Cardiovascular disease is the number one cause of mortality globally, responsible for approximately one-third of deaths. Patients also, suffer considerable morbidity not just from illness but from the effects of surgery and medications. Cardiovascular drugs are among the most widely prescribed drugs and like all medications, have the potential to cause unwanted side effects. Traditionally, physicians have employed a ‘one size fits all policy’ when prescribing medications. However this the notion is being challenged by the evolution of genetics whereby efficacy and side effects of the particular drug can be characterised to each individual. This ‘tailor-made’ approach offers individualised prescription and has the potential to revolutionise healthcare.
Each one of us has a unique genetic code which is responsible for every aspect of our appearance and function. It governs the molecular basis of important enzyme reactions and body metabolism. Recent years have seen burgeoning growth in the field of genetics and geneticists have been able to identify genes which are responsible for various aspects of drug metabolism. This has led to widespread research in pharmacogenomics and the prospect of individualised prescriptions.
There are several noteworthy examples. Clopidogrel is a frequently prescribed drug for the prevention and treatment of coronary heart disease and strokes. A gene called CYP2C19 is responsible for clopidogrel metabolism and various changes in this gene can either increase functionality or loss of function in the enzymes metabolising clopidogrel. There are ample reports of patients having further heart attacks despite taking clopidogrel and other antiplatelet drugs. A simple genetic the test can, therefore, ensure that patients that will be poor responders to clopidogrel are offered an alternative antiplatelet drug.
Another example is warfarin, a drug used for preventing strokes. The dose of warfarin varies from patient to patient, depending on how slowly or quickly it is metabolised and various dietary factors. Patients under-prescribed warfarin receive no therapeutic benefit whereas being over-prescribed increases the risks of major bleeding. Genes called CYP2CP and VKORC1 are central to warfarin metabolism and alterations in these genes can render an individual highly sensitive to warfarin and at risk of bleeding. Once again, genetic testing can identify such individuals who can be offered lower initial doses or even different classes of anticoagulant drugs.
These are just a couple of examples but genetic testing is available for an array of cardiovascular drugs including statins, beta-blockers, and ACE Inhibitors. It is envisaged that the rapid growth of this field will lead to genetic profiling for even more cardiovascular and non-cardiovascular drugs.
Genetic drug testing such as that provided by Rightangled offers unique and personalised feedback which also includes genetic risk of various cardiovascular diseases. This empowers both patients and physicians by ensuring novel precision medicine. It improves compliance with medication as patients feel less worried about potential side effects.
Finally, It is plausible that it would reduce healthcare costs by bypassing the ‘trial and error’ method of using different medications and from a reduction in side effects requiring hospitalisation and further treatment.