A health analytics tool for the detection of genetic polymorphisms associated with cardiovascular disease, hypertension, diabetes, insulin resistance, atrial fibrillation, stroke and dyslipidemia.
CardiaX aims to reduce the prevalence of heart disease and associated conditions by empowering patients and physicians with a vital resource for early risk detection and an enhanced focus on personalized primary prevention.
CardiaX is the largest collection of genetic mutations and serological tests that provides potential risks for heart, metabolic, and vascular conditions for individuals with the following risks:
- Family history of heart disease
- Uncontrolled hypertension
- History of cardiac events
- Diagnosed with metabolic syndrome
- Elevated inflammatory markers
- Increased medical risk for hypertension
Only healthcare providers licensed in their state may order laboratory testing.
CardiaX includes the following genetic SNPs (single nucleotide polymorphisms):
- ACE I/D
- Apo A1
- Apo A2
- Apo C3
CardiaX may be an appropriate test to run if you have or are suspected of having any of the following symptoms or conditions:
- Plaque rupture
- Coronary artery disease
- Myocardial infarction
- Diabetes mellitus
- Insulin resistance
- Venous thrombosis
- Atrial fibrillation
- Cardiovascular disease
- Congestive heart failure
- Ischemic stroke
- Endothelial dysfunction
CardiaX is the only genetic screening tool on the market that provides you with your predisposed risks based on advanced genetic markers.
Along with your CardiaX profile, you also get access to Vibrant’s Clinical Support Team of highly qualified clinical dietitians for advanced clinical interpretations and assistance in creating customized risk management plans in conjunction with your physician’s recommendations.
CardiaX can be performed from either a blood draw arranged through your medical provider or a cheek swab you can perform at home. Consult with your provider to determine which method they prefer.
When interpreting results, what does the “>” symbol signify? Example MTHFR 677 C>T?
For any gene that is Mendelian inherited, one allele is considered “wild type,” or normal (non-mutated), while a different allele is considered “mutant.” In genetic nomenclature, the “>” is used to signify which allele is wild. In the example of “MTHFR 677 C>T”, the C allele is wild/normal whereas T allele is mutated.
What do the terms homozygous and heterozygous mean in terms of these genetics?
The terms homozygous and heterozygous refer to the individual genotype or individual result and describe the extent of normalcy or mutation. There are three possible combinations for each gene:
- Homozygous wild type (no mutation; 2 copies of the normal allele)
- Heterozygous mutant (one copy of wild allele; one copy of mutated allele)
- Homozygous mutant (2 copies of a mutated allele)
Why do high risk genes on second page (summary) of the report look the same as the low risk genes towards the end of the report?
The genes observed on this report each have multiple alleles/SNPs. The overview on page 2 of the report show the alleles/SNPs that can denote the highest risks to health while the alleles/SNPs listed on page 10 towards the back of the report denote the lowest risk.
Do the genetics change once you make the recommended changes on the report?
No, genetics do not change, only expression of the genetics.
Dries DL, Victor RG, Rame JE, Cooper RS, Wu X, Zhu X, Leonard D, Ho SI, Wu Q, Post W, DraznerMH.Corin Gene Minor Allele Defined by 2 Missense Mutations Is Common in Blacks and Associated With High Blood Pressure and Hypertension.
The primary study sample was the Dallas Heart Study (DHS), a multistep probability-based sample of Dallas County residents 18 to 65 years of age which included over 3000 samples.
2 nonsynonymous, non-conservative single nucleotide polymorphisms (Q568P and T555I) were sequenced in near-complete linkage disequilibrium, thus describing a single minor I555 (P568) corin gene allele. The corin I555 (P568) allele remained independently associated with increased risk for prevalent hypertension (odds ratio, 1.63). The corin I555 (P568) allele also was associated with higher systolic blood pressure in subjects not using antihypertensive medication in unadjusted (133.7 ± 20.7 versus 129.4 ± 17.4 mm Hg) and adjusted (132.5 ± 1.6 versus 128.9 ± 0.6 mm Hg) analyses.
J. Eduardo Rame, S. William Tam, Dennis McNamara, Manuel Worcel, Michael L. Sabolinski, Alan Wu, and Daniel L. Dries. Dysfunctional Corin I555 (P568) Allele is Associated with Impaired BNP Processing and Adverse Outcomes in African-Americans with Systolic Heart Failure: Results from the Genetic Risk Assessment in Heart Failure A-HeFT Sub-Study.
This is a retrospective study of 354 subjects in the African-America Heart Failure Trial (A-HeFT) Genetic Risk Assessment in Heart Failure (GRAHF) sub-study. It was found that corin I555 (P568) allele was associated with increased risk for death or heart failure hospitalization Risk Ratio of 3.49.
Takeuchi F, Yamamoto K, Katsuya T, Sugiyama T, Nabika T, Ohnaka K, Yamaguchi S, Takayanagi R, Ogihara T, Kato N. Reevaluation of the association of seven candidate genes with blood pressure and hypertension: a replication study and meta-analysis with a larger sample size.
A total of 19,426 individuals underwent testing for genetic associations with systolic BP (SBP)/diastolic BP (DBP) and 9271 individuals (3460 cases and 5811 controls) underwent testing for genetic associations with dichotomous hypertension. In their study panels, the most significant association was found for CYP11B2 rs1799998 with odd ratio of 1.15.
Ye H, Li X, Wang L, Liao Q, Xu L, Huang Y, Xu L, Xu X, Chen C, Wu H, Le Y, Liu Q, Ye M, Dong C, Duan S. Genetic associations with coronary heart disease: meta-analyses of 12 candidate genetic variants.
The meta-analysis done on a comprehensive literature search for genetic variants involved in the CHD association study showed a significant association between the GPX1 rs1050450 polymorphism and CHD odd ratio=1.61.
Zhang X, Lynch AI, Davis BR, Ford CE, Boerwinkle E, Eckfeldt JH, Leiendecker-Foster C, Arnett DK. Pharmacogenetic Association of NOS3 Variants with Cardiovascular Disease in Patients with Hypertension: The GenHAT Study.
A clinical study was conducted from hypertensive subjects n=30,280 from a multi-center, double-blind trial and results suggest that for rs3918226, a higher hazard ratio (HR) was found in minor allele carriers for CHD.
Levinsson A, Olin AC, Björck L, Rosengren A, Nyberg F. Nitric oxide synthase (NOS) single nucleotide polymorphisms are associated with coronary heart disease and hypertension in the INTERGENE study.
The study consisted of 560 coronary heart disease patients and randomly selected population controls (n=2791) were genotyped at 58 SNPs in the NOS genes. NOS1 SNP rs3782218 showed the most consistent association with coronary heart disease with odds ratio of 0.89.
Ferguson JF, Phillips CM, McMonagle J, Pérez-Martínez P, Shaw DI, Lovegrove JA, Helal O, Defoort C, Gjelstad IM, Drevon CA, Blaak EE,Saris WH, Leszczyska-Goabek I, Kiec-Wilk B, Risérus U, Karlström B, Lopez-Miranda J, Roche HM. NOS3 gene polymorphisms are associated with risk markers of cardiovascular disease, and interact with omega-3 polyunsaturated fatty acids.
This study assessed association between NOS3 rs1799983 SNP and cardiovascular disease (CVD), using a case-control study of 450 metabolic syndrome patients and controls. A significant gene–nutrient interaction was observed between the NOS3 rs1799983 SNP and plasma n-3 PUFA status on plasma triacylglycerol (TAG), Where Omega-3 polyunsaturated fatty acids (n-3 PUFA) may protect against the development of cardiovascular disease (CVD).
Zee RY, Cook NR, Cheng S, Erlich HA, Lindpaintner K, Ridker PM. Polymorphism in the beta2-adrenergic receptor and lipoprotein lipase genes as risk determinants for idiopathic venous thromboembolism: a multilocus, population-based, prospective genetic analysis.
A study of 304 patients found that the Glu27 allele led to increased risk for idiopathic venous thromboembolism; the reported odds ratio was 1.40.
Markus Schürks, Tobias Kurth, Paul M Ridker, Julie E. Buring, and Robert Y. L. Zee. Association between polymorphisms in the 2-adrenergic receptor gene with myocardial infarction and ischemic stroke in women.
A clinically well-characterized case-control sample that included 294 cases of ischemic stroke and 286 controls. The presence of the Glu27 allelic variant (G allele for rs1042714) was associated with a significantly increased risk of stroke when assuming a recessive mode of inheritance with odds ratio of 1.68).
Song YY, Gong RR, Zhang Z, Li YH, Fan M, Ou GJ, Fang DZ. Effects of apolipoprotein A1 gene rs670 and rs5069 polymorphisms on the plasma lipid profiles in healthy adolescents with different body mass index.
A study was conducted with 723 adolescents of various BMI. Result shows a carriers of the rs670 mutant polymorphism had significantly higher systolic blood pressure (P=0.017) and blood glucose levels (P=0.009) than the adolescents with the GG genotype.
Dolores Corella Donna K. The -256T>C polymorphism in the apolipoprotein A-II gene promoter is associated with body mass index and food intake in the genetics of lipid lowering drugs and diet network study.
A study was conducted for 514 men and 564 women who participated in the Genetics of Lipid Lowering Drugs and Diet Network (GOLDN) study. Odds ratio for obesity in CC individuals compared with T allele carriers was 1.70. Total energy, total fat, and total protein intake were all significantly higher in (C/C) individuals.
James V. Gainer, Michael S. Lipkowitz, Chang Yu, Michael R. Waterman, Elliott P. Dawson, Jorge H. Capdevila,Nancy J. Brown and and the AASK Study Group. Association of a CYP4A11 Variant and Blood Pressure in Black Men.
In a study comprising of 732 black Americans, men with the 8590CC genotype had significantly higher systolic BP (CC 156.5 ± 22.6 versus 148.4 ± 24.3 mmHg in CT and TT combined; P = 0.04) and pulse pressure (P = 0.04) at baseline.
Bjoern Mayer, Wolfgang Lieb, Anika Götz, InkeR.König, ZouhairAherrahrou, Annett Thiemig, Stephan Holmer, Christian Hengstenberg,Angela Doering, Hannelore Loewel, Hans-Werner Hense, HeribertSchunkert, Jeanette Erdmann. Association of the T8590C Polymorphism of CYP4A11 With Hypertension in the MONICA Augsburg Echocardiographic Substudy.
A MONICA (MONitoring trends and determinants In CArdiovascular disease) survey (n=1397) indicates that individuals with the CC genotype have higher systolic (CC 141.4 ± 3.17 mm Hg versus CT 134.2 ± 0.97 mm Hg and TT 134.3 ± 0.53 mm Hg; P=0.03) and diastolic blood pressure levels (CC 85.4 ± 2.06 mm Hg versus CT 80.3±0.63 mm Hg and TT 80.7 ± 0.34 mm Hg; P=0.02). Accordingly, the odds ratio of the CC genotype versus the CT and TT genotypes for hypertension was 3.31 (95% confidence interval [CI]), 1.38 to 7.96; P=0.016) in the entire study population.
ZhenyanFua, Tomohiro Nakayamaa, NaoyukiSatoa, Yoichi Izumic, Yuji Kasamakid, Atsushi Shindod, MasakatsuOhtad, Masayoshi Somac,Noriko Aoia, MikanoSatoa, Yukio Ozawad, Yitong Mab, Koichi Matsumotoc, NobutakaDobae, ShigeakiHinoharae. A haplotype of the CYP4F2 gene associated with myocardial infarction in Japanese men.
This study assessed associations between the CYP4F2 gene and myocardial infarction (MI), using a haplotype-based case-control study of 234 MI patients and 248 controls. For men, G allele frequency of rs2108622 were significantly higher for MI patients than for controls.
Wang WY, Zee RY, Morris BJ. Association of angiotensin II type 1 receptor gene polymorphism with essential hypertension. The cohort used consisted of 108 unrelated essential Hypertensive (HT) and 84 normotensive (NT) subjects.
The rs5186(C) allele is associated with increased risk for essential hypertension in Caucasian populations with an odds ratio of 7.3 (homozygote (C/C) compared to (A/C) and (A/A).
The TG and HDL Working Group of the Exome Sequencing Project, National Heart, Lung, and Blood Institute. Loss-of-function mutations in APOC3, triglycerides, and coronary disease.
The data from the Exome sequencing study of 3734 participants showed the rs138326449 (A) is one of the several loss of function mutations in the APOC3 gene associated for a >40% lower average triglyceride level and a corresponding decrease in coronary artery disease.