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Articles by R. J De Winter
Total Records ( 3 ) for R. J De Winter
  C. M van Tiel , P. I Bonta , S. Z.H Rittersma , M. A.M Beijk , E. J Bradley , A. M Klous , K. T Koch , F Baas , J. W Jukema , D Pons , M. L Sampietro , H Pannekoek , R. J de Winter and C. J.M. de Vries

Background— The cyclin-dependent kinase inhibitor p27kip1 is a key regulator of smooth muscle cell and leukocyte proliferation in vascular disease, including in-stent restenosis. We therefore hypothesized that common genetic variations or single nucleotide polymorphisms in p27kip1 may serve as a useful tool in risk stratification for in-stent restenosis.

Methods and Results— Three single nucleotide polymorphisms concerning the p27kip1 gene (–838C>A, rs36228499; –79C>T, rs34330; +326G>T, rs2066827) were determined in a cohort of 715 patients undergoing coronary angioplasty and stent placement. We discovered that the p27kip1-838C>A single nucleotide polymorphism is associated with clinical in-stent restenosis; the –838AA genotype decreases the risk of target vessel revascularization (hazard ratio, 0.28; 95% confidence interval, 0.10 to 0.77). This finding was replicated in another cohort study of 2309 patients (hazard ratio, 0.61; 95% confidence interval, 0.40 to 0.93). No association was detected between this end point and the p27kip1-79C>T and +326G>T single nucleotide polymorphisms. We subsequently studied the functional importance of the –838C>A single nucleotide polymorphism and detected a 20-fold increased basal p27kip1 transcriptional activity of the –838A allele containing promoter.

Conclusions— Patients with the p27kip1-838AA genotype have a decreased risk of in-stent restenosis corresponding with enhanced promoter activity of the –838A allele of this cell-cycle inhibitor, which may explain decreased smooth muscle cell proliferation.

  F Windhausen , A Hirsch , J Fischer , P. M van der Zee , G. T Sanders , J. P van Straalen , J. H Cornel , J. G.P Tijssen , F. W.A Verheugt , R. J de Winter and for the Invasive versus Conservative Treatment in Unstable Coronary Syndromes (ICTUS) Investigators

Background: We assessed the value of cystatin C for improvement of risk stratification in patients with non–ST elevation acute coronary syndrome (nSTE-ACS) and increased cardiac troponin T (cTnT), and we compared the long-term effects of an early invasive treatment strategy (EIS) with a selective invasive treatment strategy (SIS) with regard to renal function.

Methods: Patients (n = 1128) randomized to an EIS or an SIS in the ICTUS trial were stratified according to the tertiles of the cystatin C concentration at baseline. The end points were death within 4 years and spontaneous myocardial infarction (MI) within 3 years.

Results: Mortality was 3.4%, 6.2%, and 13.5% in the first, second, and third tertiles, respectively, of cystatin C concentration (log-rank P < 0.001), and the respective rates of spontaneous MI were 5.5%, 7.5%, and 9.8% (log-rank P = 0.03). In a multivariate Cox regression analysis, the cystatin C concentration in the third quartile remained independently predictive of mortality [hazard ratio (HR), 2.04; 95% CI, 1.02–4.10; P = 0.04] and spontaneous MI (HR, 1.95; 95% CI, 1.05–3.63; P = 0.04). The mortality rate in the second tertile was lower with the EIS than with the SIS (3.8% vs 8.7%). In the third tertile, the mortality rates with the EIS and the SIS were, respectively, 15.0% and 12.2% (P for interaction = 0.04). Rates of spontaneous MI were similar for the EIS and the SIS within cystatin C tertiles (P for interaction = 0.22).

Conclusions: In patients with nSTE-ACS and an increased cTnT concentration, mild to moderate renal dysfunction is associated with a higher risk of death and spontaneous MI. Use of cystatin C as a serum marker of renal function may improve risk stratification.

  D. M Charytan , L Wallentin , B Lagerqvist , R Spacek , R. J De Winter , N. M Stern , E Braunwald , C. P Cannon and N. K. Choudhry

Background and objectives: In the general population, an early invasive strategy of routine coronary angiography is superior to a conservative strategy of selective angiography in patients who are admitted with unstable angina or non–ST segment elevation myocardial infarction (MI), but the effectiveness of this strategy in individuals with chronic kidney disease (CKD) is uncertain.

Design, setting, participants, & measurements: We conducted a collaborative meta-analysis with data provided by the main authors of identified trials to estimate the effectiveness of early angiography in patients with CKD. The Cochrane, Medline, and EMBASE databases were searched to identify randomized trials that compared invasive and conservative strategies in patients with unstable angina or non-ST MI. Pooled risks ratios were estimated using data from enrolled patients with estimated GFR <60 ml/min per 1.73 m2.

Results: Five randomized trials that enrolled 1453 patients with CKD were included. An early invasive strategy was associated with nonsignificant reductions in all-cause mortality, nonfatal MI, and a composite of death or nonfatal MI. The invasive strategy significantly reduced rehospitalization.

Conclusions: This collaborative study suggests that the benefits of an early invasive strategy are preserved in patients with CKD and that an early invasive approach reduces the risk for rehospitalization and is associated with trends of reduction in the risk for death and nonfatal re-infarction in patients with CKD. Coronary angiography should be considered for patients who have CKD and are admitted with non–ST elevation acute coronary syndromes.

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