Your cardiovascular genetic risk profile extends far beyond cholesterol levels. And much of it won't appear on a standard lipid panel.
Lipoprotein(a), the 9p21 locus, endothelial nitric oxide, statin pharmacogenomics, thrombophilia, and hereditary hemochromatosis. 21 variants across the cardiovascular system.
The Biology
The most dangerous cardiovascular risk factors are often the ones routine bloodwork misses. Lipoprotein(a). An LDL-like particle that causes atherosclerosis through a cholesterol-independent mechanism. Is almost entirely genetically determined and is not measured in standard lipid panels. The 9p21 chromosomal locus confers independent coronary artery disease risk through arterial biology pathways that statins and dietary intervention cannot reach. Your endothelial nitric oxide production, statin metabolism, and thrombosis risk all have significant genetic components that clinical guidelines increasingly recognize as actionable.
What Varia Analyzes
21 variants covering Lp(a) genetic architecture (rs10455872, rs3798220), PCSK9 loss-of-function status, independent CAD risk at the 9p21 locus (rs1333049, rs10757278), NOS3 endothelial function (rs1799983, rs2070744), SLCO1B1 statin pharmacogenomics (rs4149056), VKORC1 warfarin sensitivity (rs9923231), FADS1 omega-3 conversion efficiency (rs174537), thrombophilia risk (Factor V Leiden rs6025, Prothrombin G20210A rs1799963), and hereditary hemochromatosis (HFE C282Y rs1799945 and H63D rs1800562). One of the most common and most treatable serious genetic conditions in people of Northern European descent.
Why It Matters
The SLCO1B1 finding alone may be the most immediately actionable result in your entire report if you are on or considering statin therapy. CPIC clinical guidelines specifically address statin prescribing based on this variant. The Lp(a) findings identify a cardiovascular risk factor that cannot be modified by lifestyle or statins and is currently the focus of novel RNA-based therapeutic development. The HFE findings, if positive for C282Y homozygosity, represent one of the clearest examples of a serious, common condition that is entirely manageable when detected early through regular phlebotomy.
Key sources
- Clarke R, et al. Genetic variants associated with Lp(a) lipoprotein level and coronary disease. N Engl J Med. 2009.
- Cohen JC, et al. Sequence variations in PCSK9, low LDL, and protection against coronary heart disease. N Engl J Med. 2006.
- Helgadottir A, et al. A common variant on chromosome 9p21 affects the risk of myocardial infarction. Science. 2007.
- SEARCH Collaborative Group. SLCO1B1 variants and statin-induced myopathy. A genomewide study. N Engl J Med. 2008.
- Feder JN, et al. A novel MHC class I-like gene is mutated in patients with hereditary haemochromatosis. Nat Genet. 1996.