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      Cardiac hemodynamics and proinflammatory cytokines during biatrial and right atrial appendage pacing in patients with interatrial block

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          Abstract

          Purpose

          Interatrial block (IAB) frequently coexists with sinus node disease and is considered a risk factor of left atrial dysfunction, atrial arrhythmias, and heart failure development. Conventional right atrial appendage (RAA) pacing impairs intra- and interatrial conductions and consequently prolongs P wave duration. Biatrial (BiA) pacing helps correct IAB, but its advantageous influence remains controversial. The aim of the study was to compare the effects of BiA and RAA pacing on cardiac hemodynamics and serum concentrations of inflammatory markers and neuropeptides.

          Methods

          Twenty-eight patients with IAB and preserved atrio-ventricular conduction treated with BiA pacing were studied. Standard invasive hemodynamic measurements were performed during BiA and RAA pacings. Furthermore, the influence of 1 week of BiA and RAA pacing on neuropeptides: atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) and markers of inflammation: high sensitivity C-reactive protein (hs-CRP), interleukin 6 (IL-6), and neopterin was examined.

          Results

          BiA pacing resulted in significant increase of cardiac output (CO) and reduction of pulmonary capillary wedge pressure. We demonstrated significantly lower concentrations of ANP, hs-CRP, IL-6, and neopterin after 1 week of BiA in comparison to RAA pacing. BNP levels remained unchanged.

          Conclusions

          BiA pacing in comparison to RAA pacing improves hemodynamic performance in patients with IAB and preserved atrio-ventricular conduction. BiA pacing is associated with reduction of ANP and markers of inflammation (hs-CRP, IL-6, and neopterin).

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          Most cited references42

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          Inflammatory markers and onset of cardiovascular events: results from the Health ABC study.

          Inflammation plays an important role in cardiovascular disease. The aim of this study is to investigate the predictive value of several inflammatory markers on the incidence of cardiovascular events in well-functioning older persons. The subjects were 2225 participants 70 to 79 years old, without baseline cardiovascular disease, who were enrolled in the Health, Aging, and Body Composition study. Incident coronary heart disease (CHD), stroke, and congestive heart failure (CHF) events were detected during an average follow-up of 3.6 years. Blood levels of interleukin-6 (IL-6), C-reactive protein (CRP), and tumor necrosis factor-alpha (TNF-alpha) were assessed. After adjustment for potential confounders, IL-6 was significantly associated with all outcomes (CHD events, per IL-6 SD increase: RR, 1.27; 95% CI, 1.10 to 1.48; stroke events, per IL-6 SD increase: RR, 1.45; 95% CI, 1.12 to 1.86; CHF events, per IL-6 SD increase: RR, 1.72; 95% CI, 1.40 to 2.12). TNF-alpha showed significant associations with CHD (per TNF-alpha SD increase: RR, 1.22; 95% CI, 1.04 to 1.43) and CHF (per TNF-alpha SD increase: RR, 1.59; 95% CI, 1.30 to 1.95) events. CRP was significantly associated with CHF events (per CRP SD increase: RR, 1.48; 95% CI, 1.23 to 1.78). A composite summary indicator of inflammation showed a strong association with incident cardiovascular events, with an especially high risk if all 3 inflammatory markers were in the highest tertile. Findings suggest that inflammatory markers are independent predictors of cardiovascular events in older persons.
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            Associations of elevated interleukin-6 and C-reactive protein levels with mortality in the elderly.

            To investigate whether interleukin-6 and C-reactive protein levels predict all-cause and cause-specific mortality in a population-based sample of nondisabled older people. A sample of 1,293 healthy, nondisabled participants in the Iowa 65+ Rural Health Study was followed prospectively for a mean of 4.6 years. Plasma interleukin-6 and C-reactive protein levels were measured in specimens obtained from 1987 to 1989. Higher interleukin-6 levels were associated with a twofold greater risk of death [relative risk (RR) for the highest quartile (> or = 3.19 pg/mL) compared with the lowest quartile of 1.9 [95% confidence interval, CI, 1.2 to 3.1]). Higher C-reactive protein levels (> or = 2.78 mg/L) were also associated with increased risk (RR = 1.6; CI, 1.0 to 2.6). Subjects with elevation of both interleukin-6 and C-reactive protein levels were 2.6 times more likely (CI, 1.6 to 4.3) to die during follow-up than those with low levels of both measurements. Similar results were found for cardiovascular and noncardiovascular causes of death, as well as when subjects were stratified by sex, smoking status, and prior cardiovascular disease, and for both early (<2.3 years) and later follow-up. Results were independent of age, sex, body mass index, and history of smoking, diabetes, and cardiovascular disease, as well as known indicators of inflammation including fibrinogen and albumin levels and white blood cell count. Higher circulating levels of interleukin-6 and C-reactive protein were associated with mortality in this population-based sample of healthy older persons. These measures may be useful for identification of high-risk subgroups for anti-inflammatory interventions.
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              Role of inflammation in initiation and perpetuation of atrial fibrillation: a systematic review of the published data.

              Atrial fibrillation (AF) is the most common arrhythmia in clinical practice. Recent studies have indicated that inflammation might play a significant role in the initiation, maintenance, and perpetuation of AF. Inflammatory markers such as interleukin-6 and C-reactive protein are elevated in AF and correlate to longer duration of AF, success of cardioversion, and thrombogenesis. Furthermore, the inflammatory process might be modulated by the use of statins, angiotensin-converting enzyme inhibitors, or glucocorticoids. The purpose of this study is to analyze the current published reports on the relationship between inflammation and AF and the potential therapeutic options available to modulate the inflammatory milieu in AF.
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                Author and article information

                Contributors
                +48-81-7244151 , +48-81-7244151 , r_troj@hotmail.com
                Journal
                J Interv Card Electrophysiol
                J Interv Card Electrophysiol
                Journal of Interventional Cardiac Electrophysiology
                Springer US (Boston )
                1383-875X
                1572-8595
                28 April 2013
                28 April 2013
                August 2013
                : 37
                : 2
                : 147-154
                Affiliations
                [ ]Department of Cardiology, Medical University of Lublin, 8 Jaczewskiego Str, Lublin, Poland
                [ ]Department of Cardiology and Electrotherapy, Medical University of Gdansk, Gdańsk, Poland
                Article
                9792
                10.1007/s10840-013-9792-8
                3698432
                23625090
                9f45719e-19f9-4cdc-8433-f9aa06099097
                © The Author(s) 2013

                Open Access This article is distributed under the terms of the Creative Commons Attribution License which permits any use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited.

                History
                : 24 May 2012
                : 12 February 2013
                Categories
                Article
                Custom metadata
                © Springer Science+Business Media New York 2013

                Cardiovascular Medicine
                biatrial pacing,cardiac hemodynamics,anp,hs-crp,il-6,neopterin
                Cardiovascular Medicine
                biatrial pacing, cardiac hemodynamics, anp, hs-crp, il-6, neopterin

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