Managing cardiovascular health conditions presents a unique challenge for healthcare providers because individual responses to medications are so varied. Several classes of medications, including blood pressure and cholesterol-lowering drugs, anti-platelet agents, antiarrhythmic drugs, and agents to control bleeding and clotting can provoke adverse effects based on an individual’s genetic makeup.1,2 Now, there is a more informed way to prescribe medication for cardiovascular health.
Mitigate ineffective treatments and adverse drug reactions
There are several common, well-documented genetic variations that can substantially reduce or increase the functionality of enzymes responsible for the body’s breakdown of frequently-prescribed medications.2,3 If a patient harbors any of these genetic mutations, it may have a dramatic effect on their body’s ability to metabolize many commonly-prescribed cardiovascular drugs.4 The result is either reduced efficacy of the medication, which increases the risk of a major cardiovascular event, or increased risk of an adverse drug reaction, diminishing patient safety and quality of life.
Major medical centers in the United States—including Vanderbilt Medical Center and the University of Florida–are beginning to implement molecular genetic tests in patients undergoing certain procedures or taking certain medications.5,6 Implementation of pharmacogenetic testing at these institutions highlights the growing role that genetic testing can play in tailoring safe and effective treatments to an individual’s genetic make-up.
Here’s one example of how understanding genetics can play a major role in prescribing:
A patient taking statins may experience muscle aches, commonly termed myalgia, as a result of the medication.7 Some patients have a small chance of developing a serious, life-threatening adverse drug reaction called statin-induced myopathy.8 Yet in one genome-wide association study of patients taking 80 mg of simvastatin a day, more than 60 percent of such infrequent reactions were explained by a single base pair substitution in a gene encoding a liver transporter enzyme involved in the clearance of statins.8 In fact, the Clinical Pharmacogenetics Implementation Consortium recently issued guidelines surrounding the use of genetic testing and simvastatin for preventing adverse myopathy reactions,9 indicating the role that genetic testing can play in tailoring safe and effective therapy to your patient.
Kashi’s Cardiac Panel provides physicians with the genetic information they need to select the best drugs and dosing regimens for patients who are either at risk, or currently undergoing treatment for a cardiovascular disease. This intelligent approach to prescribing the correct medications for cardiovascular health management may significantly improve long-term patient wellness and outcomes.
Benefits of Kashi’s Cardiac Panel
- Improved medication selection and dosage recommendations for better therapeutic effect
- Reduced trial-and-error period in finding effective medications
- Decreased adverse drug reactions
Gene Tests Included in the Cardiac Panel
|GENE TESTS||EFFECT ON CARDIAC HEALTH|
|CYP2C9||A key metabolizer of the anticoagulant drug, warfarin, NSAIDS, sulfonylureas, and angiotensin II receptor antagonists2,10|
|CYP2C19||A major activator of the anti-platelet prodrug, clopidogrel and metabolizer of proton pump inhibitors such as omeprazole 2,11|
|CYP2D6||Plays a role in metabolizing certain beta-blockers and anti-arrhythmic drugs 2,12|
|VKORC1||A key site of action for the anticoagulant drug, warfarin 10,12|
|Factor II||Affects the body’s ability to form blood clots. Certain genetic variants linked to an increased risk of thromboembolisms.13|
|Factor V||Certain genetic variants enhance the body’s coagulability which may lead to thromboembolisms 14|
|MTHFR||Contributes to increased levels of homocysteine, a risk factor for heart disease, atherosclerosis, and diabetic peripheral neuropathy 15,16,17|
|CYP3A4/5||Plays a role in metabolizing statin medications, which are commonly prescribed to improve cholesterol. 18|
|SLCO1B1||Modulates the body’s ability to metabolize statin medications, which are commonly prescribed to improve cholesterol levels8,9|
- Ganesh SK et al. Genetics and genomics for the prevention and treatment of cardiovascular disease: update: a scientific statement from the American Heart Association. Circulation. 2013; 128(25):2813-51.
- Samer CF et al. Applications of CYP450 testing in the clinical setting. Mol Diagn Ther. 2013; 17(3):165-84.
- Sim SC et al. Pharmacogenomics of drug-metabolizing enzymes: a recent update on clinical implications and endogenous effects. Pharmacogenomics J. 2013; 13(1):1-11.
- Kitzmiller JP et al. Pharmacogenomic testing: relevance in medical practice: why drugs work in some patients but not in others. Cleve Clin J Med. 2011; 78(4):243-57.
- Van Driest SL et al. Clinically actionable genotypes among 10,000 patients with preemptive pharmacogenomic testing. Clin Pharmacol Ther. 2014; 95(4):423-31.
- Johnson JA et al. Institutional profile: University of Florida and Shands Hospital Personalized Medicine Program: clinical implementation of pharmacogenetics. Pharmacogenomics. 2013; 14(7):723-6.
- Tomaszewski M et al. Statin-induced myopathies. Pharmacol Rep. 2011; 63(4):859-866.
- Link E et al. SLCO1B1 variants and statin-induced myopathy–a genomewide study. N Engl J Med. 2008; 359(8):789-99.
- Ramsey LB et al. The clinical pharmacogenetics implementation consortium guideline for SLCO1B1 and simvastatin-induced myopathy: 2014 update. Clin Pharmacol Ther. 2014; 96(4):423-8.
- Johnson J et al. Clinical Pharmacogenetics Implementation Consortium Guidelines for CYP2C9 and VKORC1 genotypes and warfarin dosing. Clin Pharmacol Ther. 2011; 90(4):625-9.
- Scott S et al. Clinical Pharmacogenetics Implementation Consortium guidelines for cytochrome P450-2C19 (CYP2C19) genotype and clopidogrel therapy. Clin Pharmacol Ther. 2011; 90(2):328-332.
- Voora D and Ginsburg GS. Clinical application of cardiovascular pharmacogenetics. J Am Coll Cardiol. 2012; 60(1):9-20.
- Varga E and Moll S. Prothrombin 20210 mutation (factor II mutation). Circulation. 2004; 110:e15-8.
- Shaheen K et al. Factor V Leiden: how great is the risk of venous thromboembolism? Cleve Clin J Med. 2012; 79(4):265-72.
- McNulty H et al. Homocysteine, B-vitamins and CVD. Proc Nutr Soc. 2008; 67(2):232-7.
- Miranda-Massari JR et al. Metabolic Correction in the Management of Diabetic Peripheral Neuropathy: Improving Clinical Results Beyond Symptom Control. Curr Clin Pharmacol. 2011; 6(4):260-273.
- Refsum H et al. The Hordaland Homocysteine Study: A Community-Based Study of Homocysteine, Its Determinants, and Associations with disease. J Nutr. 2006; 136:1731S-1740S.
- Kitzmiller JP et al. Statin pharmacogenomics: pursuing biomarkers for predicting clinical outcomes. Discov Med. 2013; 16(86):45-51.