That's because the well-known risk factors for atherosclerosis, such as high cholesterol, smoking, diabetes and high blood pressure, appear to account for only about half the variation of rates of coronary disease observed in human populations. The balance of variation is likely explained by a combination of inherited variants in or near genes that are important in the pathogenesis of disease in addition to other unrecognized, adverse environmental exposures.
"Using genetics to help improve our ability to predict coronary disease is particularly important because we have several different classes of drugs at our disposal that can substantially reduce the risk of heart attacks" said Assimes. "But we still need to be careful about what we put into practice and not get carried away too quickly. We know from previous experience that a positive association between a genetic variant and a common disease, such as coronary disease, needs to be consistently observed in many human population studies before it can be believed."
In fact, Quertermous points out that even for the roughly one dozen genetic markers that have been successfully validated to date, evidence to support their use in clinical practice is lacking. However, this situation will likely change in the near future as researchers reliably identify more genetic markers.
The data collections used in this study were supported by more than 30 institutions including government and nonprofit agencies and the following companies: Astra Zeneca, Berlin Chemie, Boots Healthcare, deCODE genetics, Glaxo-Smith-Kline, McNeil Pharma (former Woelm Pharma), MSD Sharp & Dohme and Pfizer.
|Contact: Susan Ipaktchian|
Stanford University Medical Center