Publications by authors named "Sami O Simons"

26 Publications

  • Page 1 of 1

A VIRTUAL Sleep Apnoea management pathway For the work-up of Atrial fibrillation patients in a digital Remote Infrastructure: VIRTUAL-SAFARI.

Europace 2021 Oct 31. Epub 2021 Oct 31.

Department of Cardiology, Maastricht University Medical Centre and Cardiovascular Research Institute Maastricht, Maastricht, The Netherlands.

Aims: In atrial fibrillation (AF) patients, untreated sleep-disordered breathing (SDB) is associated with lower success rates of rhythm control strategies and as such structured SDB testing is recommended. Herein, we describe the implementation of a virtual SDB management pathway in an AF outpatient clinic and examine the utility and feasibility of this new approach.

Methods And Results: Prospectively, consecutive AF patients accepted for AF catheter ablation procedures without previous diagnosis of SDB were digitally referred to a virtual SDB management pathway and instructed to use WatchPAT-ONE (ITAMAR) for one night. Results were automatically transferred to a virtual sleep laboratory, upon which a teleconsultation with a sleep physician was planned. Patient experience was measured using surveys. SDB testing was performed in 119 consecutive patients scheduled for AF catheter ablation procedures. The median time from digital referral to finalization of the sleep study report was 18 [11-24] days. In total, 65 patients (55%) were diagnosed with moderate-to-severe SDB. Patients with SDB were prescribed more cardiovascular drugs and had higher body mass indices (BMI, 29 ± 3.3 vs. 27 ± 4.4kg/m2, P < 0.01). Patients agreed that WatchPAT-ONE was easy to use (91%) and recommended future use of this virtual pathway in AF outpatient clinics (86%). Based on this remote SDB testing, SDB treatment was recommended in the majority of patients.

Conclusion: This novel virtual AF management pathway allowed remote SDB testing in AF outpatient clinics with a short time to diagnosis and high patient satisfaction. Structured SDB testing results in a high detection of previously unknown SDB in AF patients scheduled for AF ablation.
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http://dx.doi.org/10.1093/europace/euab229DOI Listing
October 2021

Alterations in plasma hyaluronic acid in patients with clinically stable COPD versus (non)smoking controls.

Sci Rep 2021 08 5;11(1):15883. Epub 2021 Aug 5.

Department of Research and Education, Ciro, Horn, The Netherlands.

Hyaluronic acid (HA) is a key component of the extracellular matrix. HA and its metabolism are suggested to be altered in the lungs of patients with chronic obstructive pulmonary disease (COPD). The present study explored systemic HA, and its metabolic regulators, in patients with clinically stable COPD and smoking and non-smoking controls. Furthermore, associations of HA with acute exacerbations (AECOPD), airway-related hospitalizations, systemic inflammation and cardiovascular risk were studied. In total, 192 patients with moderate to very severe COPD [aged 62.3 y (± SD 7.0)], 84 smoking controls [aged 61.8 y (± 5.7)], and 107 non-smoking controls [aged 60.1 y (± 7.0)] were included. Plasma HA was reduced in patients with COPD compared to non-smoking controls (p = 0.033), but was comparable after adjusting for age and sex. Expression of HAS-3 did not differ between groups, but was substantially less detectable in more patients with COPD than (non)smoking controls (p < 0.001). Expression of HYAL-2 was enhanced in patients with COPD versus smoking (p = 0.019) and non-smoking (p < 0.001) controls, also in the age- and sex- adjusted model (p < 0.001). Plasma HA was not associated with AECOPD, airway-related hospitalizations in the previous year, or systemic inflammation in COPD. Arterial pulse wave velocity explained some of the variance (< 10%) in plasma HA (p = 0.006). Overall, these results indicate that expression of HYAL-2, but not plasma HA nor HAS-3, is enhanced in patients with COPD compared to (non)smoking controls. Furthermore, HA was not associated with clinical outcomes, yet, cardiovascular risk might play a role in its systemic regulation in stable COPD.
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http://dx.doi.org/10.1038/s41598-021-95030-6DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8342478PMC
August 2021

Healthcare use during COVID-19 and the effect on psychological distress in patients with chronic cardiopulmonary disorders in the Netherlands: a cross-sectional study.

BMJ Open 2021 06 30;11(6):e046883. Epub 2021 Jun 30.

Centre of Expertise for Palliative Care, Maastricht University Medical Centre+, Maastricht, The Netherlands.

Objectives: The COVID-19 pandemic caused a massive shift in the focus of healthcare. Such changes could have affected health status and mental health in vulnerable patient groups. We aimed to investigate whether patients with chronic pulmonary and cardiac diseases had experienced high levels of psychological distress during the COVID-19 pandemic in the Netherlands.

Design: A cross-sectional study.

Setting: COVID-19 pandemic-related changes in healthcare use, health status and psychological distress were investigated among patients with chronic obstructive pulmonary disease (COPD), pulmonary fibrosis (PF) and congestive heart failure (CHF), using an online nationwide survey.

Participants: 680 patients completed the survey. COPD was the most often reported diagnosis 334 (49%), followed by congestive heart failure 219 (32%) and PF 44 (7%). There were 79 (12%) patients with primary diagnosis 'other' than chronic cardiopulmonary disease, who also completed this survey.

Interventions: Psychological distress was assessed via the DASS-21 score (Depression Anxiety Stress Scale). Moreover, specific worries and anxieties regarding COVID-19 were explored.

Results: The frequency of contact with healthcare professionals changed in 52%. Changes in treatment were reported in 52%. Deterioration in health status was self-reported in 39%. Moderate to extremely severe levels of depression, anxiety and stress was observed in 25.8%, 28.5% and 14%, respectively. Over 70% reported specific worries and anxieties, such as about their own health and fear of being alone. Both the deterioration in health status and increased levels of anxiety were significantly (p<0.001, p<0.006) associated with changes in treatment. Exploratory analyses indicated that lack of social support may further increase anxiety.

Conclusion: Healthcare use changed during the COVID-19 pandemic in the Netherlands. It was associated with a decrease in health status, and increased psychological stress among patients with chronic cardiopulmonary disorders. Provision of healthcare should be more sensitive to the mental health needs of these patients during subsequent COVID-19 waves.
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http://dx.doi.org/10.1136/bmjopen-2020-046883DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8249168PMC
June 2021

Recovery from COVID-19: a sprint or marathon? 6-month follow-up data from online long COVID-19 support group members.

ERJ Open Res 2021 Apr 24;7(2). Epub 2021 May 24.

Dept of Research and Development, Ciro, Horn, The Netherlands.

Background: It remains unknown whether and to what extent members of online "long COVID" peer support groups remain symptomatic and limited over time. Therefore, we aimed to evaluate symptoms in members of online long COVID peer support groups up to 6 months after the onset of coronavirus disease 2019 (COVID-19)-related symptoms.

Methods: Demographics, symptoms, health status, work productivity, functional status and health-related quality of life were assessed about 3 and 6 months after the onset of COVID-19-related symptoms in members of online long COVID peer support groups.

Results: Data from 239 patients with a confirmed COVID-19 diagnosis (83% women; median (interquartile range) age 50 (39-56) years) were analysed. During the infection, a median (interquartile range) of 15 (11-18) symptoms was reported, which was significantly lower 3 and 6 months later: 6 (4-9) and 6 (3-8), respectively (p<0.05). From 3 to 6 months follow-up, the proportion of patients without symptoms increased from 1.3% to only 5.4% (p<0.001). Patients also reported a significantly improved work productivity (work absenteeism and presenteeism: 73% 52% and 66% 60%, respectively), self-reported good health (9.2% 16.7%), functional status (mean±sd Post-COVID-19 Functional Status scale: 2.4±0.9 2.2±1.0) and health-related quality of life (all p<0.05).

Conclusion: Although patients with confirmed COVID-19, who were all members of online long COVID peer support groups, reported significant improvements in work productivity, functional status and quality of life between 3 and 6 months follow-up, these data clearly highlight the long-term impact of COVID-19, as approximately 6 months after the onset of COVID-19-related symptoms a large proportion still experienced persistent symptoms, a moderate-to-poor health, moderate-to-severe functional limitations, considerable loss in work productivity, and/or an impaired quality of life. Action is needed to improve the management and healthcare of these patients.
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http://dx.doi.org/10.1183/23120541.00141-2021DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8012818PMC
April 2021

Physiological Changes Differ between Responders and Nonresponders to Pulmonary Rehabilitation in COPD.

Med Sci Sports Exerc 2021 06;53(6):1125-1133

Measure, Model & Manage Bioresponses (M3-BIORES), Department of Biosystems, KU Leuven, Leuven, BELGIUM.

Purpose: Not all patients with chronic obstructive pulmonary disease (COPD) experience similar benefits after pulmonary rehabilitation (PR). This pre-post PR study used a large sample of patients with COPD to determine whether PR-induced changes of oxygen uptake (V˙O2) kinetics and exercise responses of V˙O2, carbon dioxide output (V˙CO2), minute ventilation (V˙E), V˙E/V˙CO2, breathing frequency, and tidal volume differed between responders and nonresponders to PR.

Methods: Responders to PR were defined as patients with a minimal clinically important increase in endurance time of 105 s. Isotime (=180 s) values of V˙O2, V˙CO2, V˙E, V˙E/V˙CO2, breathing frequency, and tidal volume; gains of V˙O2, V˙CO2, and V˙E; and V˙O2 mean response time of 183 patients with COPD (forced expiratory volume in 1 s: 56% ± 19% predicted) were compared between pre- and post-PR constant work rate tests.

Results: After PR, only the group of responders significantly decreased V˙O2 mean response time (P < 0.05), V˙CO2 gain, V˙E gain, and isotime values of V˙CO2, V˙E, and V˙E/V˙CO2 (all, P < 0.001), while also improving their breathing pattern (e.g., decreased breathing frequency isotime value; P < 0.0001). These changes were not observed in the group of nonresponders. Changes in physiological exercise responses were correlated with changes in physical performance (e.g., correlation between changes in V˙O2 mean response time and endurance time: P = 0.0002, r = -0.32).

Conclusions: PR-induced changes in physiological exercise responses differed between responders and nonresponders. Physiological changes are relevant to explain the variable improvements of physical performance after PR in patients with COPD.
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http://dx.doi.org/10.1249/MSS.0000000000002578DOI Listing
June 2021

Treatable traits qualifying for nonpharmacological interventions in COPD patients upon first referral to a pulmonologist: the COPD sTRAITosphere.

ERJ Open Res 2020 Oct 2;6(4). Epub 2020 Nov 2.

Dept of Respiratory Medicine, Maastricht University Medical Centre, NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht, The Netherlands.

Introduction: The present study assessed the prevalence of nine treatable traits (TTs) pinpointing nonpharmacological interventions in patients with COPD upon first referral to a pulmonologist, how these TTs co-occurred and whether and to what extent the TTs increased the odds having a severely impaired health status.

Methods: Data were collected from a sample of 402 COPD patients. A second sample of 381 patients with COPD was used for validation. Nine TTs were assessed: current smoking status, activity-related dyspnoea, frequent exacerbations <12 months, severe fatigue, depressed mood, poor physical capacity, low physical activity, poor nutritional status and a low level of self-management activation. For each TT the odds ratio (OR) of having a severe health status impairment was calculated. Furthermore, a graphic representation was created, the COPD sTRAITosphere, to visualise TTs prevalence and OR.

Results: On average 3.9±2.0 TTs per patient were observed. These TTs occurred relatively independently of each other and coexisted in 151 unique combinations. A significant positive correlation was found between the number of TTs and Clinical COPD Questionnaire total score (r=0.58; p<0.001). Patients with severe fatigue (OR: 8.8), severe activity-related dyspnoea (OR: 5.8) or depressed mood (OR: 4.2) had the highest likelihood of having a severely impaired health status. The validation sample corroborated these findings.

Conclusions: Upon first referral to a pulmonologist, COPD patients show multiple TTs indicating them to several nonpharmacological interventions. These TTs coexist in many different combinations, are relatively independent and increase the likelihood of having a severely impaired health status.
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http://dx.doi.org/10.1183/23120541.00438-2020DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7682701PMC
October 2020

Chronic obstructive pulmonary disease and atrial fibrillation: an interdisciplinary perspective.

Eur Heart J 2021 02;42(5):532-540

Centre for Heart Rhythm Disorders, University of Adelaide and Royal Adelaide Hospital, 1 Port Road, SA 5000 Adelaide, Australia.

Chronic obstructive pulmonary disease (COPD) is highly prevalent among patients with atrial fibrillation (AF), shares common risk factors, and adds to the overall morbidity and mortality in this population. Additionally, it may promote AF and impair treatment efficacy. The prevalence of COPD in AF patients is high and is estimated to be ∼25%. Diagnosis and treatment of COPD in AF patients requires a close interdisciplinary collaboration between the electrophysiologist/cardiologist and pulmonologist. Differential diagnosis may be challenging, especially in elderly and smoking patients complaining of unspecific symptoms such as dyspnoea and fatigue. Routine evaluation of lung function and determination of natriuretic peptides and echocardiography may be reasonable to detect COPD and heart failure as contributing causes of dyspnoea. Acute exacerbation of COPD transiently increases AF risk due to hypoxia-mediated mechanisms, inflammation, increased use of beta-2 agonists, and autonomic changes. Observational data suggest that COPD promotes AF progression, increases AF recurrence after cardioversion, and reduces the efficacy of catheter-based antiarrhythmic therapy. However, it remains unclear whether treatment of COPD improves AF outcomes and which metric should be used to determine COPD severity and guide treatment in AF patients. Data from non-randomized studies suggest that COPD is associated with increased AF recurrence after electrical cardioversion and catheter ablation. Future prospective cohort studies in AF patients are needed to confirm the relationship between COPD and AF, the benefits of treatment of either COPD or AF in this population, and to clarify the need and cost-effectiveness of routine COPD screening.
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http://dx.doi.org/10.1093/eurheartj/ehaa822DOI Listing
February 2021

Sleep apnea, obesity and COPD depress respiration during catheter ablation procedures: Implications for transcutaneous carbon dioxide monitoring.

Int J Cardiol 2021 03 3;327:102-104. Epub 2020 Nov 3.

Department of Pulmonology, Maastricht University Medical Centre, Maastricht, the Netherlands.

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http://dx.doi.org/10.1016/j.ijcard.2020.10.080DOI Listing
March 2021

Role of acute exacerbations in skeletal muscle impairment in COPD.

Expert Rev Respir Med 2021 01 10;15(1):103-115. Epub 2020 Nov 10.

NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht University Medical Centre, Department of Respiratory Medicine , Maastricht, The Netherlands.

: Muscle impairments are prevalent in COPD and have adverse clinical implications in terms of physical performance capacity, disease burden, quality of life and even mortality. During acute exacerbations of COPD (AECOPDs) the respiratory symptoms worsen and this might also apply to the muscle impairments. : This report includes a review of both clinical and pre-clinical peer-reviewed literature of the past 20 years found in PubMed providing a comprehensive view on the role of AECOPD in muscle dysfunction in COPD, the putative underlying mechanisms and the treatment perspectives. : The contribution of AECOPD and its recurrent nature to muscle impairment in COPD cannot be ignored and can be attributed to the acutely intensifying and converging disease-related drivers of muscle deterioration, in particular disuse, systemic inflammation and corticosteroid treatment. The search for novel treatment options should focus on the AECOPD-enhanced drivers of muscle dysfunction as well as on the underlying, mainly catabolic, mechanisms. Considering the impact of AECOPD on muscle function, and that of muscle impairment on the recurrence of exacerbations, counteracting muscle deterioration in AECOPD provides an unprecedented therapeutic opportunity.
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http://dx.doi.org/10.1080/17476348.2021.1843429DOI Listing
January 2021

Caring for patients with COPD and COVID-19: a viewpoint to spark discussion.

Thorax 2020 12 2;75(12):1035-1039. Epub 2020 Sep 2.

Groningen Research Institute of Asthma and COPD (GRIAC), University of Groningen, Groningen, the Netherlands.

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http://dx.doi.org/10.1136/thoraxjnl-2020-215095DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7474898PMC
December 2020

Acute exacerbations of COPD are associated with a prothrombotic state through platelet-monocyte complexes, endothelial activation and increased thrombin generation.

Respir Med 2020 09 25;171:106094. Epub 2020 Jul 25.

Department of Respiratory Medicine, Gelre Ziekenhuizen, Apeldoorn, the Netherlands; Department of Respiratory Medicine, Maastricht University Medical Centre, Maastricht, the Netherlands; NUTRIM School of Nutrition and Translational Research in Metabolism, University of Maastricht, Maastricht, the Netherlands.

Introduction: Patients with chronic obstructive pulmonary disease (COPD) are at increased risk for cardiovascular events, particularly following an acute exacerbation (AE-COPD). Exacerbations are associated with increased systemic inflammation, which may drive coagulation. This prospective cohort study aimed to determine how an AE-COPD affects platelet activation, the endothelium, plasmatic coagulation and fibrinolysis, and its association with systemic inflammation.

Materials And Methods: Fifty-two patients with an AE-COPD were included. Blood samples at admission, at day 3 of treatment and at convalescence were available for 32 patients. Platelet-monocyte complex (PMC) formation, monocyte Mac-1 expression and platelet (re)activity (P-selectin expression, αIIbβ3 activation) were measured by flow cytometry. Von Willebrand Factor (VWF), thrombin generation (TG) and clot lysis time (CLT) were determined as measures of endothelial activation, plasmatic coagulation and fibrinolysis, respectively.

Results: Exacerbations were associated with increased PMCs (MFI 31.3 vs 23.8, p = 0.004) and Mac-1 (MFI 38.2 vs 34.8, p = 0.006) compared to convalescence, but not with changes in platelet (re)activity. VWF (antigen, activity, active fraction) and TG (peak, ETP and velocity index) were all significantly higher during AE-COPD compared to convalescence. PMCs, Mac-1, VWF and TG were positively associated with systemic inflammation (CRP). CLT was prolonged in AE-COPD patients with systemic inflammation. Moreover, platelet hyperreactivity on admission was associated with an increased risk for exacerbation relapse.

Conclusions: Acute exacerbations are associated with an inflammation-associated prothrombotic state, characterized by increased PMCs, endothelial activation and plasmatic coagulation. Our findings provide direction for future studies on biomarkers predicting the risk of exacerbation relapse and cardiovascular events.
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http://dx.doi.org/10.1016/j.rmed.2020.106094DOI Listing
September 2020

Increased Platelet-Monocyte Interaction in Stable COPD in the Absence of Platelet Hyper-Reactivity.

Respiration 2018;95(1):35-43. Epub 2017 Oct 12.

Department of Respiratory Medicine, Radboud University Medical Center, Nijmegen, The Netherlands.

Background: Chronic obstructive pulmonary disease (COPD) is well known for its cardiovascular co-morbidities. Increased platelet-monocyte interaction is found in COPD and may reflect altered platelet function and a potential role for anti-platelet therapy.

Objectives: The objectives were to investigate platelet-monocyte interaction, platelet activation and reactivity and plasmatic coagulation in stable COPD.

Methods: Platelet-monocyte interaction and platelet activation were determined by flow cytometry in 30 stable COPD patients and 25 controls. Platelet activation was measured by binding of fibrinogen to the activated fibrinogen receptor and platelet P-selectin expression at baseline and after platelet stimulation with platelet agonists. Plasmatic coagulation was measured by D-dimer and thrombin generation.

Results: Platelet-monocyte interaction was increased in stable COPD (median fluorescence intensity of platelet CD61 was 19.8 [IQR 14.0-33.2] vs. 10.0 [IQR 8.7-16.7], p = 0.002). In contrast, platelet activation and reactivity, reflected by fibrinogen binding and P-selectin expression, were the same in both groups. Plasma P-selectin and interleukin-6 were increased in COPD (p = 0.01 and p = 0.02, respectively), whereas soluble fibrinogen, D-dimer and thrombin generation were similar.

Conclusions: Increased platelet-monocyte interaction was found in the absence of platelet hyper-reactivity and activation of plasmatic coagulation in stable COPD. Future clinical evaluation of the effects of different anti-platelet drugs in COPD is warranted, as anti-platelet therapy may interfere with platelet-monocyte interaction.
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http://dx.doi.org/10.1159/000480457DOI Listing
October 2018

Differences in systemic adaptive immunity contribute to the 'frequent exacerbator' COPD phenotype.

Respir Res 2016 10 28;17(1):140. Epub 2016 Oct 28.

UCL Respiratory, University College London, London, UK.

Background: Some COPD patients are more susceptible to exacerbations than others. Mechanisms underlying these differences in susceptibility are not well understood. We hypothesized that altered cell mediated immune responses may underlie a propensity to suffer from frequent exacerbations in COPD.

Methods: Peripheral blood mononuclear cells (PBMCs) were obtained from 24 stable COPD patients, eight frequent exacerbators (≥3 diary-card exacerbations/year) and 16 infrequent exacerbators (< 3 diary-card exacerbations/year). Detailed multi-parameter flow cytometry was used to study differences in innate and adaptive systemic immune function between frequent and infrequently exacerbating COPD patients.

Results: The 24 COPD patients had a mean (SD) age of 76.3 (9.4) years and FEV 1.43 (0.60)L, 53.3 (18.3)% predicted. PBMCs of frequent exacerbators (FE) contained lower frequencies of CD4+ T central memory cells (CD4+ Tcm) compared to infrequent exacerbators (IE) (FE = 18.7 %; IE = 23.9 %; p = 0.035). This observation was also apparent in absolute numbers of CD4+ Tcm cells (FE = 0.17 × 10^6/mL; IE = 0.25 × 10^6/mL; p = 0.035). PBMCs of FE contained a lower frequency of CD8+ T effector memory cells expressing HLA-DR (Human Leukocyte Antigen - D Related) compared to IE COPD patients (FE = 22.7 %; IE = 31.5 %; p = 0.007).

Conclusion: Differences in the adaptive systemic immune system might associate with exacerbation susceptibility in the 'frequent exacerbator' COPD phenotype. These differences include fewer CD4+ T central memory cells and CD8+ T effector memory cells.

Trial Registration: Not applicable.
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http://dx.doi.org/10.1186/s12931-016-0456-yDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5084432PMC
October 2016

Prevalence and Localization of Pulmonary Embolism in Unexplained Acute Exacerbations of COPD: A Systematic Review and Meta-analysis.

Chest 2017 03 12;151(3):544-554. Epub 2016 Aug 12.

Department of Respiratory Medicine, Radboud University Medical Center, Nijmegen, The Netherlands.

Background: Patients with COPD experience episodes of increased inflammation, so-called acute exacerbations of COPD (AE-COPD). In 30% of AE-COPD cases, no clear cause is found. Since there is well-known cross talk between inflammation and thrombosis, the objectives of this study were to determine the prevalence, embolus localization, clinical relevance, and clinical markers of pulmonary embolism (PE) in unexplained AE-COPD.

Methods: A systematic search was performed using MEDLINE and EMBASE platforms from 1974 to October 2015. Prospective and cross-sectional studies that included patients with AE-COPD and used pulmonary CT-angiography for diagnosis of PE were included.

Results: The systematic search resulted in 1,650 records. The main reports of 22 articles were reviewed, and 7 studies were included. The pooled prevalence of PE in unexplained AE-COPD was 16.1% (95% CI, 8.3%-25.8%) in a total of 880 patients. Sixty-eight percent of the emboli found were located in the main pulmonary arteries, lobar arteries, or interlobar arteries. Mortality and length of hospital admission seemed to be increased in patients with unexplained AE-COPD and PE. Pleuritic chest pain and cardiac failure were more frequently reported in patients with unexplained AE-COPD and PE. In contrast, signs of respiratory tract infection was less frequently related to PE.

Conclusions: PE is frequently seen in unexplained AE-COPD. Two-thirds of emboli are found at locations that have a clear indication for anticoagulant treatment. These findings merit clinical attention. PE should receive increased awareness in patients with unexplained AE-COPD, especially when pleuritic chest pain and signs of cardiac failure are present, and no clear infectious origin can be identified.
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http://dx.doi.org/10.1016/j.chest.2016.07.034DOI Listing
March 2017

Non-resolving pneumonia in patient with obsessive--compulsive disorder.

Thorax 2014 Feb 1;69(2):193. Epub 2013 Nov 1.

Department of Pulmonary Medicine, Radboud University Medical Center, , Nijmegen, The Netherlands.

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http://dx.doi.org/10.1136/thoraxjnl-2013-203759DOI Listing
February 2014

[Maternal pulmonary oedema due to the use of atosiban in cases of multiple gestation].

Ned Tijdschr Geneeskd 2013 ;157(1):A5316

Universitair Medisch Centrum St. Radboud, Afd. Gynaecologie en Obstetrie, Nijmegen, the Netherlands.

Background: Nifedipine is used as a first choice tocolytic agent in many Dutch hospitals, but its use is discouraged in multiple gestations. Atosiban, a selective oxytocin receptor antagonist that rarely causes systemic side effects, is used as an alternative.

Case Description: A 32-year-old primigravida with spontaneous triplet pregnancy was admitted at 33 3/7 weeks for threatened preterm labour. For tocolysis, atosiban was administered for 48 hours together with betamethasone for foetal lung maturation. One day after treatment with atosiban she developed dyspnoea caused by pulmonary oedema. After a caesarean section and furosemide treatment the pulmonary oedema resolved. Analysis showed that atosiban was a likely cause of the pulmonary oedema.

Conclusion: Every patient with multiple gestation is at increased risk of pulmonary oedema. Any tocolytic agent may elicit that response, even the relatively safe atosiban.
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February 2013

Role of rpsA gene sequencing in diagnosis of pyrazinamide resistance.

J Clin Microbiol 2013 Jan;51(1):382

Department of Pulmonary Medicine Radboud University Nijmegen Medical Centre, Nijmegen, the Netherlands.

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http://dx.doi.org/10.1128/JCM.02739-12DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3536190PMC
January 2013

All that glitters is not gold in pursuing the diagnosis of pulmonary embolism.

Chest 2012 Jan;141(1):276-277

Department of Pulmonary Medicine, Radboud University Nijmegen Medical Centre Nijmegen, The Netherlands.

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http://dx.doi.org/10.1378/chest.11-1976DOI Listing
January 2012

Montelukast for bronchiolitis obliterans syndrome after lung transplantation.

Chest 2012 Jan;141(1):275-276

Department of Pulmonary Medicine, Radboud University Nijmegen Medical Centre Nijmegen, The Netherlands.

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http://dx.doi.org/10.1378/chest.11-1979DOI Listing
January 2012

Validation of pncA gene sequencing in combination with the mycobacterial growth indicator tube method to test susceptibility of Mycobacterium tuberculosis to pyrazinamide.

J Clin Microbiol 2012 Feb 16;50(2):428-34. Epub 2011 Nov 16.

Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands.

Pyrazinamide is important in the treatment of tuberculosis. Unfortunately, the diagnosis of pyrazinamide resistance is hampered by technical difficulties. We hypothesized that mutation analysis combined with the mycobacterial growth indicator tube (MGIT) phenotypic method would be a good predictor of pyrazinamide resistance. We prospectively analyzed 1,650 M. tuberculosis isolates referred to our tuberculosis reference laboratory in 2008 and 2009. In our laboratory, the MGIT 960 system was used for pyrazinamide resistance screening. If a pyrazinamide-resistant strain was detected, we performed a pncA gene mutation analysis. A second MGIT 960 susceptibility assay was performed afterwards to evaluate the accuracy of the pncA mutation analysis to detect true- or false-positive MGIT results. We observed pyrazinamide resistance in 69 samples using the first MGIT 960 analysis. In a second MGIT 960 analysis, 47 of the 69 samples proved susceptible (68% false positivity). Sensitivity of nonsynonymous pncA mutations for detecting resistant isolates was 73% (95% confidence interval [CI], 61% to 73%), and specificity was 100% (95% CI, 95% to 100%). A diagnostic algorithm incorporating phenotypic and molecular methods would have a 100% positive predictive value for detecting pyrazinamide-resistant isolates, indicating that such an algorithm, based on both methods, is a good predictor for pyrazinamide resistance in routine diagnostics.
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http://dx.doi.org/10.1128/JCM.05435-11DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3264162PMC
February 2012

Tissue plasminogen activator and DNase in empyema.

N Engl J Med 2011 11;365(20):1936; author reply 1936-7

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http://dx.doi.org/10.1056/NEJMc1110599DOI Listing
November 2011

Drug susceptibility testing for optimizing tuberculosis treatment.

Curr Pharm Des 2011 ;17(27):2863-74

Radboud University Medical Centre, the Netherlands National Institute for Public Health and the Environment, Bilthoven, The Netherlands.

The principles of our current drug susceptibility testing (DST) for tuberculosis (TB) have already been laid out in 1963. Since then, DST has not gained much popularity owing to the long turn-around time and the introduction of potent antituberculosis drug regimens. These and other barriers have led to a critical gap in laboratory capacity in DST of Mycobacterium tuberculosis. However, owing to the emergence of multidrug resistant tuberculosis there is a pressing need for adequate and rapid DST. In recent years, methods for fastening the diagnosis of drug resistant tuberculosis have been developed. Semi-automated (non)- radiometric liquid culture systems reduced the turn-around-time significantly. With the introduction of molecular diagnostic methods, such as reverse line probes and the recently introduced semi-automated real-time PCR, the turn-around time of at least an indicative resistance testing has dropped from days to hours. However, much more can be gained in the development of fast phenotypic and molecular DST methodologies. Recently also pharmacodynamic studies have also added significantly to our understanding of resistance development in tuberculosis treatment. This article provides an overview of the most important DST techniques now available, with their characteristics, biosafety aspects, reproducibility and required quality control. Also the findings in pharmacodynamic studies and required future research are discussed. We will argue that drug susceptibility testing in TB treatment is an essential tool for adequate TB control and prevention of resistance and should be applied to all patients to guide TB treatment. Perhaps in the near future even individualized treatment doses could be an important help to prevent further emergence or further development of resistance.
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http://dx.doi.org/10.2174/138161211797470255DOI Listing
March 2012
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