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MI-GENES: Disclosure of genetic risk for CVD linked with statin initiation, reduced LDL
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ORLANDO, Fla. — Patients whose risk for CVD was disclosed on the basis of genetic risk factors plus conventional risk factors were more likely to lower their LDL than those whose risk was disclosed on the basis of conventional risk factors alone, according to a study presented at the American Heart Association Scientific Sessions.
The LDL lowering was driven by increased statin prescriptions as opposed to changes in fat intake or physical activity, and was most pronounced in people who learned they have high genetic risk for CVD, Iftikhar J. Kullo, MD, professor of medicine, College of Medicine, Consultant Division of Cardiovascular Diseases, Mayo Clinic, said during a press conference.
Iftikhar J. Kullo
Kullo and colleagues investigated whether disclosing genetic risk for CHD based on 28 variants not related to BP or lipids would lower LDL.
The study included 207 adults (mean age, 59 years; 48% men) who were not using a statin and had odds of 5% to 20% for developing CHD within 10 years. The researchers randomly assigned participants to receive a conventional 10-year risk score for CHD or to receive the conventional score plus genetic risk information.
The primary outcome was LDL at 6 months after disclosure of risk information.
At 6 months, those who received genetic risk information had lower LDL (P = .04) and greater reduction in LDL (P = .03) compared with those who received a conventional risk score alone, according to Kullo. The effect was more pronounced compared with controls in those who learned they had a high genetic risk for CHD (LDL level, P = .02; LDL change over time, P = .007), he said.
The researchers reported no differences between the groups in fat intake or physical activity level and no significant change in anxiety score, according to Kullo.
Rather, he said, the results were almost entirely driven by new statin prescriptions “as a result of shared decision-making.” Forty percent of the genetic risk group had a statin prescribed during the study period compared with 22% of controls, he noted.
“The take-home points for our study are that genetic risk information for [CHD], which is the leading cause of death in this country, can be effectively incorporated in the electronic health record and used at the point of care to guide drug therapy,” Kullo said. “Such a disclosure led to lower LDL levels, more so in those at higher genetic risk. Our study exemplifies precision medicine and warrants further investigation of the clinical utility of genetic risk assessment for [CHD] prevention.” – by Erik Swain
Reference:
Kullo IJ, et al. Late-Breaking Clinical Trials 2. Presented at: American Heart Association Scientific Sessions; Nov. 7-11, 2015; Orlando, Fla.
Disclosure: Kullo reports no relevant financial disclosures.
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Robert Roberts, MD, FRSC, FRCPC, MACC, LLD (Hon.)
This study used the same genetic risk factors as the study published in The Lancet in March, which is the only other study applying genetic risk scores to outcomes (Mega JL, et al. Lancet. 2015;doi:10.1016/S0140-6736(14)61730-X). That was a retrospective study, but this is the first prospective study comparing genetic risk with conventional risk, again showing that genetic risk not only further stratifies independent of known risk factors, but also predicts the response to statins. This is a major step forward in the beginning of what I think will be the new generation of personalized medicine and treating on the basis of one’s genetic risk.
I think this is a landmark study. Since it only involves about 200 individuals, it will need confirmation in a larger sample size. But in many ways, showing such a statistically different effect in such a small sample size is further confirmation of the larger Lancet study, in a prospective manner. This will be a major finding and will certainly enhance the clinical application of genetic risk as a means of both detecting and predisposing to the disease, as well as treating it.
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