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Articles by E de Groot
Total Records ( 3 ) for E de Groot
  R Duivenvoorden , E de Groot , B.M Elsen , J.S Lameris , R.J van der Geest , E.S Stroes , J.J.P Kastelein and A.J. Nederveen
 

Background— Our aim was to compare common carotid mean wall thickness (MWT) measurements by 3.0-T MRI with B-mode ultrasound common carotid intima-media thickness (CCIMT) measurements, a validated surrogate marker for cardiovascular disease.

Methods and Results— B-mode ultrasound and 3.0-T MRI scans of the left and right common carotid arteries were repeated 3 times in 15 healthy younger volunteers (age, 26±2.6 years), 15 healthy older volunteers (age, 57±3.2 years), and 15 subjects with cardiovascular disease and carotid atherosclerosis (age, 63±9.8 years). MWT was 0.711 (SD, 0.229) mm and mean CCIMT was 0.800 (SD, 0.206) mm. MWT and CCIMT were highly correlated (r=0.89, P<0.001). The intraclass correlation coefficients for interscan and interobserver and intraobserver agreements of MRI MWT measurements were larger than 0.95 with small confidence intervals, indicating excellent reproducibility. Power calculations indicate that 89 subjects are required to detect a 4% difference in MRI MWT compared with 469 subjects to detect similar differences with ultrasound IMT in follow-up studies.

Conclusions— The study data for carotid MRI and ultrasound IMT showed strong agreement, indicating that both modalities measure the thickness of the intima and media. The advantage of MRI over ultrasound is that the measurement variability is smaller, enabling smaller sample sizes and potentially shorter study duration in cardiovascular prevention trials.

  M Vergeer , R Zhou , M. L Bots , R Duivenvoorden , J Koglin , F Akdim , Y. B Mitchel , R Huijgen , A Sapre , E de Groot , E. J. G Sijbrands , R. C Pasternak , C Gagne , A. D Marais , C. M Ballantyne , J. L Isaacsohn , A. F Stalenhoef and J. J. P. Kastelein
  Background—

Until recently, patients with heterozygous familial hypercholesterolemia (HeFH) were considered the best subjects for the assessment of changes in carotid intima-media thickness (cIMT) in randomized intervention trials. Our aims were to investigate whether contemporary statin-treated HeFH patients still show accelerated cIMT increase and to assess the impact of statin treatment, before and after random assignment, on atherosclerosis progression.

Methods and Results—

We retrospectively evaluated cIMT change, and prior statin treatment and postbaseline LDL-C change as predictors of cIMT change, in 1513 HeFH patients who were randomly assigned to the statin arms of the early ASAP and more recent RADIANCE 1, CAPTIVATE, and ENHANCE studies. In the 3 recent studies combined, mean cIMT increased at only 33%of the rate of the simvastatin-treated patients in the ASAP study (0.014 mm/2 years [95% confidence interval, –0.0003–0.028] versus 0.041 mm/2 years [95% confidence interval, 0.020–0.061]; P<0.05). Patients whose statin therapy could be intensified, as evidenced by an LDL-C decrease after the initiation of on-trial statin therapy, showed cIMT decrease in the first 6 to 12 months and a much lower cIMT increase measured over the full 2 years. In line with this, previously statin-naive HeFH patients showed a lower overall cIMT increase.

Conclusions—

Over the years, intensification of statin therapy in HeFH patients has resulted in an impressive decrease in carotid atherosclerosis progression. In studies that assess other antiatherosclerotic modalities, statin therapy may still induce rapid changes in cIMT. For future cIMT studies, our analyses suggest that patient populations other than intensively pretreated HeFH patients should be selected and that the statin regimen should not be changed on study initiation.

  R Duivenvoorden , E VanBavel , E de Groot , E. S. G Stroes , J. A Disselhorst , B. A Hutten , J. S Lameris , J. J. P Kastelein and A. J. Nederveen
  Background—

Low endothelial shear stress (ESS) elicits endothelial dysfunction. However, the relationship between ESS and arterial remodeling and arterial stiffness is unknown in humans. We developed a 3.0-T MRI protocol to evaluate the contribution of ESS to arterial remodeling and stiffness.

Methods and Results—

Fifteen young (aged 26±3 years) and 15 older (aged 57±3 years) healthy volunteers as well as 15 patients with cardiovascular disease (aged 63±10 years) were enrolled. Phase-contrast MRI of the common carotid arteries was used to derive ESS data from the spatial velocity gradients close to the arterial wall. ESS measurements were performed on 3 occasions and showed excellent reproducibility (intraclass correlation coefficient, 0.79). Multiple linear regression analysis accounting for age and blood pressure revealed that ESS was an independent predictor of the following response variables: carotid wall thickness (regression coefficient [b], –0.19 mm2 per N/m2; P=0.02), lumen area (b, –15.5 mm2 per N/m2; P<0.001), and vessel size (b, –24.0 mm2 per N/m2; P<0.001). Segments of the artery wall exposed to lower ESS were significantly thicker than segments exposed to higher ESS within the same artery (P=0.009). Furthermore, ESS was associated with arterial compliance, accounting for age, blood pressure, and wall thickness (b, –0.003 mm2/mm Hg per N/m2; P=0.04).

Conclusions—

Our carotid MRI data show that ESS is an important determinant of arterial remodeling and arterial stiffness in humans. The data warrant further studies to evaluate use of carotid ESS as a noninvasive tool to improve the understanding of individual cardiovascular disease risk and to assess novel drug therapies in cardiovascular disease prevention.

 
 
 
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