© 2003 by BMJ Publishing Group & British Cardiac Society
EDITORIAL
Outcome following percutaneous coronary intervention: not, so far, in our genes
Correspondence to:
Correspondence to:
Dr Bernard Keavney, Institute of Human Genetics, Central Parkway, Newcastle-upon-Tyne NE1 3BZ, UK;
b.d.keavney@ncl.ac.uk
The contribution of genes to outcome following percutaneous coronary intervention appears to be somewhat limited
Keywords: percutaneous coronary intervention
Abbreviations: ACE, angiotensin I converting enzyme; I/D, insertion/deletion; MACE, major adverse coronary events; PCI, percutaneous coronary intervention; PCR, polymerase chain reaction
| The first 150 words of the full text of this article appear below. |
Certain well recognised clinical and angiographic factors predict a poor outcome following percutaneous coronary intervention (PCI). The majority of such poor outcomes, particularly after elective PCI, are caused by restenosis requiring re-intervention. Restenosis has been fitted, somewhat uncomfortably, into the standard multifactorial model of complex disease in which genetic susceptibility, combined with environmental exposure, determines disease risk. The basic tenet of this model is almost uniquely untestable for restenosis, since classical genetic epidemiologic studies of twins or extended families to establish the heritability of the phenotype are not practical. However, given the known importance of anatomical factors, procedural factors and diabetes in determining the risk of restenosis, any genetic effect seems a priori likely to be small. Possible genetic contributions to outcome after PCI can be relatively simply tested by comparing genotype frequencies at polymorphisms of candidate genes between cases—for example, of major adverse coronary events (MACE) after PCI—and suitably
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