Circadian variation in onset of acute cardiogenic pulmonary edema is independent of patients' features and underlying pathophysiological causes

BACKGROUND: The present study aimed to confirm the existence of a circadian pattern in the onset of acute pulmonary edema (APE) and to verify whether sex, age, preexisting diseases, and clinical causes determining the event may influence it. SUBJECTS AND METHODS: The study considered all consecutive cases of APE observed at the St. Anna General Hospital of Ferrara, Italy, during a 7-year period from January 1, 1992, to December 31, 1998. The sample population was divided into subgroups by sex, age (<75 and > or =75 years), presence or absence of diabetes and hypertension, clinical causes determining the event (i.e., acute myocardial infarction (AMI), pulmonary embolism, arrhythmias). The most important associated or concomitant diseases were also considered (i.e., coronary heart disease and angina, previous myocardial infarction, chronic cardiac failure, dilatative cardiopathy, chronic atrial fibrillation, valvular disease, chronic obstructive pulmonary disease, chronic cor pulmonale, malignancy, chronic renal failure). Time of symptom onset of each event was recorded accurately, then tabulated into 24 increments of 1h (e.g., 06:00 to 06:59 was reported as 6 A.M.). For statistical chronobiological analysis, partial Fourier series were used. RESULTS: During the 7-year period, 1321 consecutive cases of APE in 1014 different subjects were observed. The majority of events occurred at night, and statistical analysis showed a 24h rhythmicity both in the total sample population and in all considered subgroups, with the only exception being patients with pulmonary embolism and arrhythmias, for which the small number of cases made the study of rhythms in APE impossible. CONCLUSIONS: The nighttime preference in the occurrence of APE appears to be quite independent of all demographic features or underlying pathophysiological causes.     

128层螺旋CT肺动脉造影对急性肺栓塞患者栓塞程度和右心功能的评估价值研究

目的:探讨128层螺旋CT肺动脉造影(CTPA)对急性肺栓塞(APE)患者栓塞程度和右心功能的评估价值。方法:选取2016年7月到2018年6月期间在我院行CTPA检查确诊并接受治疗的APE患者100例记为观察组,根据观察组患者的病情将其分为高危组(57例)和非高危组(43例),同时根据观察组患者肺栓塞部位及预后将患者分为中心肺栓塞死亡组(8例)、中心肺栓塞存活组(38例)、周围肺栓塞组(54例)。另选择同期于我院进行CTPA检查的无肺栓塞患者50例记为对照组。记录所有患者的右心功能参数[右心室短轴最大径(RVMSA)、左心室短轴最大径(LVMSA)以及二者的比值(RV:LV)],计算APE患者的CT肺动脉阻塞指数,并分析APE患者CT肺动脉阻塞指数与右心功能指标的相关性。结果:观察组的RVMSA、RV:LV均明显高于对照组(P0.05),高危组的CT肺动脉阻塞指数、RVMSA、RV:LV均明显高于非高危组(P0.05)。中心肺栓塞死亡组的CT肺动脉阻塞指数、RVMSA、RV:LV均明显高于中心肺栓塞存活组和周围肺栓塞组,中心肺栓塞存活组的CT肺动脉阻塞指数、RVMSA、RV:LV均明显高于周围肺栓塞组(P0.05)。经Pearson相关分析显示,APE患者CT肺动脉阻塞指数与RVMSA、RV:LV均呈正相关(P0.05),与LVMSA无明显的相关性(P0.05)。结论:CTPA检查可有效评估APE患者的栓塞程度和右心功能,且栓塞程度与右心功能存在相关性,CTPA检查有助于APE患者的诊断和病情评估。     

The Wall Eclipsing Sign on Pulmonary Artery Computed Tomography Angiography Is Pathognomonic for Pulmonary Artery Sarcoma

Background

The objective of this study was to evaluate the imaging characteristics of pulmonary artery sarcoma (PAS) on pulmonary artery computed tomography angiography (PACTA) that can be used to differentiate between PAS and pulmonary thromboembolic diseases, including chronic thromboembolic pulmonary hypertension (CTEPH) and acute pulmonary embolism (APE).

Methods

The clinical data and imaging characteristics of 12 patients with PAS, 156 patients with CTEPH, and 426 patients with APE who were treated at Beijing Anzhen Hospital from January 2007 to August 2013 were retrospectively analyzed. All patients underwent PACTA before treatment, and the diagnoses of PAS and CTEPH were all confirmed by surgical biopsy.

Results

All 12 PAS patients were initially misdiagnosed and received inappropriate thrombolytic and/or anticoagulant therapy before they were referred for surgical intervention. The mean time from PACTA to surgical intervention was 5.5±3.7 months (range 2–11 months). On PACTA, the PAS lesion always eclipsed the wall of the pulmonary artery before infiltrating outside the pulmonary artery, which was termed the wall eclipsing sign. This sign was observed in all PAS patients but was not observed in any CTEPH or APE patients.

Conclusions

PAS is a rare neoplasm with a poor prognosis, and is easily misdiagnosed as thromboembolic disease. The wall eclipsing sign on PACTA is pathognomonic for PAS, and patients with this sign should be investigated to confirm the diagnosis and should undergo surgical intervention as soon as possible, rather than receiving thrombolytic or anticoagulant therapy.     

不同危险分层急性肺栓塞患者D-二聚体与纤维蛋白原比值、中性粒细胞与淋巴细胞比值、白蛋白的变化及其与预后的关系研究

摘要 目的：探讨不同危险分层急性肺栓塞（APE）患者D-二聚体与纤维蛋白原比值（DFR）、中性粒细胞与淋巴细胞比值（NLR）、白蛋白（Alb）的变化及其与预后的关系。方法：选择2019年3月至2021年12月我院收治的APE患者154例作为APE组,根据《肺血栓栓塞症的诊断与治疗指南(2015)》分为低危组48例、中危组69例和高危组37例,另选择同期我院体检健康志愿者40例作为对照组,比较各组DFR、NLR、Alb水平。根据不同预后将APE患者分为存活组125例,死亡组29例,比较两组DFR、NLR、Alb水平。应用受试者工作特征（ROC）曲线分析DFR、NLR、Alb对APE预后的预测价值。结果：APE组DFR、NLR显著高于对照组,Alb水平显著低于对照组（P<0.05）。随着危险分层增加,APE患者DFR、NLR逐渐升高,Alb水平逐渐降低,不同危险分层APE患者DFR、NLR、Alb水平比较有统计学意义（P<0.05）。死亡组DFR、NLR显著高于存活组,Alb水平显著低于存活组（P<0.05）。ROC曲线分析显示,DFR、NLR、Alb对APE死亡预测具有较高的敏感度、特异度,其中DFR、NLR、Alb联合检测对APE死亡预测的曲线下面积（AUC）、敏感度、特异度最高。结论：APE患者DFR、NLR异常升高,Alb异常降低与APE危险分层增加及不良预后相关,DFR、NLR、Alb联合检测对APE患者预后不良的预测价值更高。     

Likelihood and Predictors of ST-Elevation in Patients Hospitalized for Myocardial Infarction

Importance

Emergency treatment options in myocardial infarction are guided by presence or absence of ST-elevations in electrocardiography. Occurrence and factors associated with ST-presentation in different population groups are however inadequately known.

Objective

To determine likelihood and patient features associated with ST-elevations in myocardial infarction.

Design

Nationwide registry study including 22 hospitals with angiolaboratory during an eight year period in Finland.

Setting

Hospitalized care.

Participants

68,162 consecutive patients aged ≥30 with myocardial infarction.

Measures

Likelihood and patient features associated with presence of ST-elevations.

Results

Myocardial infarction presented with ST-elevation in 37.5% (CI 37.0–37.9%) and without in 62.5% (CI 61.9–63.1%) of patients, p<0.0001. Majority of patients aged 30–59 years with myocardial infarction had ST-elevation, but among octogenarians ST-elevations were present in only 24.7%. Presence of ST-elevations decreased with age by estimated 15.6% (CI 15.0–16.2%) per 10 year increase (p<0.0001). Men aged 40–79 years had significantly higher rate for ST-elevation myocardial infarction compared to women. Sex-based difference in presentation of myocardial infarction declined with increasing age. Overall, men had a 13% (CI 11–15%, p<0.0001) higher relative risk for ST-elevations compared to women when adjusted for age and co-morbidities. Diabetes, atrial fibrillation, peripheral or cerebral artery disease, chronic pulmonary disease, malignancy, and renal insufficiency were associated with absence of ST-elevations in myocardial infarction in multivariate analysis.

Conclusions and Relevance

Myocardial infarction presents with ST-elevations more commonly in men. Presence of ST-elevations decreases with increasing age. Diabetes, atrial fibrillation, peripheral or cerebral artery disease, chronic pulmonary disease, malignancy, and renal insufficiency are associated with absence of ST-elevations in myocardial infarction. These findings may help to predict likelihood of ST-elevations in a patient with myocardial infarction.     

New Insights into the Circadian Rhythm of Acute Myocardial Infarction in Subgroups

The aim of this study was to determine the existence of the circadian rhythm (CR) in the onset of acute myocardial infarction (AMI) in different patient subgroups. Information was collected about 41,244 infarctions from the database of the ARIAM (Analysis of Delay in AMI) Spanish multicenter study. CR in AMI were explored in subgroups of cases categorized by age, gender, previous ischemic heart disease (PIHD), outcome in coronary care unit, infarction electrocardiograph (ECG) characteristics (Q wave or non‐Q wave), and location of AMI. Cases were classified according to these variables in the different subgroups. To verify the presence of CR, a simple test of equality of time series based on the multiple‐sinusoid (24, 12, and 8 h periods) cosinor analysis was developed. For the groups as a whole, the time of pain onset as an indicator of the AMI occurrence showed a CR (p<0.0001), with a morning peak at 10:10 h. All the analyzed subgroups also showed CR. Comparison between subgroups showed significant differences in the PIHD (p<0.01) and infarction ECG characteristics (p<0.01) groups. The CR of the subgroup with Q‐wave infarction differed from that of non‐Q wave subgroup (p<0.01) when the patients had PIHD (23% in Q wave infarction vs. 39.2% in non‐Q wave). AMI onset followed a CR pattern, which is also observed in all analyzed subgroups. Differences in the CR according to the Q/non‐Q wave infarction characteristics could be determined by PIHD. The cosinor model fit with three components (24, 12, and 8 h periods) showed a higher sensitivity than the single 24 h period analysis.     

Seasonal Variation in Occurrence of Pulmonary Embolism: Analysis of the Database of the Emilia‐Romagna Region,Italy

Seasonal variation in the occurrence of cardiovascular and cerebrovascular events, including pulmonary embolism (PE), has been reported; however, recent large‐scale, population‐based studies conducted in the United States did not confirm such seasonality. The aim of this large‐scale population study was to determine whether a temporal pattern in the occurrence of PE exists. The analysis considered all consecutive cases of PE in the database of all hospital admissions of the Emilia Romagna region in Italy at the Center for Health Statistics between January 1998 and December 2005. PE cases were first grouped according to season of occurrence, and the data were analyzed by the χ² test for goodness of fit. Then, inferential chronobiologic (cosinor and partial Fourier) analysis was applied to monthly data, and the best‐fitting curve for the annual variation was derived. The total sample consisted of 19,245 patients (8,143 male, mean age 71.6±14.1 yrs; 11,102 female, mean age 76.1±13.7 yrs). Of these, 2,484 were <65 yrs, 5,443 were between 65 and 74, and 11,318 were ≥75 yrs. There were 4,486 (23.3%) fatal‐case outcomes. PE occurred least frequently in spring (n=4,442 or 23.1%) and most frequent in winter (n=5,236 or 27.2%, goodness of fit χ²=75.75, p<0.001). Similar results were obtained for subgroups formed by gender, age, fatal/non‐fatal outcome, presence/absence of major underlying co‐morbid conditions, and specific risk factors. Inferential chronobiological analysis identified a significant annual pattern in PE, with the peak between November and December for the total sample of cases (p<0.001), males (p<0.001), females (p=0.002), fatal and non‐fatal cases (p<0.001 for both), and subgroups formed by age (<65 yrs, p=0.012; 65–74 yrs, p<0.001; ≥75 yrs, p=0.012). This pattern was independent of the presence/absence of hypertension (p=0.003 and p<0.001, respectively), pulmonary disease (p<0.001 and p<0.001, respectively), stroke (p<0.001 and p=0.004, respectively), neoplasms (p=0.005 and p=0.001, respectively), heart failure (p=0.022 and p<0.001, respectively), and deep vein thrombosis (p=0.002 and p<0.001, respectively). However, only a non‐statistically significant trend was found for subgroups formed by cases of diabetes mellitus, infections, renal failure, and trauma.     

导管引导介入治疗急性中高危肺动脉栓塞临床研究

目的:评估导管引导介入治疗急性中高危肺动脉栓塞的有效性及安全性。方法:顾性分析2012年1月至2018年6月在柳州市工人医院血管外科诊治的112例急性中高危肺动脉栓塞患者资料。根据治疗方案分单纯抗凝组(共38例)、导管介入+抗凝治疗组(共74例),对比两组肺动脉压及肺动脉栓塞严重指数降低情况、肺栓塞症状改善率、住院时长和出血并发症发生率;以其随访中肺栓塞复发率和慢性血栓性肺动脉高压发生率。根据介入方案不同,介入治疗组包括AngioJet机械吸栓(共13例)、猪尾导管碎栓及溶栓(61例);分别对比两种介入方案术前及术后的动脉血氧分压、指脉氧、心率及肺动脉压、弥勒指数评估治疗效果。结果:两组术前人口学特征、发病时间、DVT并发率、肺动脉压、肺动脉栓塞严重指数等无明显差异(P均0.05)。介入治疗组在降低肺动脉压及肺动脉严重指数、症状的改善率、缩短住院时间上明显优于单纯抗凝组(P分别为0.000、0.001、0.01、0.003);而相关出血并发症发生率无统计学差异(P0.05)。通过分别对比介入治疗两种方案的术前及术后动脉血氧分压、指脉氧、心率及肺动脉压、弥勒指数,两种治疗方案在这五个指标均有明显改善(P值均0.05)。随访6月至7年,肺栓复发率在单纯抗凝组、导管介入+抗凝治疗组分别为10.5%、6.8%,统计学差异显著(P=0.004);慢性血栓性肺动脉高压发生率分别为5.3%、1.4%,统计学差异显著(P=0.000)。结论:导管引导介入治疗对急性中高危肺动脉栓塞治疗是安全有效的,且可明显降低复发及慢性肺动脉高压的发生率。     

What Caused the UK's Largest Common Dolphin (Delphinus delphis) Mass Stranding Event?

On 9 June 2008, the UK''s largest mass stranding event (MSE) of short-beaked common dolphins (Delphinus delphis) occurred in Falmouth Bay, Cornwall. At least 26 dolphins died, and a similar number was refloated/herded back to sea. On necropsy, all dolphins were in good nutritive status with empty stomachs and no evidence of known infectious disease or acute physical injury. Auditory tissues were grossly normal (26/26) but had microscopic haemorrhages (5/5) and mild otitis media (1/5) in the freshest cases. Five lactating adult dolphins, one immature male, and one immature female tested were free of harmful algal toxins and had low chemical pollutant levels. Pathological evidence of mud/seawater inhalation (11/26), local tide cycle, and the relative lack of renal myoglobinuria (26/26) suggested MSE onset on a rising tide between 06∶30 and 08∶21 hrs (9 June). Potential causes excluded or considered highly unlikely included infectious disease, gas/fat embolism, boat strike, by-catch, predator attack, foraging unusually close to shore, chemical or algal toxin exposure, abnormal weather/climatic conditions, and high-intensity acoustic inputs from seismic airgun arrays or natural sources (e.g., earthquakes). International naval exercises did occur in close proximity to the MSE with the most intense part of the exercises (including mid-frequency sonars) occurring four days before the MSE and resuming with helicopter exercises on the morning of the MSE. The MSE may therefore have been a “two-stage process” where a group of normally pelagic dolphins entered Falmouth Bay and, after 3–4 days in/around the Bay, a second acoustic/disturbance event occurred causing them to strand en masse. This spatial and temporal association with the MSE, previous associations between naval activities and cetacean MSEs, and an absence of other identifiable factors known to cause cetacean MSEs, indicates naval activity to be the most probable cause of the Falmouth Bay MSE.     

Investigations into the role of fungi in pulmonary diseases

Summary 32 cases of non tuberculous chronic pulmonary diseases and 10 cases of chronic pulmonary tuberculosis not responding to the routine treatment, were investigated to find out if fungi played any role in their etiology. Fungi were isolated from 9 cases of non-tuberculous and 2 cases of tuberculous pulmonary infections.Fungi as such seem to play some role in the etiology of Pulmonary Diseases and probably also help in keeping up the disease in tuberculous cases. Mycostatin is the drug of choice in the treatment of pulmonary moniliasis.Sputa and bronchial aspirates from 32 cases of non-tuberculous chronic pulmonary diseases and 10 cases of chronic pulmonary tuberculosis, not responding to the routine treatment, were repeatedly examined to find out if fungi played any role in their etiology. Fungi were isolated from 9 cases of non-tuberculous (C. albicans from 8 andActinomyces bovis from 1) and two cases (C. albicans from both) of tuberculous pulmonary infections. All the strains ofC. albicansandA. bovis isolated were tested for their sensitivity against Nystatin. Only strains ofC. albicans were found to be sensitive to Nystatin. Two cases treated with Mycostatin improved rapidly.

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Zusammenfassung Sputum and Bronchialsekret von 32 Fällen von nicht-tuberkulösen chronischen Lungenkrankheiten und von 10 Fällen von chronischer Lungentuberkulose, die auf Routinebehandlung nicht ansprachen, sind wiederholt daraufhin untersucht worden, ob Pilze eine aetiologische Rolle spielten. Pilze sind in 9 nicht-tuberkulösen Fällen (C. albicans in 8,Actinomyces bovis in einem Falle) und in 2 tuberkulösen Fällen (C. albicans in beiden) isoliert worden.Alle isolierten Stämme vonC. albicans andA. bovis sind auf ihre Sensitivität gegen Nystatin untersucht worden. NurC. albicans war sensitiv gegen Nystatin. Zwei Fälle, die mit Mycostatin behandelt wurden, zeigten rasche Besserung.

     

The Recent Emergence of Plague: A Process of Felonious Evolution

Yersinia pestis, the causative agent of bubonic plague, evolved from closely related Yersinia pseudotuberculosis within the past 20,000 years, an event that corresponds to the end of the last ice age and distribution of Homo sapiens throughout the world. Y. pseudotuberculosis causes chronic but generally mild enteropathogenic infections whereas plague is the most devastating acute disease experienced by mankind. The very recent evolution of plague from its progenitor assures close genomic homogeneity between the two species and thus high probability that disparities in DNA sequence mediate dramatic differences in symptoms of infection. The purpose of this minireview is to define salient distinctions between the genomes of Y. pestis and Y. pseudotuberculosis and to equate unique functions to respective acute and chronic mechanisms of virulence. The significance of these processes is then related to the procedures the organisms use to survive when between hosts (i.e., the flea vector colonized by Y. pestis and natural environments including soil and water in the case of Y. pseudotuberculosis). Next, an attempt is made to order the various mutational events that caused the recent emergence of Y. pestis as a distinct species. Finally, selective pressures such as predatory soil nematodes are considered that possibly influenced the early evolution of those yersiniae now pathogenic to humans.     

Quantifying the Role of Adverse Events in the Mortality Difference between First and Second-Generation Antipsychotics in Older Adults: Systematic Review and Meta-Synthesis

Background

Observational studies have reported higher mortality among older adults treated with first-generation antipsychotics (FGAs) versus second-generation antipsychotics (SGAs). A few studies examined risk for medical events, including stroke, ventricular arrhythmia, venous thromboembolism, myocardial infarction, pneumonia, and hip fracture.

Objectives

1) Review robust epidemiologic evidence comparing mortality and medical event risk between FGAs and SGAs in older adults; 2) Quantify how much these medical events explain the observed mortality difference between FGAs and SGAs.

Data sources

Pubmed and Science Citation Index.

Study eligibility criteria, participants, and interventions

Studies of antipsychotic users that: 1) evaluated mortality or medical events specified above; 2) restricted to populations with a mean age of 65 years or older 3) compared FGAs to SGAs, or both to a non-user group; (4) employed a “new user” design; (5) adjusted for confounders assessed prior to antipsychotic initiation; (6) and did not require survival after antipsychotic initiation. A separate search was performed for mortality estimates associated with the specified medical events.

Study appraisal and synthesis methods

For each medical event, we used a non-parametric model to estimate lower and upper bounds for the proportion of the mortality difference—comparing FGAs to SGAs—mediated by their difference in risk for the medical event.

Results

We provide a brief, updated summary of the included studies and the biological plausibility of these mechanisms. Of the 1122 unique citations retrieved, we reviewed 20 observational cohort studies that reported 28 associations. We identified hip fracture, stroke, myocardial infarction, and ventricular arrhythmias as potential intermediaries on the causal pathway from antipsychotic type to death. However, these events did not appear to explain the entire mortality difference.

Conclusions

The current literature suggests that hip fracture, stroke, myocardial infarction, and ventricular arrhythmias partially explain the mortality difference between SGAs and FGAs.     

Respiratory failure treated at the intensive care unit "R" of the Internal Disease Clinic of the Institute of Tuberculosis and Pulmonary Diseases (1986-1987)

A picture and clinical course of the acute and exacerbated chronic respiratory failure have been analysed. An analysis embraced a group of 49 patients, i.e. 16 percent of all patients treated at the Intensive Care Unit. Four subgroups were distinguished depending on the etiology of the disease in which infectious, thrombo-embolic, circulatory or toxic factors caused respiratory failure. An emphasis is on the prevalence of the infectious etiology of disease being noted in 65% of patients. Acute respiratory failure was observed in 37% of patients whereas exacerbation of the chronic respiratory failure in 63%. Complete respiration distress was noted in 55% of cases and partial respiratory failure in the remaining 45%. Gasometric differences characteristic for each subgroup of the patients have also been analysed. 41% of the patients died. The highest mortality rate was seen in pulmonary embolism complicating various pulmonary diseases. Sudden cardiac arrest, shock and not compensated acidosis have been most unfavourable factors in the prognosis.     

Epidemiology of Free-Living Ameba Infections1

Small free-living amebas belonging to the genera Acanthamoeba and Naegleria occur world-wide. They have been isolated from a variety of habitats including fresh water, thermal discharges of power plants, soil, sewage and also from the nose and throats of patients with respiratory illness as well as healthy persons. Although the true incidence of human infections with these amebas is not known, it is believed that as many as 200 cases of central nervous system infections due to these amebas have occurred world-wide. A majority (144) of these cases have been due to Naegleria fowleri which causes an acute, fulminating disease, primary amebic meningoencephalitis. The remaining 56 cases have been reported as due either to Acanthamoeba or some other free-living ameba which causes a subacute and/or chronic infection called granulomatous amebic encephalitis (GAE). Acanthamoeba, in addition to causing GAE, also causes nonfatal, but nevertheless painful, vision-threatening infections of the human cornea, Acanthamoeba keratitis. Infections due to Acanthamoeba have also been reported in a variety of animals. These observations, together with the fact that Acanthamoeba spp., Naegleria fowleri, and Hartmannella sp. can harbor pathogenic microorganisms such as Legionella and or mycobacteria indicate the public health importance of these amebas.     

Activation of muscarinic K<Superscript>+</Superscript> channels by arecaidine propargyl ester in isolated guinea-pig atrial myocytes

Summary Arecaidine propargyl ester (APE) was developed as a potential candidate compound for the treatment of Alzheimer’s disease. APE has been shown to have cardiovascular effects. APE produces negative chronotropic and inotropic effects in isolated atria. However, the ionic mechanisms underlying the cardiovascular effects of APE in guinea-pig atria are unclear. The aims of this study were: (1) to examine the shortening effect of APE on action potential duration (APD) and to compare the difference in potency between APE and muscarine in isolated single guinea-pig atrial myocytes by using the current clamp method, (2) to examine by using patch clamp techniques the ionic mechanisms underlying the cardiac effects of APE, and (3) to determine whether the cardiac effects caused by APE affect the usefulness of APE as a potential candidate for the treatment of Alzheimer’s disease. The APE significantly reduced the APD in guinea-pig atria and produced no direct effect on ventricular myocytes. APE is approximately 20 times as potent as muscarine in shortening the APD. Attenuation of the APD was consistently accompanied by a hyperpolarization of the resting membrane potential in a concentration-dependent manner. The APE activated muscarinic K⁺ channels and increased potassium conductance in guinea-pig atrial myocytes. In the cell-attached configuration, the APE contained in the pipette increased the channel-opening probability and decreased the closed-state time interval. The proposal that APE can be used as a potential remedy for the treatment of Alzheimer’s disease should be taken into consideration the undesirable cardiovascular side effects that APE causes at lower concentrations.     

引起AECOPD 精神神经异常的原因及治疗对策

目的：探讨引起慢性阻塞性肺疾病合并精神神经异常的原因,以制订有针对性的治疗对策。方法：回顾性分析我院自2010 年1 月到2013 年1 月期间收治的250 例慢性阻塞性肺疾病急性发作期患者的临床资料。结果：32 例患者出现精神神经异常症 状,占12.80%。其中17 例为肺性脑病,占53.13%（17/32）,8 例为低渗性脑病,占25.00%（8/32）,5 例为药物的不良反应,占15.63% （5/32）,2 例为脑梗死,占6.25%（2/32）。所有患者均给予慢性阻塞性肺疾病急性发作的常规治疗方案进行治疗,同时肺性脑病患 者给予积极纠正二氧化碳潴留;低渗性脑病患者给予积极纠正电解质紊乱;脑梗死的患者根据情况给予溶栓、脱水、营养脑神经、 抗凝、抗血小板聚集等治疗;药物不良反应的患者则给予停止应用相应的药物。经过治疗后,29 例症状恢复,占90.63%,3 例最终 死亡,死亡率为9.38%,其中2 例为肺性脑病患者,1 例为低渗性脑病患者。结论：对于慢性阻塞性肺疾病急性发作合并精神神经 异常的治疗,应根据患者的症状、体征以及辅助检查结果,尽早明确诊断,及时干预,尽快控制病情,防止病情恶化。     

Long-Term Survival in a Large Cohort of Patients with Venous Thrombosis: Incidence and Predictors

Background

Venous thrombosis is a common disease with a high mortality rate shortly after the event. However, details on long-term mortality in these patients are lacking. The aim of this study was to determine long-term mortality in a large cohort of patients with venous thrombosis.

Methods and Findings

4,947 patients from the Multiple Environmental and Genetic Assessment study of risk factors for venous thrombosis (MEGA study) with a first nonfatal venous thrombosis or pulmonary embolism and 6,154 control individuals without venous thrombosis, aged 18 to 70 years, were followed up for 8 years. Death and causes of death were retrieved from the Dutch death registration. Standardized mortality ratios (SMRs) were calculated for patients compared with control individuals. Several subgroups were studied as well.736 participants (601 patients and 135 controls) died over a follow-up of 54,948 person-years. The overall mortality rate was 22.7 per 1,000 person-years (95% CI 21.0–24.6) for patients and 4.7 per 1,000 person-years (95% CI 4.0–5.6) for controls. Patients with venous thrombosis had a 4.0-fold (95% CI 3.7–4.3) increased risk of death compared with controls. The risk remained increased up to 8 years after the thrombotic event, even when no additional comorbidities were present. The highest risk of death was found for patients with additional malignancies (SMR 5.5, 95% CI 5.0–6.1). Main causes of death were diseases of the circulatory system, venous thrombosis, and malignancies. Main limitation was a maximum age of 70 at time of inclusion for the first event. Therefore results can not be generalized to those in the highest age categories.

Conclusions

Patients who experienced a first venous thrombosis had an increased risk of death which lasted up to 8 years after the event, even when no comorbidities were present at time of thrombosis. Future long-term clinical follow-up could be beneficial in these patients. Please see later in the article for the Editors'' Summary     

Association between Number of Teeth and Chronic Systemic Diseases: A Cohort Study Followed for 13 Years

BackgroundThere is growing evidence of an association between oral health, specifically dental status, and chronic systemic diseases. However, varying measures of dental status across different populations and low study sample has made comparison of studies and conclusion of findings unclear. Our aim is to examine whether the number of teeth as a measure of dental status is associated with incident chronic diseases in a cohort setting.MethodsWe conducted a cohort study among 24,313 middle-aged Germans followed up for 13 years. Data on number of teeth as a measure of dental status were obtained through self-reports. Outcomes were clinically–verified incident non–fatal myocardial infarction, stroke, type 2 diabetes mellitus, and cancer. Hazard ratio (HR) and 95% confidence intervals (CI) were obtained from Cox regression models.ResultsIncreasing number of teeth is inversely related to risk of myocardial infarction (HR: 0.97; 95% CI: 0.96, 0.99). The full multivariate model of teeth groups showed a strong linear trend for myocardial infarction, a less strong trend for stroke, and no relation with type 2 diabetes mellitus and cancer in a competing risk model. Participants with 18–23 teeth and those without teeth were at 76% (95%CI: 1.04, 3) and 2.93 times (95%CI: 1.61, 5.18) higher risk of myocardial infarction compared to those with nearly all teeth (28–32 teeth).ConclusionsNumber of teeth is specifically associated with myocardial infarction and not with other chronic disease indicating that dental status further strengthens the link between oral health and cardiovascular diseases.     

Apoptosis and apoptosis related proteins in chronic viral liver disease

Background: Apoptosis may be an important mechanism of hepatocyte death in chronic viral liver disease. Methods: We studied apoptosis in liver biopsies from 30 patients with chronic viral hepatitis and 8 patients with viral cirrhosis by the TUNEL method. 12 cases of non-alcoholic steatohepatitis and 12 cases of primary biliary cirrhosis were used as non-viral disease controls. Immunohistochemical expression of p53, p21/waf1, bcl-2 and mdm-2 proteins was also studied in the same patients. Results: A statistically significant increase of apoptotic liver cells was found in severe chronic viral hepatitis (5.3 ± 0.3%), cirrhosis (3.4 ± 0.5%) and PBC (4.4 ± 0.4%) cases compared to patients with non-alcoholic steatohepatitis (0.8 ± 0.3%). The expression of p53 protein was increased in the cases of viral cirrhosis and in chronic severe viral hepatitis whereas in the cases of chronic mild hepatitis, PBC and non-alcoholic steatohepatitis we found no expression of p53. P21/waf1 expression was increased in severe chronic hepatitis, cirrhosis and PBC cases compared to mild hepatitis and non-alcoholic steatohepatitis cases. However no induction of mdm-2 was observed in the subgroups of chronic liver disease. Bcl-2 was expressed only in epithelium of bile ducts and mononuclear cells of the portal tracts and liver lobules. A weaker Bcl-2 expression was noted in the epithelium of bile ducts of 7/12 PBC cases. Conclusion: Our results provide evidence of increased apoptosis in severe chronic viral liver disease, suggesting that apoptotic cell death might be involved in the pathogenesis of hepatocellular damage of viral hepatitis and cirrhosis. Furthermore we analysed part of the apoptotic pathways implicated in the above process and found an increased expression of p21/waf1, probably p53 mediated, without overexpression of the apoptosis inhibiting bcl-2 and mdm-2 proteins. By contrast p21/waf1 overexpression in PBC seems to be propagated by a p53 independent mechanism.     

Predisposing factors for cerebral infarction: the Oxfordshire community stroke project.

The frequency of known causative factors of cerebral infarction was studied in 244 cases of first ever stroke due to cerebral infarction proved by computed tomography or at necropsy who were registered in the first two years of a prospective community based study. Risk factors for cerebral infarction were present in 196 (80%) cases; hypertension in 126 (52%); ischaemic heart disease in 92 (38%); peripheral vascular disease in 60 (25%); a cardiac lesion that was a major potential source of embolism to the brain in 50 (20%); transient ischaemic attacks in 35 (14%); cervical arterial bruit in 33 (14%); and diabetes mellitus in 24 (10%). Thirty one patients (13%) were in atrial fibrillation. Of the 48 patients who were free of risk factors or a major potential cardiac source of embolism at the time of the stroke, 18 were found to have hypertension after the stroke and 10 to have non-atheromatous non-embolic conditions (migrainous cerebral infarction (three), arteritis (two), inflammatory bowel disease (one), arterial trauma (one), autoimmune disease (one), carcinoma of the thyroid (one), and major operation (one). In 20 patients no causative factors could be identified. In this unselected series of patients with first ever stroke due to cerebral infarction most of the strokes were presumed to be due to either atheromatous arterial disease or embolism from the heart, and only 4% (95% confidence interval 2 to 7%) were probably due to non-atheromatous non-embolic causes. This has implications for research into strokes and allocation of public health expenditure.