According to a British study published Tuesday C -reactive protein, known as a key indicator of inflammation in the body and believed to be the cause of heart disease is not linked to development of the ailment.

The research published in the Journal of the American Medical Association said C-reactive protein (CRP), which has been a target for studies of treatment for coronary heart disease contrary to earlier beliefs, is not in fact directly involved in causing it.

C-reactive protein is secreted by the liver and signals tissue inflammation and a risk for heart attack or stroke.

Lead author Paul Elliott, a professor at Imperial College, London said, "Some researchers thought C-reactive protein would be a good molecule to target, as raised levels of this protein in the blood are associated with increased risk of coronary heart disease. However our research suggests that the association may not be causal, so attempts to target this protein to reduce the risk of the disease are unlikely to be fruitful."

The study conducted by Imperial College scientists and 12 other universities and institutes in Europe and North America examined a total of 28,112 people with the disease and 100,823 people without the disease.

They compared the genetic variations that play a role in the level of CRP with the prevalence of coronary heart disease in those that they studied and concluded that higher-than-normal levels of C-reactive protein were likely caused by tissue inflammation, and not a cause of the inflammation and resulting cardiovascular problems.

Dr. James Lemos of the University of Texas Southwestern Medical Center, who helped write a commentary in the journal about the studies said, "This study puts the nail in the coffin ... in the question about (C-reactive protein): does it cause cardiovascular disease?". It clearly does not, he said.

However the study did discover new genetic variations associated with coronary heart disease, Elliott added. "If confirmed in other studies, these might give clues to identify new targets to treat the disease," he said.

Researchers at Massachusetts General Hospital and Lund University in Malmo, Sweden in another study tested 5,000 Swedes for six potential biomarkers for heart disease and then monitored for up to 15 years. They found that although five of the six biomarkers -- including C-reactive protein -- were useful in predicting future cardiovascular problems such as heart attacks, they were not helpful in classifying patients' risk or determining changes in the course of treatment.

"That is the goal of these tests -- to pick up these individuals (at risk for heart attack)," Lemos said.

"Both as a clinician and as an investigator, I still think at some point we will figure out how to use multiple biomarkers to predict risk. I don't think this is a failed idea," he said.