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Articles by B. A Hutten
Total Records ( 2 ) for B. A Hutten
  A. Q Reuwer , M. T Twickler , B. A Hutten , F. W Molema , N. J Wareham , G. M Dallinga Thie , R. L Bogorad , V Goffin , M Smink Bol , J. J.P Kastelein , S. M Boekholdt and K. T. Khaw
 

Background— Prolactin is increasingly recognized to play a stimulatory role in the inflammatory response. Because inflammation is considered of crucial importance in the development of atherosclerosis, we aimed to evaluate whether prolactin levels are associated with the occurrence of coronary artery disease (CAD).

Methods and Results— We performed a nested case-control study in the prospective EPIC-Norfolk cohort. Cases were apparently healthy men and women, aged 45 to 79 years, who developed fatal or nonfatal CAD (n=882). Controls remained free of CAD (n=1490). Overall, systemic prolactin levels did not differ between cases and controls, and people in the highest prolactin tertile did not have a significantly increased risk of developing future CAD (in men, odds ratio, 1.21; 95% CI, 0.92 to 1.61; in women, odds ratio, 1.12; 95% CI, 0.76 to 1.64). However, in a separate immunohistochemical study, the presence of prolactin receptors could be demonstrated in postmortem human coronary artery plaques (preliminary data).

Conclusions— Elevated systemic prolactin levels do not predict CAD in the general population. However, prolactin receptors were found in human coronary artery plaques. This observation may indicate a role of prolactin within atherosclerotic plaques. More studies are needed to define the possible role of prolactin in atherosclerotic plaque development.

  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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