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Nieuwegein, Netherlands

Van Lammeren G.W.,University Utrecht | Peeters W.,University Utrecht | De Vries J.-P.P.M.,University Utrecht | De Kleijn D.P.V.,St. Antonius Hospital Nieuwegein | And 3 more authors.
Stroke | Year: 2011

Background and Purpose- Carotid endarterectomy (CEA) of stable atherosclerotic plaques is associated with an increased risk for restenosis. Patients with transient ischemic attack and patients with and stroke have relatively unstable atherosclerotic plaques. However, carotid plaques stabilize over time after a cerebrovascular event due to plaque repair after rupture. These findings raised 2 questions: (1) Is preoperative clinical presentation related to restenosis after CEA? (2) Does delayed revascularization result in a higher risk for restenosis compared with CEA in the short term after a cerebrovascular event? Methods- Between 2002 and 2009, 1203 patients undergoing CEA were included. The impact of clinical presentation on the occurrence of restenosis 1 year after CEA was investigated and corrected for cardiovascular risk factors, medication use, and type of arteriotomy closure. Patency was assessed with standardized duplex ultrasound imaging at 1 year after CEA. Restenosis was defined as recurrent luminal narrowing 50% at the endarterectomy site. Results- At 1 year of follow-up, restenosis was observed more frequently in asymptomatic patients than in patients with transient ischemic attack and patients with stroke. The adjusted odds ratio (95% CI) for restenosis was 0.56 (0.35 to 0.89) for patients with transient ischemic attack and 0.49 (0.27 to 0.87) for patients with stroke compared with asymptomatic patients. Subgroup analysis showed an increased risk for restenosis if CEA was performed >30 days after stroke (adjusted OR, 2.23; 1.02 to 5.73). Conclusions- Asymptomatic patients have an increased risk for restenosis at 1 year after CEA compared with patients with transient ischemic stroke and patients with stroke. CEA within 30 days after stroke is associated with a decreased risk of restenosis, which supports the current strategy for early surgical intervention after stroke. © 2011 American Heart Association. All rights reserved. Source


Vriesendorp P.A.,Erasmus University Rotterdam | Schinkel A.F.L.,Erasmus University Rotterdam | Liebregts M.,St. Antonius Hospital Nieuwegein | Theuns D.A.M.J.,Erasmus University Rotterdam | And 4 more authors.
Circulation: Arrhythmia and Electrophysiology | Year: 2015

Background - The recently released 2014 European Society of Cardiology guidelines of hypertrophic cardiomyopathy (HCM) use a new clinical risk prediction model for sudden cardiac death (SCD), based on the HCM Risk-SCD study. Our study is the first external and independent validation of this new risk prediction model. Methods and Results - The study population consisted of a consecutive cohort of 706 patients with HCM without prior SCD event, from 2 tertiary referral centers. The primary end point was a composite of SCD and appropriate implantable cardioverter-defibrillator therapy, identical to the HCM Risk-SCD end point. The 5-year SCD risk was calculated using the HCM Risk-SCD formula. Receiver operating characteristic curves and C-statistics were calculated for the 2014 European Society of Cardiology guidelines, and risk stratification methods of the 2003 American College of Cardiology/European Society of Cardiology guidelines and 2011 American College of Cardiology Foundation/American Heart Association guidelines. During follow-up of 7.7±5.3 years, SCD occurred in 42 (5.9%) of 706 patients (ages 49±16 years; 34% women). The C-statistic of the new model was 0.69 (95% CI, 0.57-0.82; P=0.008), which performed significantly better than the conventional risk factor models based on the 2003 guidelines (C-statistic of 0.55: 95% CI, 0.47-0.63; P=0.3), and 2011 guidelines (C-statistic of 0.60: 95% CI, 0.50-0.70; P=0.07). Conclusions - The HCM Risk-SCD model improves the risk stratification of patients with HCM for primary prevention of SCD, and calculating an individual risk estimate contributes to the clinical decision-making process. Improved risk stratification is important for the decision making before implantable cardioverter-defibrillator implantation for the primary prevention of SCD. © 2015 American Heart Association, Inc. Source


Verschuur-Maes A.H.J.,University Utrecht | De Bruin P.C.,St. Antonius Hospital Nieuwegein | Van Diest P.J.,University Utrecht
Breast Cancer Research and Treatment | Year: 2012

Promoter hypermethylation of several tumour suppressor genes often occurs during breast carcinogenesis, but little is known about epigenetic silencing in the possible precursor columnar cell lesion (CCL). Promoter hypermethylation of 50 different tumour suppressor genes was assessed in normal breast tissue (N = 10), CCL (N = 15), ductal carcinoma in situ (DCIS) grade I originating in CCL (N = 5) and paired CCL (N = 15) with DCIS (N = 7) and/or invasive carcinoma (N = 14) by Methylation-specific multiplex ligation-dependent probe amplification. Increasing mean cumulative methylation levels were found from normal breast tissue to CCL to DCIS and invasive carcinoma (P < 0.001) with similar methylation levels in DCIS and invasive carcinoma. Methylation levels and frequencies (in the overall analysis and analysis of only the synchronous lesions) were the highest for RASSF1, CCND2, ID4, SCGB3A1 and CDH13. The methylation levels of ID4, CCND2, and CDH13 increased significantly from normal breast tissue to CCL and to DCIS/invasive carcinoma. RASSF1, SCGB3A1 and SFRP5 had significant higher methylation levels in CCL compared to normal breast tissue, but showed no significant differences between CCL, DCIS and invasive carcinoma. Also, no difference was found between CCLs with and without atypia, or CCLs with or without synchronous cancer. In conclusion, promoter hypermethylation for several established tumour suppressor genes is already present in CCLs, underlining that promoter hypermethylation is an early event in breast carcinogenesis. Atypia in CCL or the presence of synchronous more advanced lesions does not seem to be accompanied by higher methylation levels. © 2012 Springer Science+Business Media New York. Source


Vlieger A.M.,St. Antonius Hospital Nieuwegein
Journal of Pediatric Gastroenterology and Nutrition | Year: 2014

Conclusions: Pediatric patients with IBS and those with FAPS have similar psychosocial profiles. These results may explain why treatment response of psychological therapies in these AP-FGIDs is similar. These results may indicate that pediatric IBS and FAPS are different expressions of 1 underlying functional disorder, but similarities in psychosocial characteristics do not exclude the possibility that these disorders are different entities, because these similarities can exist between disorders of various causes. Therefore, future research is required on the role of other (physiological) factors in pediatric IBS and FAPS.Methods: A total of 259 children, ages 8 to 18 years, fulfilling Rome III criteria for IBS or FAPS were included in a randomized controlled trial evaluating the effect of hypnotherapy. At inclusion, questionnaires assessed demographics, clinical features, abdominal pain frequency and intensity, depression and anxiety, somatization, health-related quality of life, pain beliefs, and coping strategies.Objectives: It has been suggested that different subcategories of childhood abdominal pain-related functional gastrointestinal disorders (AP-FGIDs) are not separate clinical entities, but represent variable expressions of the same FGID. The aimof the present study was to compare clinical and psychological characteristics of children with irritable bowel syndrome (IBS), functional abdominal pain (FAP), and functional abdominal pain syndrome (FAPS).Results: No differenceswere found between children with IBS and those with FAPS with respect to the main outcomes: frequency and intensity of abdominal pain, symptoms of depression and anxiety, somatization, healthrelated quality of life, pain beliefs, and coping strategies. Asignificantly higher percentage of patients with IBS had a positive family history for AP-FGIDs (56.8% vs 37.8%; P=0.00). Characteristics of patients with IBS subtypes did not differ. Patients with FAP or FAPS differed only with respect to problem-focused coping strategy (2.21± 0.61 vs 2.52± 0.49; P=0.00. © 2014 by European Society for Pediatric Gastroenterology, Hepatology, and Nutrition and North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition. Source


Osnabrugge R.L.,Erasmus University Rotterdam | Head S.J.,Erasmus University Rotterdam | Zijlstra F.,Erasmus University Rotterdam | Ten Berg J.M.,St. Antonius Hospital Nieuwegein | And 4 more authors.
Genetics in Medicine | Year: 2015

We systematically investigated how 11 overlapping meta-analyses on the association between CYP2C19 loss-of-function alleles and clinical efficacy of clopidogrel could yield contradictory outcomes. The results of the meta-analyses differed because more recent meta-analyses included more primary studies and some had not included conference abstracts. Conclusions differed because between-study heterogeneity and publication bias were handled differently across meta-analyses. All meta-analyses on the clinical end point observed significant heterogeneity and several reported evidence for publication bias, but only one out of eight statistically significant meta-analyses concluded that therefore the association was unproven and one other refrained from quantifying a pooled estimate because of heterogeneity. For the end point stent thrombosis, all meta-analyses reported statistically significant associations with CYP2C19 loss-of-function alleles with no statistically significant evidence for heterogeneity, but only three had investigated publication bias and also found evidence for it. One study therefore concluded that there was no evidence for an association, and one other doubted the association because of a high level of heterogeneity. In summary, meta-analyses on the association between CYP2C19 loss-of-function alleles and clinical efficacy of clopidogrel differed widely with regard to assessment and interpretation of heterogeneity and publication bias. The substantial heterogeneity and publication bias implies that personalized antiplatelet management based on genotyping is not supported by the currently available evidence. © 2015 American College of Medical Genetics and Genomics. Source

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