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      Pulmonary Arterial Pressure Response During Exercise in COPD: A Correlation with C-Reactive Protein (hsCRP)

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          Abstract

          Background:

          The non-invasive assessment of pulmonary haemodynamics during exercise provides complementary data for the evaluation of exercise tolerance in patients with COPD.

          Methods:

          Exercise echocardiography in the semi-supine position was performed in 27 patients with COPD (C) with a forced expiratory volume in one second (FEV1) of 36±12% predicted and 13 age and gender-matched non-COPD subjects (NC). COPD patients also underwent cardiopulmonary exercise testing with gas exchange detection (CPET). Furthermore, serum high sensitive C-reactive protein (hsCRP), a marker of systemic inflammation, was also measured.

          Results:

          The maximal work rate (WRmax) and aerobic capacity (VO2peak) were significantly reduced (WRmax: 77±33 Watt, VO2peak: 50±14 %pred) in COPD. Pulmonary arterial systolic pressure (PAPs) was higher in COPD versus controls both at rest (39±5 vs. 31±2 mmHg, p<0.001), and at peak exercise (72±12 vs. 52±8 mmHg, p<0.001). In 19 (70%) COPD patients, the increase in PAPs was above 22 mmHg. The change in pressure (dPAPs) correlated with hsCRP (r2=0.53, p<0.0001) and forced vital capacity (FVC) (r2=0.18, p<0.001).

          Conclusion:

          PAPs at rest and during exercise were significantly higher in COPD patients and correlated with higher hsCRP. This may indicate a role for systemic inflammation and hyperinflation in the pulmonary vasculature in COPD.

          The study was registered at ClinicalTrials.gov webpage with NCT00949195 registration number.

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          Most cited references34

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          Pulmonary arterial pressure during rest and exercise in healthy subjects: a systematic review.

          According to current guidelines, pulmonary arterial hypertension (PAH) is diagnosed when mean pulmonary arterial pressure (Ppa) exceeds 25 mmHg at rest or 30 mmHg during exercise. Issues that remain unclear are the classification of Ppa values 30 mmHg during exercise is always pathological. We performed a comprehensive literature review and analysed all accessible data obtained by right heart catheter studies from healthy individuals to determine normal Ppa at rest and during exercise. Data on 1,187 individuals from 47 studies in 13 countries were included. Data were stratified for sex, age, geographical origin, body position and exercise level. Ppa at rest was 14.0+/-3.3 mmHg and this value was independent of sex and ethnicity. Resting Ppa was slightly influenced by posture (supine 14.0+/-3.3 mmHg, upright 13.6+/-3.1 mmHg) and age ( or = 50 yrs: 14.7+/-4.0 mmHg). Ppa during exercise was dependent on exercise level and age. During mild exercise, Ppa was 19.4+/-4.8 mmHg in subjects aged or = 50 yrs (p<0.001). In conclusion, while Ppa at rest is virtually independent of age and rarely exceeds 20 mmHg, exercise Ppa is age-related and frequently exceeds 30 mmHg, especially in elderly individuals, which makes it difficult to define normal Ppa values during exercise.
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            Noninvasive estimation of right ventricular systolic pressure by Doppler ultrasound in patients with tricuspid regurgitation.

            We evaluated the accuracy of a noninvasive method for estimating right ventricular systolic pressures in patients with tricuspid regurgitation detected by Doppler ultrasound. Of 62 patients with clinical signs of elevated right-sided pressures, 54 (87%) had jets of tricuspid regurgitation clearly recorded by continuous-wave Doppler ultrasound. By use of the maximum velocity (V) of the regurgitant jet, the systolic pressure gradient (delta P) between right ventricle and right atrium was calculated by the modified Bernoulli equation (delta P = 4V2). Adding the transtricuspid gradient to the mean right atrial pressure (estimated clinically from the jugular veins) gave predictions of right ventricular systolic pressure that correlated well with catheterization values (r = .93, SEE = 8 mm Hg). The tricuspid gradient method provides an accurate and widely applicable method for noninvasive estimation of elevated right ventricular systolic pressures.
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              Genetically elevated C-reactive protein and ischemic vascular disease.

              Elevated levels of C-reactive protein (CRP) are associated with increased risks of ischemic heart disease and ischemic cerebrovascular disease. We tested whether this is a causal association. We studied 10,276 persons from a general population cohort, including 1786 in whom ischemic heart disease developed and 741 in whom ischemic cerebrovascular disease developed. We examined another 31,992 persons from a cross-sectional general population study, of whom 2521 had ischemic heart disease and 1483 had ischemic cerebrovascular disease. Finally, we compared 2238 patients with ischemic heart disease with 4474 control subjects and 612 patients with ischemic cerebrovascular disease with 1224 control subjects. We measured levels of high-sensitivity CRP and conducted genotyping for four CRP polymorphisms and two apolipoprotein E polymorphisms. The risk of ischemic heart disease and ischemic cerebrovascular disease was increased by a factor of 1.6 and 1.3, respectively, in persons who had CRP levels above 3 mg per liter, as compared with persons who had CRP levels below 1 mg per liter. Genotype combinations of the four CRP polymorphisms were associated with an increase in CRP levels of up to 64%, resulting in a theoretically predicted increased risk of up to 32% for ischemic heart disease and up to 25% for ischemic cerebrovascular disease. However, these genotype combinations were not associated with an increased risk of ischemic vascular disease. In contrast, apolipoprotein E genotypes were associated with both elevated cholesterol levels and an increased risk of ischemic heart disease. Polymorphisms in the CRP gene are associated with marked increases in CRP levels and thus with a theoretically predicted increase in the risk of ischemic vascular disease. However, these polymorphisms are not in themselves associated with an increased risk of ischemic vascular disease. 2008 Massachusetts Medical Society
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                Author and article information

                Journal
                Open Respir Med J
                Open Respir Med J
                TORMJ
                The Open Respiratory Medicine Journal
                Bentham Open
                1874-3064
                29 January 2016
                2016
                : 10
                : 1-11
                Affiliations
                [1 ]Department of Pulmonology, University of Szeged, Deszk, Hungary
                [2 ]National Koranyi Institute for TB and Pulmonology, Budapest, Hungary
                [3 ]Department of Medical Physics and Informatics, University of Szeged, Szeged, Hungary
                [4 ]Department of Internal Medicine, Elisabeth Hospital, Hodmezovasarhely, Hungary
                Author notes
                [* ]Address correspondence to this author at the Department of Pulmonary Rehabilitation, National Koranyi Institute for TB and Pulmonology, No 1, Piheno Street, H-1121 Budapest, Hungary, Fax No: +3613913285, E-mail: varga@ 123456koranyi.hu
                Article
                TORMJ-10-1
                10.2174/1874306401610010001
                4787317
                27019674
                3e21e732-ea64-4461-9d8f-6ae19c6ac303
                © Varga et al.; Licensee Bentham Open.

                This is an open access article licensed under the terms of the Creative Commons Attribution-Non-Commercial 4.0 International Public License (CC BY-NC 4.0) ( https://creativecommons.org/licenses/by-nc/4.0/legalcode), which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

                History
                : 25 June 2015
                : 20 October 2015
                : 21 October 2015
                Categories
                Article

                Respiratory medicine
                chronic obstructive pulmonary disease,exercise,hs-crp,pulmonary hypertension,systemic inflammation

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