Meeting News Coverage

Genetics can be useful for CV risk assessment

NEW ORLEANS — Genetics can refine risk levels for CAD and identify individuals at high risk earlier than conventional risk factors, an expert said at the National Lipid Association Scientific Sessions. 

In many cases, the risk that genetics can identify is independent of traditional risk factors, and the risk can be identified inexpensively, Nathan O. Stitziel, MD, PhD, assistant professor of medicine and genetics, director of the Center for Cardiovascular Genetics and assistant director of McDonnell Genome Institute at Washington University, St. Louis, said during a presentation.

Nathan O. Stitziel, MD

Nathan O. Stitziel

What that means, he said, is that genetic information might be able to help physicians determine who should receive preventive CV care before traditional CV risk factors manifest. Certain individuals may benefit from being started on therapy at a much younger age than current guidelines recommend.

“The top 20% of the population [in terms of genetic CV risk] is at about a 70% increased risk compared with the bottom 20% of the population,” he said.

Studies of single mutations known to be linked with increased risk for CAD have not yielded much predictive value beyond traditional risk factors. However, according to Stitziel, studies of multiple such mutations have the potential to identify certain individuals at high risk for CAD who would have been missed had only clinical risk factors been considered.

Of the known genes and mutations associated with increased risk for CAD, one-third are linked with conventional risk factors such as lipids and BP, but the other two-thirds are not, he said.

“This means there is a whole lot that we still don’t understand” about the relationship between genetics and CAD, he said.

A study of the placebo arms of four statin therapy trials (Mega JL, et al. Lancet. 2015;doi:10.1016/S0140-6736(14)61730-X) demonstrated that genetic risk scores significantly stratified CAD risk even when adjusted for traditional risk factors (HR for intermediate-risk vs. low-risk = 1.34; 95% CI, 1.22-1.47; HR for high-risk vs. low risk = 1.72; 95% CI, 1.55-1.92).

Individuals at high genetic risk for CHD appear to derive greater benefit from statin therapy than those at low genetic risk, Stitziel said. He cited an analysis of the ASCOT trial, in which the number needed to treat to prevent one event was 100 in those with low genetic risk, but 33 in those with high genetic risk.

“Hopefully in the future, we will incorporate this information into allocation of preventive therapies,” he said. – by Erik Swain

Reference:

Stitziel N. Human Genetics and CV Risk Assessment. Presented at: National Lipid Association Scientific Sessions; May 19-22, 2016; New Orleans.
Disclosure: Stitziel reports receiving grant support from AstraZeneca and consulting for Aegerion.

NEW ORLEANS — Genetics can refine risk levels for CAD and identify individuals at high risk earlier than conventional risk factors, an expert said at the National Lipid Association Scientific Sessions. 

In many cases, the risk that genetics can identify is independent of traditional risk factors, and the risk can be identified inexpensively, Nathan O. Stitziel, MD, PhD, assistant professor of medicine and genetics, director of the Center for Cardiovascular Genetics and assistant director of McDonnell Genome Institute at Washington University, St. Louis, said during a presentation.

Nathan O. Stitziel, MD

Nathan O. Stitziel

What that means, he said, is that genetic information might be able to help physicians determine who should receive preventive CV care before traditional CV risk factors manifest. Certain individuals may benefit from being started on therapy at a much younger age than current guidelines recommend.

“The top 20% of the population [in terms of genetic CV risk] is at about a 70% increased risk compared with the bottom 20% of the population,” he said.

Studies of single mutations known to be linked with increased risk for CAD have not yielded much predictive value beyond traditional risk factors. However, according to Stitziel, studies of multiple such mutations have the potential to identify certain individuals at high risk for CAD who would have been missed had only clinical risk factors been considered.

Of the known genes and mutations associated with increased risk for CAD, one-third are linked with conventional risk factors such as lipids and BP, but the other two-thirds are not, he said.

“This means there is a whole lot that we still don’t understand” about the relationship between genetics and CAD, he said.

A study of the placebo arms of four statin therapy trials (Mega JL, et al. Lancet. 2015;doi:10.1016/S0140-6736(14)61730-X) demonstrated that genetic risk scores significantly stratified CAD risk even when adjusted for traditional risk factors (HR for intermediate-risk vs. low-risk = 1.34; 95% CI, 1.22-1.47; HR for high-risk vs. low risk = 1.72; 95% CI, 1.55-1.92).

Individuals at high genetic risk for CHD appear to derive greater benefit from statin therapy than those at low genetic risk, Stitziel said. He cited an analysis of the ASCOT trial, in which the number needed to treat to prevent one event was 100 in those with low genetic risk, but 33 in those with high genetic risk.

“Hopefully in the future, we will incorporate this information into allocation of preventive therapies,” he said. – by Erik Swain

Reference:

Stitziel N. Human Genetics and CV Risk Assessment. Presented at: National Lipid Association Scientific Sessions; May 19-22, 2016; New Orleans.
Disclosure: Stitziel reports receiving grant support from AstraZeneca and consulting for Aegerion.

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