Pulmonary Hypertension In COPD Research Articles

Treatment of Pulmonary Hypertension in COPD: Implications for Exercise Tolerance and Mortality

Treatment of Pulmonary Hypertension in COPD: Implications for Exercise Tolerance and Mortality

Pulmonary Hypertension in COPD

Pulmonary hypertension (PH) is a common consequence of COPD. It has been speculated that patients showing serious PH and vascular remodeling without severe airway obstruction might benefit from vasoactive treatment. There is no approved drug available for COPD-induced PH. Most trials assessing the efficacy of vasoactive drugs in PH have had a follow-up of 12-16 weeks. We report on 4 subjects with COPD and PH. Pulmonary arterial hypertension associated diseases and pulmonary embolism were ruled out. PH persisted despite optimized treatment of underlying COPD and comorbidities, so bosentan was started in all 4 subjects. With bosentan the mean pulmonary artery pressure improved. The average gains in 6-min walk distance at 2-3 months and 8-9 months were 36 m and 145 m, respectively. The maximum gains in 6-min walk distance of the individual subjects were at the 9th, 13th, and 18th month. Oxygenation was stable, and no side effects were observed. We suggest from this experience that in clinical trials of PH in COPD, a follow-up of 16 weeks might cause underestimation of the treatment effects.

Investigation on irbesartan combined with low molecular weight heparin in the treatment of COPD patients with pulmonary hypertension

Objective To evaluate the clinical effect,the changes of pulmonary hypertension,serum D-dimer and side effect of irbesartan combined with low molecular weight heparin in the treatment of pulmonary hypertension in COPD patients.Methods 49 patients of COPD were randomly allocated into two groups:the control group( n =22 )and the treatment group( n =27).The patients of the control group were treated with common treatments,for the treatment group,irbesartan 80mg qd combined with low molecular weight heparin 0.4ml IH bid were additionally administered for 14 days.To evaluate the clinical effect,the changes of pulmonary hypertension,serum D-dimer and side effects.Results The treatment group and the control group could reduce the pulmonary artery pressure.The clinical effects of the former were statistically significant better than the control(P ＜0.01 ).Side effect had no statistically significant difference between two groups.Conclusion Irbesartan combined with low molecular weight heparin have better clinical effects in the treatment of pulmonary hypertension in COPD patients and it was convenient,safe and worthy of extending in clinic. Key words: Irbesartan; Low molecular weight heparin; Pulmonary hypertension

Pulmonary Hypertension Secondary to COPD.

The development of pulmonary hypertension in COPD adversely affects survival and exercise capacity and is associated with an increased risk of severe acute exacerbations. Unfortunately not all patients with COPD who meet criteria for long term oxygen therapy benefit from it. Even in those who benefit from long term oxygen therapy, such therapy may reverse the elevated pulmonary artery pressure but cannot normalize it. Moreover, the recent discovery of the key roles of endothelial dysfunction and inflammation in the pathogenesis of PH provides the rationale for considering specific pulmonary vasodilators that also possess antiproliferative properties and statins.

Pulmonary Hypertension in COPD: Epidemiology, Significance, and Management: Pulmonary Vascular Disease: The Global Perspective

Pulmonary hypertension (PH) associated with parenchymal lung diseases is one of the most common forms of PH. Studies in patients with advanced COPD and hypoxemia have shown a very high prevalence of PH; however, prevalence in mild and moderate COPD is not known. Typical hemodynamic abnormalities include mild-to-moderate elevations in pulmonary artery pressure (PAP) and pulmonary vascular resistance with a preserved cardiac output. A small proportion (< 5%) of patients may have significant elevations in PAP (mean PAP > 35-40 mm Hg) in the presence of mild airflow limitation and are believed to have disproportionate PH. COPD-associated PH has significant clinical implications because it can produce functional limitation and has a negative impact on prognosis. Doppler echocardiography is the best noninvasive test, but noninvasive methods used for diagnosis are prone to error and cannot be relied on when making or refuting the diagnosis of PH. All patients require right-sided heart catheterization if treatment with PH-specific medications is contemplated. The most important steps in managing these patients are: (1) confirm the diagnosis; (2) optimize COPD management; (3) rule out comorbidities; (4) assess and treat hypoxemia; and (5) enroll the patient in pulmonary rehabilitation, if indicated. In patients with PH and advanced airflow limitation, lung transplantation offers the best opportunity for long-term benefit. The role of PH-specific medications remains poorly defined and requires further study but may be considered in patients with disproportionate PH.

Right Heart Function in COPD

Pulmonary hypertension is a common complication in patients with severe hypoxic COPD, but the elevation in pulmonary arterial pressure (PAP) is usually relatively mild, although its presence indicates a poor prognosis. A minority of patients have severe pulmonary hypertension, whose prognosis is very poor with the development of right heart failure. Pulmonary hypertension in COPD is thought to result from hypoxic pulmonary vasoconstriction leading to structural remodeling of all layers of the pulmonary arterial walls. The simple hypothesis that hypoxemia in patients with chronic lung disease results in pulmonary hypertension, which adversely affects right ventricular function and hence increases morbidity and decreases exercise tolerance, leading to the development of peripheral edema and increased mortality, is still somewhat controversial. Whether therapeutic interventions that directly affect PAP or right ventricular function have a significant effect on long-term survival in patients with pulmonary hypertension secondary to hypoxic lung disease is still a matter of debate. Furthermore, whether such interventions will have an effect on symptoms or exercise tolerance remains unproven. Present therapies are limited to the correction of hypoxemia over the long term, which has been shown to have proven benefits on survival. Further studies are required of more specific pulmonary vasodilators or therapies to improve right ventricular function in these patients.

Role for Interleukin-6 in COPD-Related Pulmonary Hypertension

Pulmonary artery remodeling triggered by alveolar hypoxia is considered the main mechanism of pulmonary hypertension (PH) in COPD patients. We hypothesized that the risk for PH in COPD is increased by an elevation in the proinflammatory cytokines interleukin (IL)-6, monocyte chemoattractant protein-1 (MCP-1), and IL-1beta, as well as by specific genetic polymorphisms of these cytokines. We assessed cytokine plasma levels and the polymorphisms G(-174)C IL-6, C(-511)T IL-1beta, and A(-2518)G MCP-1 in 148 COPD patients (recruited at two centers) with right heart catheterization data and 180 control subjects including smokers and nonsmokers. Human pulmonary artery smooth muscle cells (PA-SMCs) were cultured for IL-6 messenger RNA assays under normoxic and hypoxic conditions. Patients with PH (mean pulmonary artery pressure [PAP], >or= 25 mm Hg) had lower Pao(2) and higher plasma IL-6 values than those without PH; there were no differences in terms of pulmonary function test results or CT scan emphysema scores. Plasma IL-6 correlated with mean PAP (r = 0.39; p < 0.001) and was included in a multiple stepwise regression analysis, with mean PAP as the dependent variable. In patients with the IL-6 GG genotype, the mean PAP value was significantly higher and PH was more common than in CG or CC patients (adjusted odds ratio, 4.32; 95% confidence interval, 1.96 to 9.54). Exposure to 4 h of hypoxia led to an about twofold increase in IL-6 messenger RNA in cultured human PA-SMCs. Inflammation, most likely involving IL-6, may contribute substantially to PH complicating COPD.

Pulmonary hypertension in COPD: a review of the literature

Pulmonary hypertension in COPD: a review of the literature

AGE AND DIFFUSION CAPACITY PREDICT PULMONARY HYPERTENSION IN COPD

PURPOSE: Pulmonary hypertension (PHTN) is a known risk factor for morbidity and mortality in patients with COPD. Identifying COPD patients at risk for developing PHTN may improve outcomes. Hypoxic pulmonary vasoconstriction, destruction of alveolar capillaries and hyperinflation are proposed mechanisms of PHTN in COPD, but only a few studies have evaluated the ability of pulmonary function testing to identify PHTN in these patients.

45 Pulmonary hypertension in COPD

45 Pulmonary hypertension in COPD

Is there a relationship between FEV1 and pulmonary hypertension in COPD?

Is there a relationship between FEV1 and pulmonary hypertension in COPD?

Noninvasive diagnosis of latent pulmonary hypertension in copd by exercise-load impedance rheopneumogram: a comparative study with right heart catheterization

Impedance rheopneumogram (IRP) and right heart Swan-Ganz catheter examinations were simultaneously carried out in 63 patients. Two equations for calculating after-exercise-pulmonary-pressure (PAPm) were obtained by stepwise regression analysis: 1) PAPm (kPa) = -1.40-0.88.InHs+8.30.(B-F)+5.78.Q-B/B-Y (r = 0.730, IRP is measured at rest); 2) PAPm(kPa) = 6.46-5.04.Hs/square root of R-R +4.35.Q-B/B-Y-19.34.(Q-C) (r = 0.648, IRP is measured after exercise). This is a new method for diagnosing latent pulmonary hypertension noninvasively.

Pulsed Doppler Echocardiography in the Diagnosis of Pulmonary Hypertension in COPD

We used pulsed Doppler echocardiography to examine the systolic ejection flow from the right ventricle in 66 patients with chronic obstructive pulmonary disease. Adequate recordings were obtained in 60 patients, in conjunction with right heart catheterization. Patients without pulmonary artery hypertension at rest (mean pulmonary artery pressure less than 20 mm Hg) underwent an exercise test which identified a group with PAH during exercise (MPAP greater than 30 mm Hg). The patients were divided into four groups: group 1, or control group: 17 healthy nonsmokers without normal respiratory function data; group 2: COPD without PAH (n = 12); group 3: PAH during exercise (n = 26); group 4: PAH at rest (n = 22). Analysis of Doppler data included time to peak velocity, right ventricular pre-ejection period, and ejection period. Pulsed Doppler echocardiography was a simple and reliable method of detecting PAH. Latent PAH, revealed by the exercise test, was accompanied by significant changes in Doppler findings, confirming the sensitivity of the method.