While cholesterol-lowering drugs have undoubtedly been a success for some people cholesterol does not decrease as much as it should. For others, cholesterol may decrease without reducing the risk of heart attack as much as doctors expect.
It is for this reason that the prospect of pharmacogenomics - the study of the interaction of an individual's genetic makeup and response to a drug, could become the solution to this potentially life-threatening problem.
A study published in the Journal of the American Medical Association could provide some of the answers. Researchers at Harvard Medical School found that patients with either one of two DNA mutations saw their cholesterol decrease by about 20 per cent less than other patients when they took the same cholesterol-lowering drug, Pravachol (pravastatin)
However, Paul Ridker, the Harvard cardiologist who headed up the study said that all these patients should still be taking cholesterol drugs and this latest discovery is a long way off from becoming a viable diagnostic test.
Ridker added: "The scope of these studies is very large and very complex. You do get a sense that pharmacogenomics might have a role."
Eric Topol, chairman of the Cleveland Clinic's department of cardiovascular medicine said: "There are a lot of people out there spending a hundred dollars a month on drugs and they're not going to benefit."
"This is a nice step forward for a principal that many of us have believed was just a matter of time."
Certainly in the future, such diagnostic tests may become a necessity as a whole new generation of cardiovascular drugs are under development. Pfizer, Merck, GlaxoSmithKline and Eli Lilly are all in the race to develop drugs that differentiate in their target.
The study focussed on evaluating systematically whether genetic variation influences response to pravastatin therapy.
The DNA of 1536 individuals were analysed for 148 single-nucleotide polymorphisms (SNPs) within 10 candidate genes related to lipid metabolism. Variation within these genes was then examined for associations with changes in lipid levels observed with pravastatin therapy during a 24-week period.
Researchers discovered that individuals heterozygous (carrying two different alleles of a gene) for a genetic variant in the HMG-CoA reductase gene (the target enzyme that is inhibited by pravastatin) experienced significantly smaller reductions in cholesterol when treated with pravastatin.
The absolute difference in total cholesterol reduction associated with the HMG-CoA reductase genotype was 9 mg/dL (0.23mmol/L), a figure large enough to affect health on a population basis.
The data is sure to have considerable pathophysiological interest and provides strong clinical evidence towards "personalised medicine" and the use of genetic screening to target certain therapies.
However the researchers were adamant that further research must be carried out in order to determine whether this difference can be offset by dose adjustment or the choice of an alternative nonstatin lipid-lowering therapy.