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Genetic risk scores failed to predict cardiac events

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Two risk scores based on genetic markers for CVD were unable to distinguish between women at risk for CV events and those not at risk, and neither remained associated with CVD incident after adjusting for traditional risk factors, study results indicated.

“While the importance of genetic data in understanding biology and etiology is unchallenged, we did not find evidence in this study of more than 19,000 women to incorporate the current body of known genetic markers into formal clinical tools for [CV] risk assessment,” the researchers wrote.

The researchers analyzed data from 19,313 white women who participated in the Women’s Genome Health Study. The primary outcome measured during the median 12-year follow-up was a composite of MI, stroke, CV death and revascularization procedures.

Two genetic risk scores were evaluated. One consisted of 101 single nucleotide polymorphisms that were previously associated with CVD or known risk factors, including high LDL-cholesterol and hypertension. The second consisted of 12 single nucleotide polymorphisms associated only with incident CVD.

During the follow-up period, participants experienced 777 CVD events, including 199 MI, 203 strokes, 63 CV deaths and 312 revascularizations. After adjusting for age, the HR for CVD was 1.02 per risk allele included in the genetic risk score (95% CI, 1.00-1.03; P=.006), for a corresponding absolute CVD risk of 3% during a 10-year period for those in the lowest tertile of genetic risk (73-99 risk alleles) and a corresponding absolute CVD risk of 3.7% for those in the highest tertile (106-125 alleles). But after adjusting for traditional CV risk factors, the genetic risk score did not improve discrimination or reclassification per risk-associated allele (HR=1.00; 95% CI, 0.99-1.01). However, self-reported family history remained associated with incident CVD.

Although “genome-wide testing is increasingly available and marketed to the general public,” the researchers wrote, they found “no clinical utility in a multilocus panel of [single nucleotide polymorphisms] for [CV] risk based on the best available literature.”

Paynter NP. JAMA. 2010;303:631-637.

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