For years, scientists suspected that heart disease had a genetic component, making observations like people with a parent who developed coronary artery disease before the age of 55 faced a much greater risk of becoming afflicted with it themselves. Now the evidence written in our genes is coming to light on an almost daily basis. Here are some of the latest headlines:
Genes have been linked to high blood pressure. Poring through the genetic data of about 30,000 people from the United States, Sweden, and Finland, researchers just announced in the journal Nature that people with two particular variants of genes called NFPA and NFPB, respectively, were anywhere from 11 percent to 18 percent more likely to develop hypertension. The genes in question produce proteins that are responsible for the relaxation of the blood vessels and the excretion of dietary salt; people with variations on these genes have lower levels of these proteins and therefore face a greater risk of high blood pressure, which is a major cause of heart disease.
The genetic locus associated with triglyceride levels has been mapped. In April 2008, scientists claimed they had located a region on chromosome 1 containing genes that can control triglyceride levels. Many factors contribute to elevated triglyceride levels—smoking, eating foods high in fat and cholesterol, forsaking physical activity—but genetic variation accounts for 40 percent of cases in which this form of dietary fat fails to accumulate on arterial walls, increasing the risk of atherosclerosis and, as a consequence, heart disease. By mapping this region, scientists may be able to develop drugs that can selectively coax these genes to decrease triglyceride levels.
Stopping heart failure with gene therapy is now in trials. Patients at New York Presbyterian Hospital/Columbia University Medical Center are currently undergoing a procedure in which a cardiac catheter injects a specially engineered gene. This gene will stimulate the production of an enzyme that will help the heart pump more efficiently. Among the 5 million Americans who suffer from heart failure, the test subjects have a depressed level of SERCA2a. If the therapy proves effective, it will provide an attractive alternative to heart transplant surgery.
