Outcome following percutaneous coronary intervention: not, so far, in our genes

The contribution of genes to outcome following percutaneous coronary intervention appears to be somewhat limited 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 matched controls. A very large number of single nucleotide polymorphisms can now be easily typed by using the polymerase chain reaction (PCR) to amplify the genetic segment of interest, followed by a variety of techniques to identify the different alleles. As has been shown for a number of genetic polymorphisms hypothesised to contribute to the risk of coronary heart disease and other “complex” diseases, reliable results regarding the presence or absence of such small effects require individual studies or meta-analyses of thousands of cases.1 A variety of polymorphisms have been typed in a large number of studies of patients undergoing PCI, most …