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Study Suggests Genetic Risk of Heart Disease May Inform Statin Use

NEW YORK (GenomeWeb) – A new Lancet study suggests genetic profiling may hold the key to identifying groups of individuals most apt to benefit from statin therapy.

Researchers from the US, Sweden, and the UK brought together genetic and other data for tens of thousands of individuals enrolled in five cohort or randomized trial studies. They then looked at how coronary heart disease events in the individuals varied depending on statin therapy and genetic profiles, using information from more than two-dozen variants previously implicated in coronary heart disease.

As it turned out, the apparent coronary heart disease prevention benefit associated with statin therapy differed alongside genetic risk of such conditions: statin therapy was linked to especially pronounced declines in relative and absolute risks of heart disease in those carrying coronary heart disease-prone genetic variant patterns.

"[P]atients with a high genetic risk score appear to benefit more from statin therapy because they're starting at a higher baseline risk, even controlling for all the clinical measures we routinely examine," co-first author Nathan Stitziel, a cardiologist and human geneticist at Washington University, said in a statement.

The team was interested in exploring ways of more carefully tailoring statin prescriptions. Ideally, it hopes to find ways to balance the potential disease reduction attributed to cholesterol-lowering drugs with personalized treatment that prevents overuse of the drugs.

"Some have said we should be treating more people [with statins], while others say we need to treat fewer," Stitziel explained in a statement. "[A]nother approach is to identify people at high risk and preferentially prescribe statin therapy to those individuals."

With that in mind, the researchers looked at genetic and coronary heart disease data for 48,421 individuals enrolled through the community-based Malmo Diet and Cancer Study, the JUPITER or ASCOT primary prevention randomized control trials, or through two secondary prevention-focused randomized trials known as CARE and PROVE IT-TIMI 22.

Using information at 27 genetic variants, they stratified the individuals genetically into low-, intermediate-, and high-risk groups for coronary heart disease. While traditional risk factors such as high-density lipoprotein and low-density lipoprotein cholesterol levels were measured and used to adjust genetic risk models, the analysis largely hinged on variant profiles.

Across the combined group, individuals experienced 3,477 coronary heart disease events, the team noted. Such events were more common amongst those in the highest genetic risk group, as expected.

When researchers folded in data on statin treatment for participants of the primary and secondary prevention trials, they found that the drug was associated with a 48 percent dip in coronary heart disease risk in those deemed at high risk genetically.

The team estimated that 25 genetically high-risk participants from the JUPITER trial — or 20 high-risk participants from the ASCOT trial — would have to be treated for a decade to prevent one coronary heart disease event. For the intermediate- and low-risk groups, that jumped to between 42 and 66 individuals treated over the same time frame for every coronary event prevented.

Relatively speaking, statin therapy was linked to a 13 percent risk reduction in the group carrying the fewest genetic risk factors, and a 29 percent decline in events for those using statins in the intermediate genetic group.

"The panel of genetic markers we analyzed provide[d] a way to identify the patients starting out at higher baseline risk," Stitziel said, noting that this statin effect stratification "appears to be independent of cholesterol levels and other traditional markers of heart disease that we typically use to estimate risk."