Signs Of Chronic Obstructive Pulmonary Disease Research Articles

Deep Transfer Learning for Chronic Obstructive Pulmonary Disease Detection Utilizing Electrocardiogram Signals

The primary objective and contribution of this research is the development and design of an artificial intelligence system that will diagnose Chronic Obstructive Pulmonary Disease (COPD) utilizing only the heart signal (ECG) of the patient. In contrast to the traditional way of diagnosing COPD, which requires spirometer tests and a laborious workup in a hospital setting, the proposed system uses the classification capabilities of deep transfer learning and the patient’s heart signal, which provides COPD signs in itself and can be received from any modern smart device. The motivation of this research is that it introduces the first research on automated COPD diagnosis using deep learning and utilizes the first annotated dataset in this field. Since the disease progresses slowly and conceals itself until the final stage, hospital visits for diagnosis are uncommon. Hence, the medical goal of this research is to detect COPD using a simple heart signal before it becomes incurable. Deep transfer learning frameworks, which were previously trained on a general image data set, are transferred to carry out an automatic diagnosis of COPD by classifying patients’ electrocardiogram (ECG) signal equivalents, which are produced by signal-to-image transform techniques. Xception, VGG-19, InceptionResNetV2, DenseNet-121, and "trained-from-scratch" convolutional neural network architectures have been investigated for the detection of COPD, and it is demonstrated that they are able to obtain high performance rates in classifying nearly 33.000 instances using diverse training strategies. The highest classification rate was obtained by the Xception model at 99%. This research shows that the newly introduced COPD detection approach is effective, easily applicable, and eliminates the burden of considerable effort in a hospital. It could also be put into practice and serve as a diagnostic aid for chest disease experts by providing a deeper and faster interpretation of ECG signals. Using the knowledge gained while identifying COPD from ECG signals may aid in the early diagnosis of future diseases for which little data is currently available.

Frustrated Caring: Family Members' Experience of Motivating COPD Patients Towards Self-Management.

AimThe aim of this phenomenological study was to explore principal family members’ experience of motivating patients with chronic obstructive pulmonary disease (COPD) towards self-management.MethodsInterviews were conducted with 10 family members (spouses and adult children) of COPD patients. The interviews were audio recorded, transcribed and analyzed thematically.ResultsBeing a principal family member of a COPD patient is characterized by frustrated caring; wanting the best for him/her and yet carrying a heavier burden than the person feels equipped for, lacking both knowledge about the disease progress and information about available healthcare resources. The situation demands much energy, due to COPD patients’ lack of stamina; family members’ fear of the patient’s possible breathlessness; willingness to help, though sometimes meeting with negative reactions from the patient; and feeling ignored by health professionals (HPs). Family members expressed a need for a formal connection between patient–family–HPs. The increasing burden experienced by patients’ family members is characterized by a sequential process in three phases of the patient’s declining self-management. In the early phase, family and patient are ignorant of COPD yet recognize the patient’s smoking as a risky lifestyle. In the intermediary phase, signs of COPD become evident to the family. The first turning point is when the family first observes the patient’s acute exacerbation. A second turning point is in the advanced phase, when family and patient recognize COPD as a progressive disease, possibly fatal. We also identified family members’ views on COPD patients’ needs, and their own roles, main frustrations and concerns.ConclusionFamily members’ experience of motivating COPD patients towards self-management is a sequential process where the family experiences advancing caring burden and declining self-management by the patient. We propose the establishment of COPD patients’ teams consisting of patient–family–HP, aimed at the patients’ best possible self-management.

CHRONIC OBSTRUCTIVE LUNG DISEASE AS RISK FACTOR FOR CARDIOVASCULAR DISORDERS

Close relation of cardiovascular (CVD) diseases and chronic obstructive pulmonary disease (COPD) gains attention during last years as one of the aspects of systemic COPD signs. High prevalence of CVD in COPD patients can be explained by a concept of persisting systemic lowintensive inflammation. Current review regards COPD as risk factor for CVD that demands respective multidisciplinary diagnostic and management approaches.

Smoking: Is it a Risk Factor for Pulmonary Vascular Diseases?

Chronic obstructive pulmonary disease (COPD) summarizes chronic bronchitis and lung emphysema. A major trigger for this disease is cigarette smoking. However, the occurrence and role of pulmonary vascular remodeling and pulmonary hypertension (PH) in COPD is not clarified yet. Although PH and lung vascular remodeling were thought to be infrequent events in COPD, recent clinical data estimate that 30-70% of patients with COPD also have PH.[1] In 50% of COPD patients evaluated for lung transplantation, mean pulmonary arterial pressure was above 25 mmHg.[2] In addition, a much larger portion of COPD patients may be affected by morphological changes of the lung vessels and/or borderline PH.[3-5] In this regard it has recently been stated that “moderate-to-severe PH is not a rare event” in COPD[2] and “numerous studies have shown that the presence of even mild PH is of prognostic relevance in patients with COPD.”[3] Without doubt, late-stage COPD can result in a lack of oxygen, which can trigger pulmonary vascular remodeling, similar to chronic alveolar hypoxia. However, recently it has been proposed that pulmonary vascular alterations are not secondary to lung emphysema development but can even be the driving force of COPD. Indeed, there is increasing evidence that cigarette smoke may have a major direct impact on the pulmonary vasculature, suggesting that PH and subsequent cor pulmonale are not necessarily secondary to hypoxia in patients with COPD.[6-8] This field of research was largely driven by investigations from Joan Barbera's group, who documented that pulmonary vascular remodeling (resembling pulmonary vascular remodeling occurring in PH patients) occurs in smokers who have not yet developed COPD.[5] For detailed investigations of the time course of possible tobacco-smoke induced pulmonary vascular remodeling processes and emphysema development, animal experiments can be helpful. They may decipher 1) whether lung vascular remodeling generally occurs during tobacco smoke exposure, 2) whether it leads to PH, and 3) whether it precedes lung emphysema development. Early studies already clearly showed that tobacco smoke causes vascular remodeling with thickening of the vessel wall, and studies in guinea pigs and recently in mice described that pulmonary vascular remodeling may be observed prior to lung emphysema development.[9-12] An investigation from our group showed that pulmonary vascular remodeling and PH induced by tobacco smoke occur in the absence of hypoxia and precede the development of alveolar destruction and emphysema formation. This study furthermore revealed that emphysema and PH development are not essentially linked but can occur independently—at least in mice. Whereas emphysema development was dependent on the inducible NO synthase (iNOS) in non-bone marrow derived cells, PH was dependent on iNOS in bone marrow-derived cells (Fig. 1).[12] Nevertheless, this study proposed that a vascular iNOS upregulation induced by tobacco smoke, even in the absence of vascular remodeling, can trigger emphysema. Smoke-induced vascular alterations and emphysema development. A recent study in mice revealed that tobacco smoke-induced vascular remodeling and PH is dependent on iNOS activity in bone marrow-derived cells, whereas lung emphysema development was dependent on iNOS activity in non-bone marrow-derived cells. iNOS inhibition with L-N6-(1-iminoethyl)-lysine (L-NIL) could not only prevent but also reversed established PH and emphysema in mice.[15] Provided that such animal studies also apply to the human situation—which is supported by studies in smokers that have not yet developed COPD, but display pulmonary vascular remodeling—[5,13] it is clear that tobacco smoke can trigger vascular alterations even without signs of COPD. Such alterations, which can affect biochemical pathways, vascular function, as well as the morphology of the pulmonary vessels,[14] may also—going beyond pulmonary vascular disease—drive emphysema development.

Comparison of Fenspiride with Beclomethasone as Adjunctive Anti-Inflammatory Treatment in Patients with Chronic Obstructive Pulmonary Disease

This study aimed to compare the clinical efficacy of two anti-inflammatory medications (fenspiride and inhaled beclomethasone [beclomethasone dipropionate]) in patients with stable chronic obstructive pulmonary disease (COPD) over 6 months. DESIGN, METHODS AND PATIENTS: This was a randomised comparison of 58 patients with COPD, divided into five treatment groups: fenspiride (stages 1 and 2), beclomethasone (stage 2), and two control groups (stages 1 and 2). In addition, 64 patients with exacerbations of COPD were evaluated over a 2-week treatment period during which they received either fenspiride or prednisolone. Clinical signs and symptoms of COPD were evaluated every 2 months (aggregated numerical index of signs and symptoms), as were lung function tests (forced vital capacity [FVC], forced expiratory volume in 1 second [FEV1], FEV1/FVC) and a 6-minute walking test. Statistically significant reductions in all evaluated COPD signs and symptoms were achieved with fenspiride in stage 1 COPD. Fenspiride therapy significantly reduced the indices of sputum parameters (8-fold decrease), incidence of dry rales (6-fold decrease), dyspnoea (4-fold decrease) and cough (2.5-fold decrease). In comparison with beclomethasone, fenspiride was superior in stage 2 COPD. In patients with stage 2 COPD, reductions were less marked, but remained significantly superior in the fenspiride group in comparison with the beclomethasone group and the control groups. In patients with exacerbations of COPD, fenspiride had equivalent efficacy to that of systemic corticosteroids. Anti-inflammatory therapy with fenspiride in addition to bronchodilators significantly improved clinical signs and symptoms, external respiratory function tests and physical activity tests in patients with stage 1 COPD. Adjunctive fenspiride therapy was superior to inhaled beclomethasone in stage 2 COPD. Anti-inflammatory therapy in COPD may be more effective at an early stage of this disease.

Polymerized α1‐antitrypsin is present on lung vascular endothelium. New insights into the biological significance of α1‐antitrypsin polymerization

The damage to lung tissue in chronic obstructive pulmonary disease (COPD) may involve the progressive loss of pulmonary vascular endothelial cells. Endothelial binding of alpha1-antitrypsin (alpha1-AT) derived from plasma has been identified, and alpha1-AT deficiency is a known genetic risk factor associated with alpha1-AT polymerization and COPD development. Therefore, in the present study we aimed to investigate if alpha1-AT is present on the lung vascular endothelium, and if it is in a polymeric form. Postmortem paraffin-embedded tissue specimens from 15 COPD (chronic bronchitis and emphysema) cases with and without Z alpha1-AT (Glu342Lys) deficiency and from 10 cases without signs of COPD were studied. Immunohistochemistry was performed using the streptavidin-biotin method with a monoclonal ATZ11 antibody specific for polymeric alpha1-AT, and polyclonal antibodies against human alpha1-AT and neutrophil elastase. Vascular endothelium showed intense staining for alpha1-AT with the ATZ11 antibody in all cases; however, intensity of staining in patients with alpha1-AT deficiency was greater. No endothelial staining was observed with the anti-elastase antibody. This is the first demonstration that alpha1-AT bound to the vascular endothelium of lungs is in a polymeric form, which also suggests a possible previously unknown role for polymeric alpha1-AT in vivo.

Compliance During Long-Term Treatment with Fluticasone Propionate in Subjects with Early Signs of Asthma or Chronic Obstructive Pulmonary Disease (COPD): Results of the Detection, Intervention, and Monitoring Program of COPD and Asthma (DIMCA) Study

In a prospective study, we investigated the long-term compliance to fluticasone propionate (FP) by dry powder inhalation (Rotadisk®) in subjects with early signs of asthma and chronic obstructive pulmonary disease (COPD) without an established diagnosis. Subjects were selected from a large screening program on early stages of asthma and COPD (Detection, Intervention, and Monitoring Program of COPD and Asthma [DIMCA] program) in the general practice. Forty-eight adult subjects with “early signs of COPD” (slightly increased forced expiratory volume in 1 sec [FEV1] decline of >0.04L/year) and 29 adult subjects with “early signs of asthma” (signs of bronchial hyperresponsiveness or reversibility) participated in a randomized placebo-controlled trial with FP (Flixotide® 500 jag daily) versus placebo with a duration of 2 years or 1 year, respectively. Compliance was measured by counting Rotadisks returned. By means of a questionnaire, participants were asked about perceived effects and/or side effects of the trial drug. The mean overall individual compliance rates of 72% (range 7%-102%) in the early COPD trial and 71% (range 8%-99%) in the early asthma trial were maintained throughout the study. Perceived effectiveness (12% of the participants) or side effects (30% of the participants) of the trial drug were not related to compliance. The willingness of patients to use the trial drug in daily practice if efficacy would be proved was statistically significantly related to compliance during the trial (p = 0.017). It was concluded that the compliance rates found were relatively high in patients with symptoms of mild asthma or COPD without an established diagnosis. Conviction of the importance of treatment influenced compliance more positively than perceived (side) effects. These results again emphasize the importance of patient education in establishing early treatment with inhaled corticosteroids.

CT of saber-sheath trachea

The diagnosis of saber-sheath trachea is easy at CT due to its cross-sectional imaging, but the significance of this CT sign has not been evaluated in the diagnosis of chronic obstructive pulmonary disease (COPD). Various signs of COPD were compared between a series of 20 patients with a saber-sheath trachea at CT (tracheal index ≤ 66%) and a group of 20 pneumologic control patients without saber-sheath trachea (tracheal index ≥ 70%). These signs included clinical and standard radiographic indices of COPD, sternum-spine distance and 3 functional tests of COPD: forced expiratory volume in one second, carbon monoxide diffusing lung capacity, and functional residual capacity (FRC). A significant difference was found between the 2 groups, concerning the values of FRC (p<10−4) and of sternum-spine distance (p<10−2). The tracheal index was significantly correlated with the FRC values (r= −0.611; p<10−5) and with the sternum-spine distance (r= −0.322; p<0.05). No other significant difference was observed. It is ...

CT of Saber-Sheath Trachea

The diagnosis of saber-sheath trachea is easy at CT due to its cross-sectional imaging, but the significance of this CT sign has not been evaluated in the diagnosis of chronic obstructive pulmonary disease (COPD). Various signs of COPD were compared between a series of 20 patients with a saber-sheath trachea at CT (tracheal index < or = 66%) and a group of 20 pneumologic control patients without saber-sheath trachea (tracheal index > or = 70%). These signs included clinical and standard radiographic indices of COPD, sternum-spine distance and 3 functional tests of COPD: forced expiratory volume in one second, carbon monoxide diffusing lung capacity, and functional residual capacity (FRC). A significant difference was found between the 2 groups, concerning the values of FRC (p < 10(-4)) and of sternum-spine distance (p < 10(-2)). The tracheal index was significantly correlated with the FRC values (r = -0.611; p < 10(-5)) and with the sternum-spine distance (r = -0.322; p < 0.05). No other significant difference was observed. It is concluded that saber-sheath trachea is basically a sign of hyperinflation.