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      Frequency of Pulmonary Hypertension in Patients with COPD due to Biomass Smoke and Tobacco Smoke

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          Abstract

          Objectives; Pulmonary hypertension (PH) is a common and well established complication of chronic obstructive pulmonary disease (COPD). Its presence is associated with decreased survival. This study was designed to investigate the PH frequency and its relations in hospitalized tobacco and biomass related COPD patients. Methods and Results; The study was a retrospective review of inpatients with COPD defined as a history of tobacco or biomass smoking, Pulmonary function tests (PFT) within stable status, an echocardiogram within stable status. PH was defined as systolic pulmonary artery pressure (sPAP) >35 mmHg. Of the 694 individuals, 600 had suitable aspects for inclusion of study. All Females were biomass exposer and males were tobacco smoker. The Prevalence of PH was found more frequent in females than males. It was more prominent in moderate level COPD cases (56,2% and 37,5%, P<0,002). Both groups had airflow limitation, hypercapnia and hypoxemia, but no differences were found in terms of PaCO 2 and PaO2. However, FEV1 % was lower in males than females (p<0,005). On the other hand, FVC % was lower in the females compared with the males (p < 0.02). When analyzing the influence of PFT and demographic parameters on PH in separate COPD level groups, the results a bit varied among the groups. Conclusion; Our study demonstrated that PH frequency is higher in female COPD cases due to biomass smoke than in male COPD cases due to tobacco smoke. The influence of FVC % on the risk of a person having PH increased with increasing COPD level.

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          Most cited references39

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          Diagnosis and assessment of pulmonary arterial hypertension.

          The diagnosis and assessment of pulmonary arterial hypertension is a rapidly evolving area, with changes occurring in the definition of the disease, screening and diagnostic techniques, and staging and follow-up assessment. The definition of pulmonary hypertension has been simplified, and is now based on currently available evidence. There has been substantial progress in advancing the imaging techniques and biomarkers used to screen patients for the disease and to follow up their response to therapy. The importance of accurate assessment of right ventricular function in following up the clinical course and response to therapy is more fully appreciated. As new therapies are developed for pulmonary arterial hypertension, screening, prompt diagnosis, and accurate assessment of disease severity become increasingly important. A clear definition of pulmonary hypertension and the development of a rational approach to diagnostic assessment and follow-up using both conventional and new tools will be essential to deriving maximal benefit from our expanding therapeutic armamentarium.
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            Pulmonary hypertension in COPD.

            Mild-to-moderate pulmonary hypertension is a common complication of chronic obstructive pulmonary disease (COPD); such a complication is associated with increased risks of exacerbation and decreased survival. Pulmonary hypertension usually worsens during exercise, sleep and exacerbation. Pulmonary vascular remodelling in COPD is the main cause of increase in pulmonary artery pressure and is thought to result from the combined effects of hypoxia, inflammation and loss of capillaries in severe emphysema. A small proportion of COPD patients may present with "out-of-proportion" pulmonary hypertension, defined by a mean pulmonary artery pressure >35-40 mmHg (normal is no more than 20 mmHg) and a relatively preserved lung function (with low to normal arterial carbon dioxide tension) that cannot explain prominent dyspnoea and fatigue. The prevalence of out-of-proportion pulmonary hypertension in COPD is estimated to be very close to the prevalence of idiopathic pulmonary arterial hypertension. Cor pulmonale, defined as right ventricular hypertrophy and dilatation secondary to pulmonary hypertension caused by respiratory disorders, is common. More studies are needed to define the contribution of cor pulmonale to decreased exercise capacity in COPD. These studies should include improved imaging techniques and biomarkers, such as the B-type natriuretic peptide and exercise testing protocols with gas exchange measurements. The effects of drugs used in pulmonary arterial hypertension should be tested in chronic obstructive pulmonary disease patients with severe pulmonary hypertension. In the meantime, the treatment of cor pulmonale in chronic obstructive pulmonary disease continues to rest on supplemental oxygen and a variety of measures aimed at the relief of airway obstruction.
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              Severe pulmonary hypertension and chronic obstructive pulmonary disease.

              Severe pulmonary hypertension occurs occasionally in patients with chronic obstructive pulmonary disease (COPD), but no detailed description of these patients is available. To identify and characterize patients with COPD and severe pulmonary hypertension. Retrospective study of 27 patients with COPD with severe pulmonary hypertension (pulmonary artery mean pressure [Ppa], > or = 40 mm Hg) among 998 patients who underwent right heart catheterization between 1990 and 2002 as part of a workup for chronic respiratory failure during a period of disease stability. Of the 27 patients, 16 had another disease capable of causing pulmonary hypertension. The remaining 11 (11 of 998, 1.1%) patients had COPD as the only cause of pulmonary hypertension, with a median Ppa of 48 mm Hg (interquartile range, 46-50). They had an unusual pattern of cardiopulmonary abnormalities with mild to moderate airway obstruction, severe hypoxemia, hypocapnia, and a very low diffusing capacity for carbon monoxide (p < 0.01 compared with a control group of patients with COPD). Exertional dyspnea was more severe (p < 0.01) and survival was shorter (p = 0.0026) than in the control subjects. Severe pulmonary hypertension is uncommon in patients with COPD. When it occurs, another cause must be sought. COPD with severe pulmonary hypertension and no other possible cause shares features with pulmonary vascular diseases, such as idiopathic pulmonary hypertension.
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                Author and article information

                Journal
                Int J Med Sci
                Int J Med Sci
                ijms
                International Journal of Medical Sciences
                Ivyspring International Publisher (Sydney )
                1449-1907
                2012
                21 July 2012
                : 9
                : 6
                : 406-412
                Affiliations
                1. Department of Pulmonary and Critical Care, Yuzuncu Yil University Medical Faculty, Turkey;
                2. Department of Cardiology, Yuzuncu Yil University Medical Faculty, Turkey;
                3. Department of Pulmonary and Critical Care, Dicle University Medical Faculty, Turkey.
                Author notes
                ✉ Corresponding author: Bunyamin Sertogullarindan, Yuzuncu Yil University Medical Faculty, Arastirma Hastanesi Kazım Karabekir caddesi, 65200 Van, Turkey. Tel: +904322150470 or +905336584452 Fax: +904322141909 E-mail: Bunyaminsert@ 123456hotmail.com .

                Competing Interests: The authors have declared that no competing interest exists.

                Article
                ijmsv09p0406
                10.7150/ijms.4715
                3410359
                22859900
                6f40d744-f702-46e6-b655-c3c20e71d337
                © Ivyspring International Publisher. This is an open-access article distributed under the terms of the Creative Commons License (http://creativecommons.org/licenses/by-nc-nd/3.0/). Reproduction is permitted for personal, noncommercial use, provided that the article is in whole, unmodified, and properly cited.
                History
                : 10 June 2012
                : 16 July 2012
                Categories
                Research Paper

                Medicine
                copd,pulmonary hypertension,environmental pollutants,smoking.
                Medicine
                copd, pulmonary hypertension, environmental pollutants, smoking.

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