Cardiac Risk Prediction Array - Simultaneous genotyping of 19 SNPs for a reliable CHD risk assessment

Coronary Heart Disease (CHD) is the leading cause of death in the developed world and its prevention is a core activity in general practice worldwide. Clinical guidelines from the Joint Cardiac Societies and NICE in the UK recommend that patients at greater than 20% risk of CHD in the next ten years should be classified as high risk and considered for intensive lifestyle intervention and lipid lowering therapy, primarily the prescription of statins.₁

Current CHD risk assessment tools based on common risk factors such as blood pressure and blood cholesterol levels have low predictive value.₂₋₅ Genome Wide Association Studies (GWAS) have been carried out to identify genetic variants associated with CHD. These studies have identified 18 variants (SNPs) as being associated with CHD. The presence of multiple ‘at risk’ alleles can increase the risk of developing CHD two fold or greater.₇

The Randox Cardiac Risk Prediction Array allows all 18 SNPs to be genotyped simultaneously. The genotype information is then put into an algorithm which weights each SNP and calculates a CHD genetic risk score. This score is combined with common risk factors and an overall CHD risk score is calculated. A SNP which can predict response to particular statin therapies is also included.

A further important SNP which can predict response to particular statin therapies has been included in the array. Individuals who are homozygous (frequency =0.13) for the risk allele are 17 times more likely to suffer from statin-induced myopathy when treated with high doses of simvastatin.₈ Identifying patients with a higher risk of suffering statin-induced myopathy would allow clinicians to make more informed decisions when prescribing lipid lowering therapies.

Key Benefits

  • Simultaneous genotyping of 18 SNPs and a statin therapy response SNP
  • Identifies patients genetically predisposed to statin-induced myopathy
  • Allows more accurate classification and preventative actions to be taken
  • Simple and rapid protocol allows patient sample to be genotyped in one day

References

  • Wood, D.A., Wray, R., Poulter, N., Williams, B., Kirby, M., Patel, V. et al JBS2: Joint British guidelines on prevention of cardiovascular disease in clinical practice. Heart 2005; 91(Suppl V): V1-52.
  • Assmann, G., Cullen, P. & Schulte, H. Simple scoring scheme for calculating the risk of acute coronary events based on the 10-year follow-up of the prospective cardiovascular Munster (PROCAM) Study. Circulation 2002;105, 310–315.
  • Sheridan S, Pignone M, Mulrow C. Framingham based tools to calculate the global risk of coronary heart disease: a systematic review of tools for clinicians. J Gen Intern Med 2003. 18(12):1039–1052.
  • Haq IU, Ramsay LE, Wallis EJ, Isles CG, Jackson PR. Population implication of lipid lowering for prevention of coronary heart disease: data from the 1995 Scottish health survey. Heart 2001;86: 289-95.
  • Expert panel on detection, evaluation and treatment of high blood cholesterol in adults. Executive summary of the third report of the national cholesterol education program (NCEP) expert panel on detection, evaluation and treatment of high blood cholesterol in adults (AdultTreatment Panel III). JAMA 2001;285:2486–2497.
  • Cooper, J. A., Miller, G. J. & Humphries, S. E. A comparison of the PROCAM and Framingham point scoring systems for estimation of individual risk of coronary heart disease in the Second Northwick Park Heart Study. Atherosclerosis 2005;181: 93–100.
  • Talmud PJ, Cooper JA, Palmen J, Lovering R, Drenos F, Hingorani AD, Humphries SE. Chromosome 9p21.3 coronary heart disease locus genotype and prospective risk of CHD in healthy middle-aged men. Clin Chem. 2008; 54: 467–474.
  • The SEARCH Collaborative Group. SLCO1B1 variants and statin-induced myopathy - A genomewide study. New Engl J Med 2008 359(8):789-799.