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DD ACE gene polymorphism is associated with increased coronary artery endothelial dysfunction: the PREFACE trial
  1. H J G H Mulder1,
  2. P P van Geel2,
  3. M J Schalij1,
  4. W H van Gilst2,
  5. A H Zwinderman3,
  6. A V G Bruschke1
  1. 1Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands
  2. 2Department of Clinical Pharmacology, University Hospital Groningen, Groningen, The Netherlands
  3. 3Department of Medical Statistics, Leiden University, Leiden, The Netherlands
  1. Correspondence to:
    Dr Han JGH Mulder, Department of Cardiology, Leiden University Medical Center, Albinusdreef 2, PO Box 9600, 2300 RC, Leiden, The Netherlands;

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Endothelial dysfunction is an early event in atherogenesis and is associated with the propensity to cause future cardiovascular events. The amelioration of endothelial dysfunction has been a research target for some years now, and success has been reported with, for example, the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors. Research has also identified the homozygous deletion (DD) subset of the angiotensin converting enzyme (ACE) insertion(I)/deletion(D) polymorphism to be associated with deteriorated endothelial function. The results, however, are conflicting. In a substudy of the PREFACE (pravastatin-related effects following angioplasty on coronary endothelium) trial1 we assessed ACE polymorphism, coronary endothelial function, and the influence of the HMG-CoA reductase inhibitor pravastatin.


PREFACE1 was a randomised, double blinded, placebo controlled, multicentre study designed to assess the effect of three months of treatment with pravastatin (40 mg, once daily) on the endothelial function of native and dilated coronary arteries in non-smoking, non-hypercholesterolaemic patients.

Coronary endothelium dependent vasomotion at three months was assessed by serial, two minute, intracoronary infusions of acetylcholine with the final intracoronary concentrations estimated to be 10-8, 10-7, and 10-6 M. Hereafter …

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