The annual meeting of the American College of Cardiology held this week in Chicago featured a number of pharmacogenomically guided studies related to treatments for cardiovascular disease.

The following is a roundup of some of the meeting's pharmacogenomics highlights.

Lack of Association in SLCO1B1 Polymorphisms and Clinical Myalgia after Crestor Treatment

Researchers led by Jacqueline Suk Danik from Brigham and Women's Hospital investigated whether individuals who are carriers of SCLCOB1 rs4363657C and rs4149056C have increased incidence of myopathic complaints when taking AstraZeneca's Crestor (rosuvastatin) compared to non-carriers. In past studies, researchers have seen a similar influence in patients taking Merck's Zocor (simvastatin).

Danik et al. retrospectively genotyped patients receiving Crestor in the JUPITER trial. The original study randomized 4,400 people without heart disease or diabetes to Crestor or placebo. "Among those allocated to active rosuvastatin, there was no difference in [the] rate of myalgia among carriers of the rs4363657C allele or the rs4149056C allele when compared to non-carriers," the researchers found. The researchers had similar findings even after expanding their definition of myalgia to include complaints of muscle weakness, stiffness, or pain.

"In contrast to data for simvastatin, there appears to be no increased risk of myalgia among users of rosuvastatin who carry the rs4363657C allele or the rs4149056C allele in the SLCO1B1 gene," Danik et al. concluded.

AstraZeneca, the National Cancer Institute, and the National Heart, Lung, and Blood Institute provided funding for this study.

Impact of CYP2C19 and CYP3A5 Genotypes in Patients Undergoing Stent Procedures, Treated with Maintenance Dose Plavix

Studies have shown that patients with high platelet reactivity after being treated with Bristol-Myers Squibb's Plavix (clopidogrel) may be at increased risk of stent thrombosis after undergoing a stent procedure. Researchers led by Tadasuke Chitose of Kumamoto University examined CYP2C19 and CYP3A5 genotypes, as well as platelet aggregation, in 62 patients. Platelet reactivity was measured twice, after patients received a loading dose (300 mg/day) of Plavix, and then after they received a maintenance dose (75 mg/day) of the drug.

In the study, 31 percent, 42 percent, and 27 percent of patients were extensive metabolizers, intermediate metabolizers, and poor metabolizers, respectively. After patients received 300 mg/day of Plavix, platelet reactivity was 4,069 +/-1,383; 4,407 +/-1,755; and 5,301 +/-807 AU*min in the extensive, intermediate, and poor metabolizer groups, respectively. After receiving the maintenance dose of Plavix, platelet reactivity levels were 2,948 +/-1,427; 3,068 +/-1,656; and 4,465 +/-1,557 AU*min in the extensive, intermediate, and poor metabolizer groups, respectively.

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PGx Highlights from American College of Cardiology Annual Meeting