as the underlying circuitry involved in euthymic and abnormal mood and anxiety states. Disrupted cortical regulation may mediate impaired concentration and memory, together with uncontrollable worry. Hypothalamic abnormalities likely contribute to altered appetite, libido, and autonomic symptoms. Thalamic and brainstem dysregulation contributes to altered sleep and arousal states. Finally, abnormal modulation of cortical-hippocampal-amygdala pathways may contribute to chronically hypersensitive stress and fear responses, possibly mediating features of anxiety, anhedonia, aggression, and affective dyscontrol. The continued appreciation of the neural circuitry mediating affective states and their modulation by neurotransmitter systems should further the understanding of the pathophysiology of affective and anxiety disorders.
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              Psychometric properties of the STAI: a reply to Ramanaiah, Franzen, and Schill.

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                Author and article information

                Journal
                CRD
                Cardiology
                10.1159/issn.0008-6312
                Cardiology
                S. Karger AG
                0008-6312
                1421-9751
                2005
                September 2005
                15 September 2005
                : 104
                : 3
                : 162-168
                Affiliations
                Department of Cardiology, Siyami Ersek Cardiovascular and Thoracic Surgery Center, Istanbul, Turkey
                Article
                87874 Cardiology 2005;104:162–168
                10.1159/000087874
                16131805
                © 2005 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: 2, Tables: 5, References: 28, Pages: 7
                Categories
                Arrhythmias and Electrophysiology

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