The scientists from many countries have together explored that a specific mutated gene can lower heart attack risk in half. It is estimated that around 170 genes associating to a greater danger for heart disease.
The discovery was made by an international research team lead by the Cardiologist Professor Heribert Schunkert, Medical Director of the German Heart Center at the Technical University of Munich (TUM). The findings indicate that people with a gene mutation may considerably 50 percent likely to have a heart attack.
“This discovery makes it considerably easier to develop new medications that simulate the effect of this mutation,” explains Prof. Schunkert. “This gives follow-on research aiming at reducing heart attacks in the future a concrete goal.”
In order to conduct this study in large scale, the researchers had to analyzed 13,000 diverse genes from 200,000 participants including people with heart attack and healthy individuals. Based on the results of analysis, they could discover correlations between gene mutations and threat for coronary artery disease.
There are a few of genes that the scientists recorded a link, consisting of the ANGPTL4 (Angiopoietin-like 4) gene. Otherwise, the triglyceride values in blood in people with the mutated ANGPTL4 gene are considerably lower than those who do not have this mutated gene.
“The blood fat triglyceride serves as an energy store for the body. However, as with LDL cholesterol, elevated values lead to an increased risk of cardiovascular disease. Low values, by contrast, lower the risk,” said Prof. Jeanette Erdmann, Director of the Institute of Integrative and Experimental Genomics at the University of Lubeck, and a collaborator on the work.
As Prof. Schunkert, the significance of triglycerides for human health so far has been underestimated: “For most patients the focus still lies on cholesterol. A differentiation is always made between the healthy HDL and the harmful LDL cholesterol variants. However, in the mean time we know that the HDL values always run inversely proportional to those of the triglycerides and that HDL itself actually tends to behave in a neutral manner.”
Until now, this study presents that the concentration of triglycerides in the blood are affected by both nutrition as well as predisposition and ANGPTL4 gene. “At the core of our data is the lipoprotein lipase (LPL) enzyme. It causes the decomposition of triglycerides in the blood,” said Prof. Erdmann.
ANGPTL4 gene typically causes higher blood fat level, which leads to a higher heart attack risk. The researchers, nevertheless, found out that individuals with inadequacies in the gene have lower levels of the blood fat, as well as lower heart attack threats. From this point, the researchers indicated that disabling the function of this gene through medication could significantly reduce triglyceride levels, and heart risks.
Prof. Shuinkert expected that the antibody preparations with a similar effect to the neutralizing antibody against ANGPTL4 in animals in order for blood fat reduction can soon be successfully used in humans.