Vectorcardiographic detection of early hemodynamic abnormalities in chronic obstructive pulmonary disease.

The ability of the vectorcardiogram to detect mild circulatory abnormalities in patients with chronic obstructive pulmonary disease (COPD) is unclear. Therefore, vectorcardiographic changes were correlated with hemodynamic measurements made at rest and during supine exercise in 32 patients with COPD and no clinical or electrocardiographic evidence of right ventricular hypertrophy. Twelve patients had normal hemodynamic data (group 1), nine had abnormal hemodynamic data only during exercise (group 2), and 11 had abnormal hemodynamic data at rest and during exercise (group 3). The extent of rightward terminal QRS forces noted on the vectorcardiogram was significantly less in group 1 (5.5 +/- 8.7 percent) than in either group 2 (19.0 +/- 10.7 percent) or group 3 (17.8 +/- 14.8 percent). Sixty-five percent (13) of the 20 patients with hemodynamic abnormalities had rightward terminal QRS forces of 15 percent or more, whereas only 8 percent (one) of the 12 patients with normal hemodynamic data had such forces of 15 percent or more. The mean of the rightward terminal QRS forces in 27 age-matched normal subjects was 5.0 +/- 5.4 percent, and only one subject had forces of 15 percent or more. We conclude that hemodynamic abnormalities are frequent in patients with COPD and no clinical evidence of right ventricular hypertrophy and that the vectorcardiogram provides an indirect method of detecting these abnormalities.     

A study on pulmonary hemodynamic in patients with stable chronic obstructive pulmonary disease]

Pulmonary hemodynamic changes in 63 chronic obstructive pulmonary disease (COPD) were studied with right heart catheter and impedance pulmonary rheogram (IPR) both at rest and during exercise. The two regression equations for estimating exercise PAPM with rest and exercise IPR parameters were established as follows: PAPM (kPa) = -1.40-0.88lnHs + 8.30B-F + 5.78Q-B/B-Y. PAPM (kPa) = 6.46-5.04Hs/square root of R-R + 4.35Q-B/B-Y-19.34Q-C.6 patients with normal rest PAPM were found to have PAPM increased during exercise and 4 patients with Cor Pulmonale had normal PAPM both at rest and at exercise. PCWP in all patients with and without Cor Pulmonale was normal. We also found that SV, SVI reduced significantly at exercise when compared with these at rest. With the patient's condition aggravating. SV, SVI decreased while RVSWI and dp/dt max of right ventricular systolic pressure increased.     

慢性阻塞性肺疾病相关性肺动脉高压的血流动力学和肺功能相关性研究

目的：观察 COPD 相关性肺动脉高压(pulmonary hypertension,PH)患者的血流动力学和肺功能的相关性。方法共入选右心导管确诊的 COPD 相关 PH 患者64例。根据平均肺动脉压和心指数分为2组：36例严重 COPD 相关 PH 和28例非严重 COPD 相关 PH。比较2组患者各项肺功能参数的差异,与血流动力学指标进行相关性分析。结果 COPD 相关 PH 患者的 FVC% pred[(55.03±22.2)%]、FEV1%pred 降低[(31.4±13.1)%];残气量%pred[(184.7±63.4)%]以及气道阻力%pred [(450.9±296.8)%]增高;并伴弥散量%pred[(58.5±31.1)%]降低。无论是肺容量通气指标、气道阻力指标还是弥散功能,严重 COPD 相关 PH 和非严重 PH 2组间差异均无统计学意义。严重 COPD 相关PH 低氧血症明显,PaO 2和 SaO 2较非严重 PH 组分别低10.6 mmHg 及6.3%(95% CI ,-16.1~-5.0;-9.1~-3.5;P <0.01)。COPD 相关 PH 的 PaO 2和 SaO 2和肺动脉平均压负相关。结论COPD 相关 PH 患者存在严重阻塞性通气功能障碍以及中度弥散功能障碍,血流动力学受损程度和两者无明显相关性。但严重 COPD 相关 PH 低氧血症更为显著,提示除了通气弥散功能外,肺血管因素有可能参与其中。     

Right-ventricular contractility in chronic obstructive pulmonary disease: a combined radionuclide and hemodynamic study

The effect of pulmonary artery hypertension on right-ventricular performance in patients with chronic obstructive pulmonary disease (COPD) is unclear. Decreased values of right-ventricular ejection fraction (RVEF) have been reported, but most patients with stable COPD are not in cardiac failure and have normal or even increased cardiac outputs. We therefore hypothesized that RVEF may be afterload dependent, and thus a poor parameter of cardiac function, and that right-ventricular contractility may be normal even in COPD patients with pulmonary hypertension. We therefore studied 24 COPD patients using a combined hemodynamic and radionuclide approach. RVEF and thermodilution stroke volume index were measured simultaneously at rest in all 24 patients and also during bicycle ergometry in 9 patients. We then calculated end-diastolic and end-systolic volume indices and derived right-ventricular systolic pressure-volume relations in all and the slopes (E) of the pressure-volume line in 9 patients. RVEF was normal in COPD patients without pulmonary hypertension, but was reduced in those with pulmonary hypertension. A strong inverse linear relation between RVEF and mean pulmonary artery pressure (r = -0.73; p less than 0.001) and pulmonary vascular resistance (r = -0.69; p less than 0.001) could be demonstrated, indicating RVEF to be highly afterload dependent. Right-ventricular end-diastolic volume index was significantly higher in patients with pulmonary hypertension, indicating increased preload as the major mechanism to maintain adequate stroke volume in the face of an increased afterload. Right-ventricular end-systolic pressure-volume relations, a good parameter to define right-ventricular contractility independent of systolic loading conditions, were not different between COPD patients with or without pulmonary hypertension, nor did the slopes of the pressure-volume lines in the 9 patients studied during exercise show any difference. From these data we conclude that (a) RVEF is a poor indicator of overall right-ventricular function; (b) right-ventricular contractility is well preserved in stable COPD patients; (c) the major mechanism of maintaining stroke volume in the face of increased right-ventricular afterload seems to be preload augmentation.     

IL-27与COPD的相关性研究

IL-27可作为促炎和抗炎双重作用的细胞因子,以防止炎症对机体引起过度的组织损伤.COPD的发病机制尚未明确,许多实验证明IL-27与其发生、发展密切相关.对IL-27与COPD的相关性进行研究可以为疾病的临床诊治提供新的研究方向,本文就其研究进展作一综述.     

维生素D与慢性阻塞性肺疾病的研究进展

慢性阻塞性肺疾病(COPD)是呼吸系统常见慢性疾病,目前发病率和病死率逐年上升,给个人和社会带来沉重的负担.近年来,人们在努力研究和开发预防和治疗COPD新药的同时,也逐渐发现维生索D这一常见药物与COPD在起病原因、发病机制、发病过程等诸多方面存在关联.     

Cardiovascular disease in chronic obstructive pulmonary disease

Smoking is a major cause of chronic obstructive pulmonary disease (COPD) and cardiovascular disorders, including coronary heart disease (CHD) and peripheral arterial disease. Smoking-induced inflammation and other risk factors like dyslipidemia cause vascular endothelial damage via oxidative stress, and a vicious cycle with the characteristics of atherosclerosis ensues. Inflammatory cytokines stimulate hepatic acute-phase protein production, and C-reactive protein is now used widely to assess inflammation in the arterial wall. Smoking is associated with many alterations in lipids and lipoproteins, and is also prothrombotic. Global risk assessment, which determines the absolute risk for developing CHD in 10 years, is used widely to determine who should receive lipid-lowering therapy. Major CHD risk factors include age, sex, smoking, blood pressure, lipoproteins, and cholesterol, but COPD is not among them. Future studies should determine the absolute risk for developing CHD in patients with COPD. The 3-hydroxy-3-methylglutaryl coenzyme-A reductase inhibitors (statins) are used widely to treat and prevent cardiovascular disease. The statins may also produce other beneficial pleiotropic effects, including increased nitric oxide and prostacyclin, antithrombosis, and decreased inflammation, perhaps indicating utility in the therapy for COPD. Efforts are currently underway to determine if such antiinflammatory effects are independent of or in addition to simply lowering low-density lipoprotein cholesterol.     

Cardiac disease in chronic obstructive pulmonary disease

The cardiac manifestations of chronic obstructive pulmonary disease (COPD) are numerous. Impairments of right ventricular dysfunction and pulmonary vascular disease are well known to complicate the clinical course of COPD and correlate inversely with survival. The pathogenesis of pulmonary vascular disease in COPD is likely multifactorial and related to alterations in gas exchange and vascular biology, as well as structural changes of the pulmonary vasculature and mechanical factors. Several modalities currently exist for the assessment of pulmonary vascular disease in COPD, but right heart catheterization remains the gold standard. Although no specific therapy other than oxygen has been generally accepted for the treatment of pulmonary hypertension in this population, there has been renewed interest in specific pulmonary vasodilators. The coexistence of COPD and coronary artery disease occurs frequently. This association is likely related to shared risk factors as well as similar pathogenic mechanisms, such as systemic inflammation. Management strategies for the care of patients with COPD and coronary artery disease are similar to those without COPD, but care must be given to address their respiratory limitations. Arrhythmias occur frequently in patients with COPD, but are rarely fatal and can generally be treated medically. Use of beta-blockers in the management of cardiac disease, while a theoretical concern in patients with increased airway resistance, is generally safe with the use of cardioselective agents.     

Prognosis in chronic obstructive pulmonary disease

We recruited 985 patients with COPD but without hypoxemia or other serious disease, treated them in a standard fashion, and followed them closely for nearly 3 yr. At the time of recruitment the patients were carefully characterized as to symptom severity, lung function, exercise tolerance, and quality of life, and studies of lung function were repeated during follow-up. Overall mortality was 23% in 3 yr of follow-up. Patient age and the initial value of the FEV1 were the most accurate predictors of death; when FEV1 before bronchodilator was used, the response to bronchodilators was directly related to survival, but this relationship became nonsignificant when postbronchodilator FEV1 was used as a primary predictor. After adjustment for age and FEV1, mortality was related positively to TLC, resting heart rate, and perceived physical disability, and related negatively to exercise tolerance. These relationships, though significant, were relatively weak. When standardized for age and FEV1, mortality in the present series was less than that of a previous series (4), and the same as that of hypoxemic patients with COPD who received continuous home O2 therapy. Changes in FEV1 with time averaged -44 ml/yr, but the standard deviation was large. Patients with low initial values of FEV1 showed relatively little further decline, probably indicating a survivor effect. In patients with well-preserved initial FEV1, rate of decline correlated negatively with bronchodilator response, symptomatic wheezing, and psychological disturbances.     

Senescence in chronic obstructive pulmonary disease

There is a growing realization that chronic obstructive pulmonary disease involves several processes present in aging and cellular senescence. The impact of these processes in the pathogenesis of the main manifestations is multiple, particularly in the propagation of a proinflammatory phenotype, loss of reparative potential, and amplification of oxidative stress, all ultimately leading to tissue damage. This review highlights salient aspects related to senescence discussed in the 2011 Aspen Lung Conference.     

Nutrition in chronic obstructive pulmonary disease

Weight loss is a frequently occurring complication in patients with chronic obstructive pulmonary disease (COPD) and is a determining factor of functional capacity, health status, and mortality. Weight loss in COPD is a consequence of increased energy requirements unbalanced by dietary intake. Both metabolic and mechanical inefficiency contribute to the elevated energy expenditure. A disbalance between protein synthesis and protein breakdown may cause a disproportionate depletion of fat-free mass in some patients. Nutritional support is indicated for depleted patients with COPD because it provides not only supportive care, but direct intervention through improvement in respiratory and peripheral skeletal muscle function and in exercise performance. A combination of oral nutritional supplements and exercise or anabolic stimulus appears to be the best treatment approach to obtaining significant functional improvement. Patients responding to this treatment even demonstrated a decreased mortality. Poor response was related to the effects of systemic inflammation on dietary intake and catabolism. The effectiveness of anticatabolic modulation requires further investigation.     

Exercise in chronic obstructive pulmonary disease

Several important differences exist between the training responses in normal patients and those in patients with chronic obstructive pulmonary disease (COPD). Chief among these is the lack of cardiovascular and metabolic changes in patients with COPD. Despite this, important and significant improvements do occur in exercise endurance after exercise training programs. Experience has shown that simple forms of exercise training and testing are effective and safe.     

Imaging in chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is divided into pulmonary emphysema and chronic bronchitis (CB). Emphysema is defined patho-anatomically as "permanent enlargement of airspaces distal to the terminal bronchiole, accompanied by the destruction of their walls, and without obvious fibrosis" (1). These lesions are readily identified and quantitated using computed tomography (CT), whereas the accompanying hyperinflation is best detected on plain chest X-ray, especially in advanced disease. The diagnosis of CB is clinical and relies on the presence of productive cough for 3 months in 2 or more successive years. The pathological changes of mucosal inflammation and bronchial wall thickening have been more difficult to identify with available imaging techniques. However, recent studies using Multi-detector row CT (MDCT) reported more reproducible assessment of air wall thickening.     

Cough in chronic obstructive pulmonary disease

Patients with chronic obstructive pulmonary disease (COPD) most commonly complain of cough, production of phlegm and breathlessness. The cough reflex sensitivity is heightened compared with that in healthy volunteers and is similar to that in subjects with asthma. The degree of airflow obstruction does not predict cough reflex sensitivity or objective cough counts, implying an independent process. Objective cough rates seem to be relatively low in COPD, despite frequent reporting of the symptom by patients. The relative contribution of cough to disability in COPD seems to be small, if assessed by subjective reporting. Effective treatments for cough in COPD have not yet been identified. Improved outcome measures of cough, a better understanding of the mechanisms underlying cough, and the importance of cough to patients is required to progress in this field.     

Osteoporosis in chronic obstructive pulmonary disease

Patients with chronic obstructive pulmonary disease (COPD) are at increased risk of osteoporosis because of their age, limited physical activity, low body mass index, smoking, hypogonadism, malnutrition, and use of corticosteroids. Systemic inflammation represents an additional pathomechanism contributing to the development of osteoporosis in COPD patients. Males in their mid to late 60s with a smoking history of greater than 60 pack-years have a prevalence rate of vertebral fractures similar to, and possibly greater than, postmenopausal women greater than or equal to 65 years old: in patients with severe COPD, up to 50-70% have osteoporosis or osteopenia, and up to 24-30% have compression vertebral fractures. Correlates of osteoporosis in COPD are mainly measures of body composition, disease severity and the use of corticosteroids, although causality has not been proven. Systemic corticosteroids remain the most common cause of drug-related osteoporosis, and a meta-analysis concluded that the use of more than 6.25 mg prednisone daily led to decreased bone mineral density (BMD) and increased fracture risk. In contrast, the effects of the long-term use of inhaled corticosteroids on BMD remain debatable. Effects of treatment of osteoporosis have not been investigated in samples consisting of COPD patients only but the recommendations follow the general recommendations for the diagnosis and treatment of osteoporosis. Early recognition of BMD loss is essential, and assumes close interdisciplinary cooperation between respirologists and reumatologists. Longitudinal follow-up to assess determinants of osteoporosis in COPD and randomised placebo-controlled trials on the effects of treatment of osteoporosis in patients with COPD only are warranted. In the future, novel therapeutical strategies such as monoclonal antibodies against osteoclasts activators may prove their beneficial effects in the treatment of COPD-related osteoporosis.     

Comorbidities in chronic obstructive pulmonary disease

Comorbidities such as cardiac disease, diabetes mellitus, hypertension, osteoporosis, and psychological disorders are commonly reported in patients with chronic obstructive pulmonary disease (COPD) but with great variability in reported prevalence. Tobacco smoking is a risk factor for many of these comorbidities as well as for COPD, making it difficult to draw conclusions about the relationship between COPD and these comorbidities. However, recent large epidemiologic studies have confirmed the independent detrimental effects of these comorbidities on patients with COPD. On the other hand, many of these comorbidities are now considered to be part of the commonly prevalent nonpulmonary sequelae of COPD that are relevant not only to the understanding of the real burden of COPD but also to the development of effective management strategies.     

自噬与慢性阻塞性肺疾病

自噬现象是一个广泛存在于真核细胞中的生命过程,最早于1962年由Ashford和Porter发现的.近年来,随着对自噬作用研究的深入,发现自噬在多种疾病中都扮演着十分重要的角色.慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)逐渐成为一个不容忽视的公共健康问题,据世界卫生组织/世界银行研究推测,截至2020年该病将成为全球经济负担的第五大疾病.但是,COPD的发病机制尚不明确,随着自噬现象及其与COPD的关系研究进一步深入,为COPD的防治寻找新的治疗策略.因此,该文着重讨论自噬在COPD发病机制中的作用及其在COPD中的临床运用价值.     

Advances in chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is characterised by progressive airflow limitation in the presence of identifiable risk factors. Inflammation is the central pathological feature in the pathogenesis of COPD. In addition to its pulmonary effects, COPD is associated with significant extrapulmonary manifestations, including ischaemic heart disease, osteoporosis, stroke and diabetes. Anxiety and depression are also common. Spirometry remains the gold standard diagnostic tool. Pharmacologic and non‐pharmacologic therapy can improve symptoms, quality of life and exercise capacity and, through their effects on reducing exacerbations, have the potential to modify disease progression. Bronchodilators are the mainstay of pharmacotherapy, with guidelines recommending a stepwise escalating approach. Smoking cessation is paramount in managing COPD, with promotion of physical activity and pulmonary rehabilitation being other key factors in management. Comorbidities should be actively sought and managed in their own right. Given the chronicity and progressive nature of COPD, ongoing monitoring and support with timely discussion of advanced‐care planning and end‐of‐life issues are recommended.