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ORLANDO, Fla. — Disclosure of information regarding genetic risk for coronary heart disease (CHD) may result in greater statin initiation and lower LDL cholesterol levels in intermediate- to high-risk patients, according to data presented at the American Heart Association Scientific Sessions.
Although genomic association studies have identified genetic variants linked to the development of heart disease, questions persist about how to use this information to improve clinical outcomes, Iftikhar J. Kullo, MD, of the Mayo Clinic in Rochester, Minnesota, said during a press conference.
To learn more, Dr Kullo and colleagues evaluated whether disclosure of genetic risk for CHD to patients would affect LDL cholesterol at 6 months.
For the MI-GENES (Myocardial Infarction Genes) study, the researchers created a genetic risk score for CHD derived from 28 genetic variants not related to blood pressure or lipids. They then evaluated whether incorporating this score into conventional risk estimates and disclosing this information to patients would lead to lower LDL cholesterol levels.
The study included 203 patients (mean age, 59.4 years; 49% men) who were randomly assigned to receive information about their conventional 10-year risk for CHD (n=100) or a CHD risk estimate that included genetic risk information in addition to conventional risk factors (n=103).
Patients were characterized as having a high or low/average genetic risk, and this information was disclosed via a genetic counselor. Afterwards, patients met with physicians to engage in shared decision making about whether to initiate statin therapy.
At 3 and 6 months, LDL cholesterol levels were checked and patients were asked about dietary fat intake, physical activity, anxiety levels, and statin therapy.
LDL cholesterol at 6 months served as the primary end point.
Results revealed decreases in LDL cholesterol at 6 months in both study groups. Patients who received genetic risk information, however, had lower LDL cholesterol levels — about 10 mg/dL lower — than those who did not at this time point (P=.04). Additionally, those who had a high genetic risk score achieved greater reductions in LDL cholesterol — about 13 mg/dL — compared with those who did not receive genetic risk information (P=.02).
There was also a trend toward the genetic risk group achieving greater reductions in LDL cholesterol than the conventional risk group over the entire study period (P=.03). The same was true for those with high genetic risk vs those who did not receive genetic risk information (P=.007).
Statin initiation was more frequent in the genetic risk group (40% vs 22%).
“We saw that the decrease in LDL cholesterol actually mirrored the frequency of initiation of statins … This difference in statin initiation accounted for most of the difference in LDL cholesterol levels,” said Dr Kullo.
Data denoted no significant differences at 6 months in dietary fat intake or physical activity between the study groups. In addition, Dr Kullo noted, there was no change in anxiety levels as a result of disclosing genetic risk to patients.
“The take-home points from our study are the genetic risk information for coronary heart disease, 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,” Dr Kullo concluded.
“Such a disclosure led to lower LDL cholesterol levels, more so in those at higher genetic risk, and our study exemplifies precision medicine and motivates further investigation into the clinical utility of genetic risk assessment for coronary heart disease prevention.”
Reference
- Kullo I. LBCT.02 – Decreasing the Global Burden of Disease: Breakthroughs in Prevention. The Effect of Disclosing Genomic Risk of Coronary Heart Disease on Low-density Lipoprotein Cholesterol Levels: The Myocardial Infarction Genes (MI-GENES) Study. Presented at the American Heart Association Scientific Sessions; November 7-11, 2015; Orlando, FL.
