Although the incidence of upper extremity deep venous thrombosis (UEDVT) diagnoses has increased, anticoagulation therapy for UEDVT remains inconsistent and of variable duration.
This study sought to analyze our institution's current treatment practices for UEDVT and assess the risk for subsequent pulmonary embolism (PE).
PURPOSE: We evaluated the safety and effectiveness of alternative endovascular methods to retrieve embedded optional and permanent filters in order to manage or reduce risk of long-term complications from implantation. Histologic tissue analysis was performed to elucidate the pathologic effects of chronic filter implantation.
METHODS: We studied the safety and effectiveness of alternative endovascular methods for removing embedded inferior vena cava (IVC) filters in 10 consecutive patients over 12 months. Indications for retrieval were symptomatic chronic IVC occlusion, caval and aortic perforation, and/or acute PE (pulmonary embolism) from filter-related thrombus. Retrieval was also performed to reduce risk of complications from long-term filter implantation and to eliminate the need for lifelong anticoagulation. All retrieved specimens were sent for histologic analysis.
RESULTS: Retrieval was successful in all 10 patients. Filter types and implantation times were as follows: one Venatech (1,495 days), one Simon-Nitinol (1,485 days), one Optease (300 days), one G2 (416 days), five Günther-Tulip (GTF; mean 606 days, range 154-1,010 days), and one Celect (124 days). There were no procedural complications or adverse events at a mean follow-up of 304 days after removal (range 196-529 days). Histology revealed scant native intima surrounded by a predominance of neointimal hyperplasia and dense fibrosis in all specimens. Histologic evidence of photothermal tissue ablation was confirmed in three laser-treated specimens.
CONCLUSION: Complex retrieval methods can now be used in select patients to safely remove embedded optional and permanent IVC filters previously considered irretrievable. Neointimal hyperplasia and dense fibrosis are the major components that must be separated to achieve successful retrieval of chronic filter implants.
Salmeterol is a β2-Adrenergic Receptor (β2-AR) agonist widely used for the treatment of asthma and chronic obstructive pulmonary disease (COPD). It has been shown that Salmeterol is also used at supra-therapeutic doses, as performance-enhancing substance in sport practice. Although, the abuse of β-agonists might determine some adverse effects, the molecular effects of Salmeterol on skeletal muscle cells remain unclear.
METHODS.: We evaluated the effects of Salmeterol (0.1-10 μM) on both proliferative and differentiated rat L6C5 and mouse C2C12 skeletal muscle cell lines. The metabolic effects were evaluated by glyceraldehyde phosphate dehydrogenase, lactate dehydrogenase, citrate synthase, 3-OH acyl-CoA dehydrogenase, and alanine transglutaminase activities. Cytotoxic and apoptotic effect were analyzed by MTS, Trypan blue exclusion assay, TUNEL assay, western blot analysis and immunofluorescence staining.
RESULTS.: We showed that Salmeterol reduced the growth rate of proliferating cells in dose and time dependent manner (6-48 hours). An increase of oxidative metabolism was found after 6 hours in C2C12 and L6C5 myoblasts and in C2C12 myotubes respect to control cells, while in L6C5 myotubes prevailed anaerobic metabolism. Exposure of myoblasts and myotubes for 48 and 72 hrs at high Salmeterol concentrations, induced apoptosis by the activation of the intrinsic apoptotic pathway, as confirmed by the modulation of the apoptotic proteins Bcl-xL, caspase-9, poly (ADP-ribose) polymerase (PARP), and by the cytoplasmic release of Smac/DIABLO.
CONCLUSION.: Altogether our results demonstrate that short-term supra-therapeutic Salmeterol exposure increased oxidative metabolic pathways on skeletal muscle cells, whereas prolonged treatment inhibits cell growth and exerts either a cytostatic, or pro-apoptotic effect in a time and dose-dependent way.
Smoking and bronchodilator treatment are both extensively studied as key elements in patients with chronic obstructive pulmonary disease. However, little is known about whether or not these elements interact in terms of developing cardiovascular diseases in patients with COPD.
Objectives: To explore to what extent the risk of developing ischemic cardiovascular disease in COPD patients is mediated by smoking status, use of bronchodilators and - specifically - their interaction.
Methods: We performed an observational pilot study on a relatively healthy Dutch COPD cohort from a primary care diagnostic center database with full information on spirometry tests, smoking status, bronchodilator use and other prescribed medication. We defined first ischemic cardiovascular events as primary outcome, measured by first prescription of antiplatelet drugs and/or nitrates. Unadjusted analyses by Kaplan-Meier were followed by adjusted Cox' proportional hazards.
Results: 845 COPD patients, totaling 2,169 observation years, were included in the analyses. We observed an increased risk for nonfatal ischemic cardiovascular events by smoking (adjusted HR = 3.58, p = 0.001) and a protective effect of bronchodilators (adjusted HR = 0.43, p = 0.01). Although the protective effect of bronchodilators appears to be substantially minimized in patients that persist in smoking, we could not statistically confirm a hazardous interaction between bronchodilators and smoking (HR 2.50, p = 0.21).
Conclusion: Our study reveals bronchodilators may protect from ischemic cardiovascular events in a relatively 'healthy' COPD population. We did not confirm a hazardous interaction between bronchodilators and smoking, although we observed current smokers benefit substantially less from the protective effect of bronchodilators.
Chronic obstructive pulmonary disease (COPD) has a rising global incidence and acute exacerbation of COPD (AECOPD) carries a high health-care economic burden. Classification and regression tree (CART) analysis is able to create decision trees to classify risk groups.
We analysed routinely collected laboratory data to identify prognostic factors for inpatient mortality with AECOPD from our large district hospital. Data from 5,985 patients with 9,915 admissions for AECOPD over a 7-year period were examined. Randomly allocated training (n = 4,986) or validation (n = 4,929) data sets were developed and CART analysis was used to model the risk of all-cause death during admission. Inpatient mortality was 15.5%, mean age was 71.5 (±11.5) years, 56.2% were male, and mean length of stay was 9.2 (±12.2) days. Of 29 variables used, CART analysis identified three (serum albumin, urea, and arterial pCO(2)) to predict in-hospital mortality in five risk groups, with mortality ranging from 3.0 to 23.4%. C statistic indices were 0.734 and 0.701 on the training and validation sets, respectively, indicating good model performance.
The highest-risk group (23.4% mortality) had serum urea >7.35 mmol/l, arterial pCO(2) >6.45 kPa, and normal serum albumin (>36.5 g/l). It is possible to develop clinically useful risk prediction models for mortality using laboratory data from the first 24 h of admission in AECOPD.