More than 170 genes have been linked to an increased risk for heart disease. But a team of international researchers has just discovered a gene defect that actually cuts the risk for heart attack in half.

The findings, led by the German Heart Center at the Technical University of Munich, indicate people with the gene mutation are 50 percent less likely to have a heart attack — paving the way to new medications that could effectively shut down the gene and reduce a person’s cardiovascular risks.

"This discovery makes it considerably easier to develop new medications that simulate the effect of this mutation," said lead researcher Dr. Heribert Schunkert, a cardiologist and medical director of the German Heart Center. "This gives follow-on research aiming at reducing heart attacks in the future a concrete goal."

For the study, the scientists analyzed 13,000 different genes from 200,000 heart attack patients and healthy individuals to identify links between gene mutations and risk for coronary artery disease.

For a number of genes, the researchers registered a correlation — including the so-called ANGPTL4 (angiopoietin-like 4) gene. In addition, people with the mutated ANGPTL4 gene had significantly lower triglyceride levels in their blood.

Normally, ANGPTL4 causes blood fats to rise, increasing heart attack risk. But individuals with defects in the gene have lower levels of the blood fat — and lower heart attack risks. As a result, the researchers said disabling the function of this gene through medication could cause triglyceride levels, and heart risks, to drop significantly.

"Based on our results, medications now need to be developed that neutralize the effect of the ANGPTL4 gene, thereby reducing the risk of a heart attack," said Schunkert. "Other researchers have already done this successfully in animal tests. They drastically reduced the blood fat levels in monkeys that received a neutralizing antibody against ANGPTL4. This feeds the hope that antibody preparations with a similar effect can soon be used successfully in humans."