* Study highlights Lp-PLA2 enzyme link to heart disease
* Link may play similar role to blood pressure, cholesterol
* Glaxo developing darapladib drug to target Lp-PLA2
(Adds comment from British Heart Foundation)
By Kate Kelland
LONDON, April 30 (Reuters) - A way of fighting heart disease being pioneered by GlaxoSmithKline (GSK.L) won a potential boost on Friday from a scientific study that stressed the significance of an artery-clogging enzyme.
A study published in The Lancet medical journal suggests that the enzyme, known as lipoprotein-associated phospholipase A2, or Lp-PLA2, plays as much of a role in the risk of heart disease as high blood pressure and bad cholesterol.
Alex Thompson and John Danesh of Cambridge University, who conducted the research, said their findings would sharpen focus on an experimental drug called darapladib being developed by Glaxo and currently being studied in two large-scale clinical trials involving 27,000 patients worldwide.
“This reinforces interest in this enzyme, and reinforces the need to see the results from these clinical trials,” Thompson said in a telephone interview.
Results of the trials are expected between 2012 and 2014.
Coronary heart disease is the leading cause of death worldwide, responsible for around 7 million deaths a year.
Smoking, diabetes, high blood pressure and high levels of “bad” cholesterol known as LDL are known to cause heart disease, but they do not entirely explain its incidence, so scientists and drug companies have been investigating other links.
Glaxo discovered darapladib through the use of gene technology from Human Genome Sciences HGSI.O, which has an agreement with Glaxo to receive clinical development milestone and royalty payments for such compounds.
It is the first in a new class of drugs targeting Lp-PLA2 and is designed to offer something beyond the hugely successful class of cholesterol-lowering statin drugs like Pfizer’s (PFE.N) Lipitor and AstraZeneca’s (AZN.L) Crestor.
Darapladib seeks to cut the risk of artery-clogging plaques rupturing, blocking blood vessels and triggering heart attacks.
Peter Weissberg, medical director of the British Heart Foundation charity, said he hoped Friday’s study would stimulate more research into other drugs that could reduce Lp-PLA2 level.
“The acid test will then be to find out if such drugs reduce the risk of heart attacks and strokes in large clinical trials,” he said. “It will be some time yet before we have the answers.” Thompson and Danesh looked at links between Lp-PLA2 and risk of heart disease, stroke and death in almost 80,000 people in 32 previous studies.
They found that higher blood levels of Lp-PLA2 were associated with increased risk. For heart disease, the size of the increased risk was similar to that from higher blood pressure or bad cholesterol, they said.
But they said their analysis, which was mostly of data for people in North America and Europe, also showed weaker than expected links between heart disease and blood pressure and bad cholesterol.
“This enzyme in this study was as strongly associated with heart disease as blood pressure and cholesterol, but we need to be cautious in interpreting that because the associations of blood pressure and cholesterol were themselves substantially lower than we would have expected,” Thompson said.
He said this may be because many patients in the studies were already taking heart medications that would alter their blood pressure or cholesterol levels. (Editing by Elaine Hardcastle and Andrew Callus)