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      Cardiac autonomic function in patients with acute exacerbation of chronic obstructive pulmonary disease with and without ventricular tachycardia

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          Abstract

          Background

          Autonomic dysfunction in patients with chronic obstructive pulmonary disease (COPD) may increase the risks of arrhythmia and sudden death. We studied cardiac autonomic function in patients with acute exacerbation of COPD (AECOPD).

          Methods

          Patients with AECOPD were classified into ventricular tachycardia (VT) and non-VT groups according to the presence or absence of VT. The following parameters derived from 24-h Holter monitoring were compared between groups: average heart rate, heart rate deceleration capacity (DC), heart rate acceleration capacity (AC), standard deviation of normal RR intervals (SDNN), standard deviation of average RR interval in 5-min segments (SDANN), root mean square of standard deviations of differences between adjacent normal RR intervals (rMSSD), low-frequency power (LF), high-frequency power (HF) and LF/HF ratio.

          Results

          Seventy patients were included, 22 in the VT group and 48 in the non-VT group. The groups had similar clinical characteristics (except for more common amiodarone use in the VT group, P < 0.05) and general ECG characteristics. DC, SDNN, SDANN and rMSSD were lower and AC higher in the VT group ( P < 0.05). In the VT group, DC was correlated positively with SDNN ( r = 0.716), SDANN ( r = 0.595), rMSSD ( r = 0.571) and HF ( r = 0.486), and negatively with LF ( r = -0.518) and LF/HF ( r = -0.458) ( P < 0.05). AC was correlated negatively with SDNN ( r = -0.682), SDANN ( r = -0.567) and rMSSD ( r = -0.548) ( P < 0.05).

          Conclusions

          DC decreased and AC increased in patients with AECOPD and VT, reflecting an imbalance in autonomic regulation of the heart that might increase the risk of sudden death.

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          Most cited references26

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          Deceleration capacity of heart rate as a predictor of mortality after myocardial infarction: cohort study.

          Decreased vagal activity after myocardial infarction results in reduced heart-rate variability and increased risk of death. To distinguish between vagal and sympathetic factors that affect heart-rate variability, we used a signal-processing algorithm to separately characterise deceleration and acceleration of heart rate. We postulated that diminished deceleration-related modulation of heart rate is an important prognostic marker. Our prospective hypotheses were that deceleration capacity is a better predictor of risk than left-ventricular ejection fraction (LVEF) and standard deviation of normal-to-normal intervals (SDNN). We quantified heart rate deceleration capacity by assessing 24-h Holter recordings from a post-infarction cohort in Munich (n=1455). We blindly validated the prognostic power of deceleration capacity in post-infarction populations in London, UK (n=656), and Oulu, Finland (n=600). We tested our hypotheses by assessment of the area under the receiver-operator characteristics curve (AUC). During a median follow-up of 24 months, 70 people died in the Munich cohort and 66 in the London cohort. The Oulu cohort was followed-up for 38 months and 77 people died. In the London cohort, mean AUC of deceleration capacity was 0.80 (SD 0.03) compared with 0.67 (0.04) for LVEF and 0.69 (0.04) for SDNN. In the Oulu cohort, mean AUC of deceleration capacity was 0.74 (0.03) compared with 0.60 (0.04) for LVEF and 0.64 (0.03) for SDNN (p<0.0001 for all comparisons). Stratification by dichotomised deceleration capacity was especially powerful in patients with preserved LVEF (p<0.0001 in all cohorts). Impaired heart rate deceleration capacity is a powerful predictor of mortality after myocardial infarction and is more accurate than LVEF and the conventional measures of heart-rate variability.
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            COPD in China

            Although, to our knowledge, there has been no exhaustive or credible review of the evidence of the disease burden of COPD in China, COPD has become an increasing public health concern to the Chinese medical community. The purpose of this article is to review the evidence and evaluate and clarify the disease burden of COPD in China with the aim of improving effective management. We reviewed previous studies of COPD in China, which included data on prevalence, mortality, disease burden, risk factors, diagnosis, and management by searching related Web sites, including PubMed, ProQuest, and Thomson Reuters' Web of Knowledge, as well as major Chinese databases and government Web sites. Reported COPD prevalence varied between 5% and 13% in different provinces/cities across China. In 2008, COPD ranked fourth as a leading cause of death in urban areas and third in rural areas. In addition, COPD accounted for 1.6% of all hospital admissions in China in that year. The high prevalence of smoking and biomass fuel use acted as major contributors to the high occurrence of COPD in China. Management of COPD in China should focus on adjusting the distribution of medical resources and on addressing public health policies to facilitate earlier diagnosis in rural areas, aim to reduce smoking prevalence, improve patients' self-management, and keep physicians' knowledge up to date and consistent with current guidelines. COPD is one of the most challenging medical issues facing China because of its influence on both personal and public health and its impact on the economy. Optimal management strategies should be adopted and strengthened immediately.
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              Cardiovascular disease in COPD: mechanisms.

              It is now well established that cardiovascular disease contributes significantly to both morbidity and mortality in COPD. Shared risk factors for cardiovascular disease and COPD, such as smoking, low socioeconomic class, and a sedentary lifestyle contribute to the natural history of each of these conditions. However, it is now apparent that alternative, novel mechanisms are involved in the pathogenesis of cardiovascular disease, and these may play an important role in driving the increased cardiovascular risk associated with COPD. In this article, we discuss the potential mechanisms that link COPD to an increased risk of cardiovascular disease.
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                Author and article information

                Contributors
                wxdwsz8@163.com
                Jzh1216@163.com
                taihe-chenbin@163.com
                601523660@qq.com
                kzb1973@tom.com
                zsfdzs@163.com
                sportliuhua@163.com
                +86-021-38297762 , yinshaojun2010@163.com
                Journal
                BMC Pulm Med
                BMC Pulm Med
                BMC Pulmonary Medicine
                BioMed Central (London )
                1471-2466
                20 August 2016
                20 August 2016
                2016
                : 16
                : 124
                Affiliations
                [1 ]Department of Cardiology, Shanghai Jiao Tong University Affiliated Sixth People’s, Hospital, Shanghai, 200233 China
                [2 ]Department of respiratory medicine, Shanghai Pu Nan Hospital, Shanghai, 200125 China
                [3 ]Department of respiratory medicine, Shanghai Jiao Tong University Affiliated Sixth, People’s Hospital, Shanghai, 200233 China
                Article
                287
                10.1186/s12890-016-0287-0
                4992314
                27544078
                fdefa8b9-0a78-4c20-a230-b62af15146fb
                © The Author(s). 2016

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 27 April 2016
                : 11 August 2016
                Funding
                Funded by: Shanghai Hospital Development Center
                Award ID: No. SHDC12013901
                Award Recipient :
                Funded by: Key Disciplines Group Construction Project of Pudong Health Bureau of Shanghai
                Award ID: No. PWZxq2014-07
                Categories
                Research Article
                Custom metadata
                © The Author(s) 2016

                Respiratory medicine
                chronic obstructive pulmonary disease,acute exacerbation,electrocardiogram,autonomic nervous system,ventricular tachycardia,phase-rectified signal averaging (prsa)

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