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      Diastolic Dysfunction in Patients with Chronic Obstructive Pulmonary Disease: A Meta-Analysis of Case Controlled Studies

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          Abstract

          Background:

          Chronic obstructive pulmonary disease (COPD) and left ventricular diastolic dysfunction (LVDD) are major causes of morbidity and mortality and have overlapping symptomatology including cough and dyspnea. Whether COPD is a risk factor for LVDD remains largely unclear.

          The objective of this meta-analysis was to determine if the prevalence of the LVDD as determined by echocardiographic parameters is increased in COPD patients.

          Methods:

          We used a time-and-language-restricted search strategy resulting in identification of 4,912 studies of which 15 studies met our apriori inclusion criteria; 4,897 were excluded, such duplicates, foreign language articles were excluded. We performed a meta-analysis of standard echo parameters on the fifteen case control studies related to diastolic dysfunction. The meta-analysis was performed using Review Manager, version 5.3 (Cochrane Collaboration).

          Results:

          A total of 15 studies with 1,403 subjects were included. There were no differences in left ventricular ejection fraction between COPD and non-COPD population. Patients with COPD had prolonged isovolumetric relaxation time (IVRT) (mean difference 20.84 [95% CI 12.21, 29.47]; P< 0.00001), lower E/A ratio (mean difference - 0.24 [95% CI −0.34, 00.14]; P < 0.00001), higher transmitral A wave peak velocity (Apv) (mean difference 11.71 [95% CI 4.80, 18.62]; P< 0.00001), higher E/e’ ratio (mean difference 1.88 [95% CI 1.23, 2.53]; P< 0.00001), lower mitral E wave peak velocity (Epv) (mean difference −8.74 [95% CI −13.63, −3.85]; P< 0.0005), prolonged deceleration time (DT) (mean difference 50.24 [95% CI 15.60, 84,89]; P< 0.004), a higher right ventricular end diastolic diameter (RVEDD) (mean difference 8.02 [95% CI 3.45, 12.60]; P< 0.0006) compared to controls. COPD patients had a higher pulmonary arterial pressure (mean difference 10.52 [95% CI 3.98, 17.05]; P< 0.002). Differences in septal e’ velocity (mean difference −2.69 [95% CI −6.07, 0.69]; P< 0.12) and in lateral e’ velocity (mean difference −2.84 [95% CI 5.91, 0.24]; P< 0.07) trended towards significance but did not meet our cutoff for statistical significance (p < 0.05).

          Conclusions:

          Patients with COPD are more likely to have LVDD as established by echocardiographic parameters. Our findings are likely explainable, in part, by factors such as lung hyperinflation, chronic hypoxia, hypercapnia, systemic inflammation, increased arterial stiffness, subendocardial ischemia, as well as ventricular interdependence; all of which might contribute to the pathogenesis of diastolic dysfunction. Further research is needed to elucidate the pathophysiologic mechanisms of increased LVDD in the COPD population with the potential impact on developing effective therapeutic interventions for these serious disorders.

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          Most cited references 42

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          Burden of systolic and diastolic ventricular dysfunction in the community: appreciating the scope of the heart failure epidemic.

          Approximately half of patients with overt congestive heart failure (CHF) have diastolic dysfunction without reduced ejection fraction (EF). Yet, the prevalence of diastolic dysfunction and its relation to systolic dysfunction and CHF in the community remain undefined. To determine the prevalence of CHF and preclinical diastolic dysfunction and systolic dysfunction in the community and determine if diastolic dysfunction is predictive of all-cause mortality. Cross-sectional survey of 2042 randomly selected residents of Olmsted County, Minnesota, aged 45 years or older from June 1997 through September 2000. Doppler echocardiographic assessment of systolic and diastolic function. Presence of CHF diagnosis by review of medical records with designation as validated CHF if Framingham criteria are satisfied. Subjects without a CHF diagnosis but with diastolic or systolic dysfunction were considered as having either preclinical diastolic or preclinical systolic dysfunction. The prevalence of validated CHF was 2.2% (95% confidence interval [CI], 1.6%-2.8%) with 44% having an EF higher than 50%. Overall, 20.8% (95% CI, 19.0%-22.7%) of the population had mild diastolic dysfunction, 6.6% (95% CI, 5.5%-7.8%) had moderate diastolic dysfunction, and 0.7% (95% CI, 0.3%-1.1%) had severe diastolic dysfunction with 5.6% (95% CI, 4.5%-6.7%) of the population having moderate or severe diastolic dysfunction with normal EF. The prevalence of any systolic dysfunction (EF < or =50%) was 6.0% (95% CI, 5.0%-7.1%) with moderate or severe systolic dysfunction (EF < or =40%) being present in 2.0% (95% CI, 1.4%-2.5%). CHF was much more common among those with systolic or diastolic dysfunction than in those with normal ventricular function. However, even among those with moderate or severe diastolic or systolic dysfunction, less than half had recognized CHF. In multivariate analysis, controlling for age, sex, and EF, mild diastolic dysfunction (hazard ratio, 8.31 [95% CI, 3.00-23.1], P<.001) and moderate or severe diastolic dysfunction (hazard ratio, 10.17 [95% CI, 3.28-31.0], P<.001) were predictive of all-cause mortality. In the community, systolic dysfunction is frequently present in individuals without recognized CHF. Furthermore, diastolic dysfunction as rigorously defined by comprehensive Doppler techniques is common, often not accompanied by recognized CHF, and associated with marked increases in all-cause mortality.
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            • Record: found
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            2016 ESC Guidelines for the Diagnosis and Treatment of Acute and Chronic Heart Failure.

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              Heart Failure with Preserved Ejection Fraction.

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                Author and article information

                Journal
                101737788
                48175
                Int J Clin Res Trials
                Int J Clin Res Trials
                International journal of clinical research & trials
                2456-8007
                5 October 2019
                19 September 2019
                2019
                24 October 2019
                : 4
                : 2
                Affiliations
                Department of Medicine, Division of Endocrinology, State University of New York-Downstate Medical Center, Brooklyn, New York
                Author notes
                [* ] Corresponding Author: Prof. Samy I. McFarlane, Division of Endocrinology, Department of Internal Medicine, State University of New York, Downstate Medical Center, Brooklyn, New York, 11203, USA, Tel: 718-270-6707, Fax: 718-270-4488; smcfarlane@ 123456downstate.edu
                Article
                NIHMS1053203
                10.15344/2456-8007/2019/137
                6812536
                f6ee9f7e-8c47-437c-8a58-54a6a4e7ec86

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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