吸烟与慢性阻塞性肺疾病的关系及对老年患者肺功能的影响

目的分析吸烟与慢性阻塞性肺疾病发病(COPD)的关系及对老年患者肺功能的影响。方法选取180例老年男性实验志愿者,其中处于病情缓解期的COPD组患者60例,健康者120例。健康者包括健康吸烟组60例与健康非吸烟组60例。COPD组又分为已戒烟(1年以上)组30例,未戒烟组30例。检查患者肺功能指标,COPD戒烟、COPD未戒烟组行支气管舒张试验。分析吸烟与COPD发病的关系及对老年患者肺功能的影响。结果 COPD组与吸烟、非吸烟组相比,第1秒用力呼气容积占用力肺活量百分比(FEV1/FVC)及FEV1%预计值明显低于吸烟、非吸烟组(P<0.05);COPD患者中戒烟组FEV1/FEC及FEV1%预计值高于未戒烟组(P<0.05);COPD戒烟、COPD未戒烟组支气管舒张试验结果显示COPD组FEV1改变率高于COPD未戒烟组,COPD戒烟组FEV1阳性率(31.2%)较COPD未戒烟组(21.8%)高,差异均有统计学意义(P<0.05)。结论吸烟是COPD的重要发病因素,对老年患者的肺功能有明显影响,及早戒烟对延缓疾病发展、改善患者生活质量有重要意义。     

老年慢性阻塞性肺疾病患者肺功能和膈肌复合动作电位的相关性研究

目的初步探讨老年慢性阻塞性肺疾病（COPD）患者肺功能的变化与相关膈神经电生理改变的关系。方法分别对50例老年COPD患者和健康老年人进行肺功能及膈神经运动传导（PNC）、膈运动诱发电位（dMEP）及膈肌复合动作电位（dCMAP）检测。结果（1）50例老年COPD患者的呼吸功能状况显著低于非COPD健康老年人（P〈0．05）。（2）老年COPD组的PNC潜伏期平均值与健康老年人的差异无统计学意义（P〉0．05），dCMAP波幅的平均值显著低于健康老年人（P〈0．01）；老年COPD组的dMEP均正常，与健康老年人相比差异无统计学意义。（3）dCMAP波幅的降低与老年COPD患者肺功能各指标的减退相关。结论老年COPD患者肺功能的下降与dCMAP降低相关。     

戒烟10年以上的健康老年人肺功能10年随访研究

目的　观察健康老年人戒烟１０ 年后肺功能的１０ 年变化。方法　５１ 名戒烟１０ 年以上的健康老年人为研究对象，并挑选条件相同的从不吸烟健康老年人１２ 名作为随访对照，肺功能检查按常规方法进行。结果　戒烟１０ 年后健康老年人在随访的１０ 年中肺功能与从不吸烟健康老年人肺功能相比，肺活量（ＶＣ）、用力肺活量（ＦＶＣ） 、一秒钟用力呼气容积（ＦＥＶ１） 年下降值差异有显著性（Ｐ＜０－０１）；呼气峰流速（ＰＥＦ）年下降值差异有显著性（Ｐ＜０－０５）；残气量（ＲＶ）、残气量／肺总量（ＲＶ／ＴＬＣ）的年增加值差异有显著性（ Ｐ＜０－０１） 。一秒钟用力呼气容积与用力肺活量比值（ＦＥＶ１／ＦＶＣ） 、最大通气量（ＭＶＶ） 、最大呼气中期流量（ＭＭＥＦ）、功能残气量（ＦＲＣ）、肺总量（ＴＬＣ） 也有一定的改变，但变化值未达到统计学意义。结论　通过随访研究发现即使戒烟后曾吸烟对肺功能仍然存在一定影响，可能与研究对象吸烟时间长，吸烟量大所形成某些不可逆病理变化有关，并建议吸烟者应尽早戒烟。     

戒烟对稳定期慢性阻塞性肺疾病的治疗作用

目的探讨戒烟对稳定期COPD的治疗作用。方法纳入2011年7月-2013年7月经福建医科大学附属泉州第一医院肺功能室检查确诊的稳定期COPD患者193例,按是否采用戒烟治疗及最终完成情况分为戒烟成功组、戒烟失败组及非戒烟组：戒烟成功亚组62例,均为男性,平均年龄为（60．82±5．63）岁,平均吸烟指数为（852±100）年·支;戒烟失败亚组36例,均为男性,平均年龄为（60．61±4．91）岁,平均吸烟指数为（812±139）年·支;非戒烟组95例,均为男性,平均年龄为（60．49±8．77）岁,平均吸烟指数为（833土143）年·支。采用FEV。为肺功能评价指标,CAT评分为COPD病情评价指标。进行为期半年的随访。结果各试验组患者在年龄、体质量指数及吸烟指数等方面差异无统计学意义。戒烟成功组患者治疗后体质量增加（2．85±1．27）kg,CAT评分下降（6．05±2．60）分,戒烟前后对比差异有统计学意义（t值分别为17．763、18．351,P值均d0．01）;FEV,增加（O．04±0．18）L,戒烟前后对比差异无统计学意义（t=1．900,P=0．062）。而戒烟失败组及未戒烟组治疗前后体质量、CAT评分及FEV,变化差异均无统计学意义（P值均〉0．05）。结论戒烟半年即对稳定期COPD具有=定的治疗作用,主要表现在体质量增加、临床症状减轻,而肺功能则无明显改善。     

合肥地区轻度慢性阻塞性肺疾病患者的特点分析

目的调查合肥地区轻度慢性阻塞性肺疾病（COPD）患者的一般情况。方法对合肥地区118例经便携式肺功能仪诊断为轻度COPD患者进行生活习惯、呼吸道症状、既往呼吸道疾病诊断及治疗的问卷调查，将患者分为无症状组和有症状组。结果无症状组和有症状组的性别、年龄、受教育程度和吸烟情况比较均无统计学差异（P均〉0．05）。肺功能检测显示，有症状组第1秒用力呼气容积占用力肺活量的比值、第1秒用力呼气容积占预计值百分比与无症状组比较均有统计学意义（P均〈0．05）。结论合肥地区COPD患病率较高，轻度无症状COPD所占比例较大。由于COPD的诊断需要依靠肺功能测定，而早期肺功能受损不太严重时临床症状不明显，因而造成COPD的漏诊和对疾病危害的低估。     

吸烟对老年慢性阻塞性肺疾病稳定期患者中性粒细胞还原型辅酶Ⅱ氧化酶的影响

目的探讨吸烟对老年慢性阻塞性肺疾病（COPD）稳定期患者外周血中性粒细胞膜蛋白质及还原型辅酶Ⅱ（NADPH）氧化酶p47-^PHOX因子磷酸化表达的影响。方法选择134名受试者，分为4组：（1）吸烟COPD组39例;（2）吸烟无COPD组36例；（3）无吸烟COPD组31例；（4）无吸烟无COPD组28例。细胞色素C还原法测外周血中性粒细胞释放超氧阴离子（O2^-）的水平。Western blot检测外周血中性粒细胞膜蛋白质和NADPH氧化酶p47-^PHOX因子磷酸化表达，并分析O2^-的水平与其肺功能、血气之间关系。结果吸烟COPD组及吸烟无COPD组外周血中性粒膜细胞蛋白质和NADPH氧化酶p47-^PHOX因子磷酸化（呈黑色）明显强于无吸烟无COPD组（呈浅灰色）。吸烟COPD组中性粒细胞释放的O2^-水平与其第1秒用力呼气容积（FEV1）、FEV1占预计值百分比（％）、FEV1／用力肺活量、动脉血氧分压呈负相关（r分别为-0．898、-0．878、-0．874、-0．890，均为P〈50．01）。结论吸烟能激活NADPH氧化酶产生O2^-，并且吸烟能使NADPH氧化酶亚单位p47-^PHOX发生磷酸化。     

慢性阻塞性肺疾病吸烟患者同型半胱氨酸与肺功能的关系

目的通过观察吸烟的慢性阻塞性肺疾病（COPD）患者血浆同型半胱氨酸（Hcy）水平和肺功能之间关系,探讨吸烟COPD患者高Hcy血症的意义。方法选择20例男性非吸烟者、19例男性吸烟对照者、40例男性COPD患者,测定各组血浆Hcy,并前瞻性观察血浆Hcy浓度和肺功能下降的关系。结果COPD组血浆Hcy水平与FEV1%呈正相关（r-=0．729,P=0．000）,但随着COPD加重,动脉氧分压和血浆Hcy水平也下降,血浆Hcy水平与年FEV1下降值呈正相关（r6=0．510,P=0．001）。结论吸烟可导致COPD患者血浆Hcy水平升高,而血浆Hcy水平升高可能导致肺功能下降。     

慢性阻塞性肺疾病患者肺组织中血管内皮生长因子和诱生型一氧化氮合酶的表达及吸烟的影响

目的探讨慢性阻塞性肺疾病（COPD）患者肺组织中血管内皮生长因子（VEGF）、诱生型一氧化氮合酶（iNOS）的表达情况及吸烟对二者表达的影响。方法取46例因肺癌行肺叶切除患者的癌旁组织，依据吸烟及肺功能情况分成：（1）吸烟伴COPD组19例；（2）吸烟不伴COPD组12例；（3）不吸烟不伴COPD组15例。用免疫组化法检测肺组织VEGF及iNOS的表达。结果吸烟不伴COPD组（1．50±0．39，1．45±0．41）与不吸烟不伴COPD组（1．18±0．33，1．09±0．41）比较，肺组织VEGF、iNOS表达增强；吸烟伴COPD组（2．19±0．51，2．39±0．45）与不吸烟不伴COPD组比较表达明显增强。肺组织VEGF表达与iNOS表达呈明显正相关（r=0．78，P〈0．01）。肺组织VEGF表达与FEV。呈明显负相关（r=-0．67，P〈0．01）。结论吸烟以及轻度COPD患者肺组织VEGF、iNOS表达上调，iNOS、VEGF的过度表达可能参与COPD患者气道与血管重建和气流受限的过程。     

重叠综合征与慢性阻塞性肺疾病患者的日间肺功能变化差异

目的探讨重叠综合征患者与慢性阻塞性肺疾病（COPD）患者在日间肺功能上的变化差异。方法随机选择60例患者,将其分为二组,重叠综合征组30例,稳定期COPD组30例,两组患者的性别构成比、年龄和体重指数相匹配,无统计学差异（P〉0．05）,所有患者均作静态肺功能检查及日间血气分析,并对各项相关指标进行统计学处理。结果重叠综合征组与稳定期COPD组患者的各项相关指标中,血气分析中两组二氧化碳分压（PaCO2）、氧分压（PaO2）及血氧饱和度（O2sat）无显著差异（P〉0．05）。静态肺功能中两组患者用力肺活量（FVC％）、1s用力呼气容积占预计值百分比（FEV1％）、FEV1／FVC％无显著差异（P〉0．05）,而最大通气量（MVV％）、用力呼气峰流量（PEF％）、呼出25％肺容积时的最大呼气流量（FEF25％）低于稳定期COPD组（P〈0．05）。结论重叠综合征患者与稳定期COPD患者的日间低氧血症差异不明显,但静态肺功能损害较严重。     

吸烟对哮喘患者FeNO和肺功能的影响

目的探讨吸烟对哮喘患者FeNO和肺功能的影响。方法选取2017年1月至2018年5月于承德医学院附属医院确诊的哮喘患者217例,其中吸烟患者81例(吸烟组),不吸烟患者74例(不吸烟组),已戒烟患者62例(已戒烟组),比较3组间FeNO值、第1秒用力呼气容积占预计值百分比(FEV_1%)、第1秒用力呼气容积/用力肺活量(FEV_1/FVC)、最大呼气流量(MEF)25-75/预计值、和哮喘控制测试(ACT)评分,探讨FeNO与肺功能各指标、ACT评分、吸烟指数、嗜酸性粒细胞百分比(EO%)的相关性。结果吸烟患者FEV_1/FVC较不吸烟组低,差异有统计学意义(P0.05)。吸烟患者MEF25-75/预计值较不吸烟及已戒烟患者低,差异有统计学意义(P0.05)。吸烟组FeNO值较不吸烟组、已戒烟组低,差异有统计学意义(P0.05)。哮喘患者FeNO水平与血EO%呈正相关(r=0.482,P=0.041),与FEV_1/FVC、MEF25～75/预计值、吸烟指数呈负相关性(r=-0.237、-0.384、-0.526,P=0.022、0.003、0.038),差异有统计学意义(P0.05)。结论吸烟可以降低哮喘患者小气道功能指标与FeNO值,使用单一的FeNO方法评估吸烟患者的气道炎症,有可能会低估其气道炎症水平。FeNO水平更能反映哮喘患者嗜酸性气道炎症,能在一定程度上反映小气道功能障碍,尤其在不吸烟的哮喘患者评估价值更高,且FeNO值越高,小气道阻力越高。     

肺动脉血栓内膜剥脱术后再灌注肺水肿的进展

肺血栓栓塞症是一种常见、多发且病死率和致残率高的疾病。大多数急性肺动脉血栓栓塞经及时的溶栓抗凝等治疗和 (或 )自身的纤溶系统能将血栓不同程度地溶解 ,另有0 1%～ 0 2 %的患者因血栓在急性期未能溶解或栓塞反复发生进而发展成慢性栓塞性肺动脉高压。慢性栓塞性肺动脉高压溶栓无效 ,抗凝、扩血管治疗效果不佳 ,其病理过程多呈进行性加重或稳定一段时间后再次加重 ,自然预后差。肺动脉平均压 >3 0ｍｍＨｇ(1ｍｍＨｇ =0 13 3ｋＰａ)的慢性栓塞性肺动脉高压患者 5年生存率为 3 0 % ,肺动脉平均压 >5 0ｍｍＨｇ者仅为 10 %。肺动脉血…     

Chronic pulmonary embolism and pulmonary hypertension

Incomplete resolution of acute pulmonary embolism (PE) is frequently observed after acute PE and may rarely result in chronic thromboembolic pulmonary hypertension (CTEPH). The underlying pathophysiological mechanism is largely unknown. Evidence underlines the concept of a dual pulmonary vascular compartment model consisting of increased pulmonary vascular resistance by both large vessel obstruction and distal small vessel obliteration, the latter initiated by pathological vascular remodeling. Up to 40% of patients with established CTEPH have no prior history of symptomatic venous thromboembolism. CTEPH is associated with a poor prognosis if left untreated. Therefore, the diagnostic approach of CTEPH aims at assessing the location and extent of the embolic obstruction, establishing the operability and prognosis of the patients and ruling out other variations of pulmonary hypertension with distinct indicated treatment. Heart catheterization for invasive pressure measurements and pulmonary catheter angiography is obligatory for the final diagnosis. Pulmonary thromboendarterectomy is the treatment of choice. In certain patients with persistent or recurrent pulmonary hypertension after surgery or with inoperable disease, pharmacotherapy might be beneficial.     

Retrograde pulmonary perfusion improves results in pulmonary embolectomy for massive pulmonary embolism

Mortality rates for pulmonary embolectomy in patients with acute massive pulmonary embolism have decreased in recent years. However, they still range from 30% to 45% when the surgery is performed on critically ill patients, and the rates reach 60% in patients who have experienced cardiac arrest before the procedure. The causes of death in these patients are generally attributed to right heart failure due to persistent pulmonary hypertension, intractable pulmonary edema, and massive parenchymal and intrabronchial hemorrhage. Clinical and experimental findings indicate that venous air embolism causes severe or even lethal damage to the pulmonary microvasculature and the lung parenchyma consequent to the release of endothelium-derived cytokines. These findings are similar to those observed when severely compromised patients undergo pulmonary embolectomy-air entrapped in the pulmonary artery during embolectomy can lead to fatal outcomes.Besides enabling the removal of residual thrombotic material from the peripheral branches of the pulmonary artery, retrograde pulmonary perfusion fills the pulmonary artery with blood and prevents pulmonary air embolism. In this retrospective study, we analyzed a series of 21 consecutive critically ill patients in whom we applied retrograde pulmonary perfusion while performing standard pulmonary embolectomy. No patient died or experienced major postoperative complications. We believe that the use of retrograde pulmonary perfusion decreases morbidity and mortality rates associated with pulmonary embolectomy in critically ill patients.     

Cavitating pulmonary infarcts revealing thromboembolic pulmonary hypertension

Several etiologies are involved in the pathogenesis of cavitating pulmonary disease including neoplastic, infectious or inflammatory processes. Another is pulmonary infarction associated with venous thromboembolism. The lung cavities tend to be located peripherally and are the result of pulmonary embolism. We report the case of a woman with chronic thromboembolic pulmonary hypertension (CTEPH), associated with familial thrombophilia, revealed by cavitating pulmonary infarcts. CTEPH is sometimes diagnosed during an episode of recurrent pulmonary embolism following previously unnoticed lesions. Thrombophilias such as isolated elevated factor VIII are risk factors for CTEPH.     

Residual pulmonary thromboemboli after acute pulmonary embolism

BackgroundAfter an acute pulmonary embolism (PE), the complete resolution of thromboemboli may not be routinely achieved. The rate of persistence may depend on the time and the diagnostic technique used for evaluation.Patients and methodsPatients were diagnosed with acute PE by means of computed tomography angiography (CTA). While they were receiving anticoagulant therapy, a second CTA was used to explore the rate of persistence of residual thromboemboli. During the initial episode, the plasma levels of Troponin I and natriuretic peptide, patient demographics, and hemodynamic and gas exchange data were evaluated as risk factors for persistence of pulmonary thromboemboli.ResultsIn this study 166 patients were diagnosed. A second CTA was not made in 46 (28%) patients for different reasons. In 120 (72%) patients a second CTA was made 4.5 [SD2.34] months after the initial episode (range 2–12 months). Complete clearance of thrombi occurred in 89 (74%, 95% CI 65–81) patients. Residual thrombi remained in 31 (26%, 95% CI 18–34) patients. In 6%, 13% and 81% of the patients the size of the residual thrombi was greater, similar to and smaller than initially diagnosed, respectively.The risk factors for residual thrombi included the thrombotic burden (OR 1.95), the alveolar to arterial difference of oxygen (OR 1.64), and the clinical antecedents of venous thromboembolic disease (OR 0.65).ConclusionsAfter 4.5 months of anticoagulant therapy, residual pulmonary thromboemboli persisted in 26% of the patients. The risk factors for residual thromboemboli include a greater initial thrombotic burden, a deeper gas exchange disturbation and a history of previous venous thromboembolism.     

Chronic solitary pulmonary nodule due to unsuspected pulmonary infarction from silent pulmonary embolism

Abstract A case of pulmonary embolism showing a longstanding solitary pulmonary nodule is presented. An asymptomatic 57 year-old man with a solitary nodule in the right lower lobe was referred to our hospital. A pulmonary perfusion-ventilation scan following a sudden onset of dyspnoea established the diagnosis of recurrent pulmonary embolism. The nodule gradually disappeared after anticoagulant treatment, indicating that the nodule was pulmonary infarction from silent pulmonary embolism. Although the incidence of pulmonary infarction is low in Japan, this case suggests that pulmonary infarction from silent pulmonary embolism should be considered as one important cause of a solitary pulmonary nodule.     

Acute pulmonary embolism and pulmonary infarction]

32 cases of pulmonary embolism were reported, 18 cases had been autopsied (massive pulmonary embolism 9 cases. moderate pulmonary embolism 23 cases). The incidence risk factors pathogenesis, clinical manifestations of pulmonary embolism were presented. The relation between pulmonary embolism and pulmonary infarction and treatment of massive pulmonary infarction were discussed.     

Reperfusion pulmonary edema after pulmonary artery thromboendarterectomy

Pulmonary artery thromboendarterectomy (PAT) is a potentially curative procedure in chronic, major vessel thromboembolic pulmonary hypertension. However, postoperative reperfusion pulmonary edema (RPE) has been a serious complication, often requiring prolonged mechanical ventilation. This entity has been described only anecdotally in the past. To characterize it more fully, we retrospectively analyzed the course and potential determinants of RPE after thromboendarterectomy in 22 patients who had PAT at our institution from 1969 through 1984. Particular attention was directed to clinical data, thrombus location, areas operated, postoperative roentgenograms, and preoperative and postoperative hemodynamic data. In all patients but 1, RPE developed within 72 h after surgery, corresponding to anatomic locations distal to vessels subjected to PAT. Regions of lung not reperfused at surgery were uniformly spared. Pulmonary capillary wedge and/or left atrial pressures preoperatively and postoperatively were not elevated. None of the preoperative data predicted which patients would develop more persistent RPE. These observations suggest that the phenomenon of RPE is a peculiar, focal form of pulmonary edema, the basis for which remains to be defined.