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      Pulmonary Hypertension in Patients with Treated Pulmonary Tuberculosis: Analysis of 14 Consecutive Cases

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          Abstract

          Background:

          Pulmonary tuberculosis (PTB) is an increasing global health problem that continues to cause significant morbidity and mortality. The impact of PTB has been measured in terms morbidity and mortality and little attention has been paid to continuing respiratory disability in those who were cured. Pulmonary hypertension (PHT) is a serious respiratory disability that results from structural lung damage and chronic hypoxia. This study was conducted to investigate the presence of PHT in a cohort of treated PTB patients who presented with shortness of breath.

          Methods:

          This is a cross-sectional study that included 14 consecutive patients who were cured of PTB and presented with shortness of breath. Demographic and clinical data were recorded for all patients. PHT was diagnosed using Doppler echocardiography.

          Results:

          Fourteen patients who were treated for PTB and were found to have PHT were studied. All patients were sputum smear negative at the time of the study. The mean age (SD) was 43.1 (13.6) and half of the patients were males. The mean number of years since PTB was diagnosed (SD) was 9.4 (10.9). All patients had abnormal chest x-rays. The commonest radiological abnormality was fibrocavitation which occurred in 50% of patients. Estimated pulmonary artery systolic pressure (PASP) of 51 to 80 mm/Hg was found in 9 patients (64.3%) whereas PASP of 40 to 50 mm/Hg was found in 4 patients (28.6%) and one patient had PASP more than 80 mm/Hg.

          Conclusions:

          Different grades of PHT occurred in this cohort of treated PTB patients on average about 9 years after cure. The findings of this study support implementation of strategies for early detection and prevention of PTB. For those who were cured from PTB, longer periods of disability should be implemented in assessment of disease burden.

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          Most cited references18

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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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            Screening, early detection, and diagnosis of pulmonary arterial hypertension: ACCP evidence-based clinical practice guidelines.

            Pulmonary arterial hypertension (PAH) occurs as an idiopathic process or as a component of a variety of disease processes, including chronic thromboembolic disease, connective tissue diseases, congenital heart disease, and exposure to exogenous factors including appetite suppressants or infectious agents such as HIV. This article reviews evidence for screening in susceptible patient groups and the approach to diagnosing PAH when it is suspected, and provides specific recommendations for applying this evidence to clinical practice.
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              Quantitative assessment of pulmonary hypertension in patients with tricuspid regurgitation using continuous wave Doppler ultrasound.

              Doppler ultrasound examination was performed in 69 patients with a variety of cardiopulmonary disorders who were undergoing bedside right heart catheterization. Patients were classified into two groups on the basis of hemodynamic findings. Group I consisted of 20 patients whose pulmonary artery systolic pressure was less than 35 mm Hg and Group II consisted of 49 patients whose pulmonary artery systolic pressure was 35 mm Hg or greater. Tricuspid regurgitation was detected by Doppler ultrasound in 2 of 20 Group I patients and 39 of 49 Group II patients (p less than 0.001). Twenty-six of 27 patients with pulmonary artery systolic pressure greater than 50 mm Hg had Doppler evidence of tricuspid regurgitation. In patients with tricuspid regurgitation, continuous wave Doppler ultrasound was used to measure the velocity of the regurgitant jet, and by applying the Bernoulli equation, the peak pressure gradient between the right ventricle and right atrium was calculated. There was a close correlation between the Doppler gradient and the pulmonary artery systolic pressure measured by cardiac catheterization (r = 0.97, standard error of the estimate = 4.9 mm Hg). Estimating the right atrial pressure clinically and adding it to the Doppler-determined right ventricular to right atrial pressure gradient was not necessary to achieve accurate results. These findings indicate that tricuspid regurgitation can be identified by Doppler ultrasound in a large proportion of patients with pulmonary hypertension, especially when the pulmonary artery pressure exceeds 50 mm Hg. Calculation of the right ventricular to right atrial pressure gradient in these patients provides an accurate noninvasive estimate of pulmonary artery systolic pressure.
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                Author and article information

                Journal
                Clin Med Insights Circ Respir Pulm Med
                Clinical Medicine Insights: Circulatory, Respiratory and Pulmonary Medicine
                Clinical Medicine Insights. Circulatory, Respiratory and Pulmonary Medicine
                Libertas Academica
                1179-5484
                2011
                13 January 2011
                : 5
                : 1-5
                Affiliations
                [1 ]Department of Medicine, University of Khartoum, Khartoum, Sudan
                [2 ]Department of Respiratory Medicine, Elshaab Teaching Hospital, Khartoum Sudan
                [3 ]Department of Cardiology, Elshaab Teaching Hospital, Khartoum Sudan
                Author notes
                Corresponding author email: drahahmed@ 123456hotmail.com
                Article
                ccrpm-2011-001
                10.4137/CCRPM.S6437
                3040077
                21339885
                ed85a5b7-478e-4a57-870a-474fbffb2429
                © the author(s), publisher and licensee Libertas Academica Ltd.

                This is an open access article. Unrestricted non-commercial use is permitted provided the original work is properly cited.

                History
                Categories
                Original Research

                Respiratory medicine
                tuberculosis,echocardiography,pulmonary hypertension
                Respiratory medicine
                tuberculosis, echocardiography, pulmonary hypertension

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