Geneticure has assembled and patented a comprehensive panel of genes that are involved in the regulation of renal Na⁺ handling, vasodilation, and cardiac function.
All of these genes have repeatedly demonstrated physiologic effects in cell, animal, and human models and have also demonstrated altered pharmacogenetic effects.
Based on current therapeutic guidelines, and our current understanding of genetics and the proteins involved in blood pressure regulation, we provide the critical information necessary for accurate therapeutic decision making in hypertension. Treating hypertension has never been easier.
The development of high blood pressure in humans is the result of one or more of three physiologic maladaptation's:
As such, common therapies for reducing blood pressure include those that inhibit Na⁺ reabsorption in the kidney, cause vasodilation, or reduce cardiac output.
Despite a significant impulse in the medical community to move towards an “individualized medicine” approach to patient centered treatment, the current clinical treatment strategy for high blood pressure, like other diseases, is based on a set algorithm which does not take into account individual genetic differences of the patient. Rather, physicians are guided to choose a drug (one out of many options) in a given class of drugs and use that specific drug as a “first line therapy” (typically initiating with the diuretic class) and titrate that specific drug of choice to therapeutic dosage.
It is only after a prolonged course of treatment with that specific class of drug that clinical efficacy is determined (typically three months). At this stage, if clinical guideline goals for blood pressure have not been met, it is often recommended that the patient remain on the “first line therapy” whilst an additional drug from a different class of drugs (typically an angiotensin converting enzyme inhibitor (ACE inhibitor) or angiotensin II receptor blocker (ARB)) is added to the pharmacologic regimen. Again, this drug is titrated to recommended therapeutic dosage and another prolonged course of treatment is initiated before clinical efficacy is determined (an additional three months – six months since initiation of treatment).
If at this point, clinical guideline goals for blood pressure have not been met, a third drug from a third class of drugs (typically a beta-blocker) is added and the process is repeated (another three months – nine months from initiation of treatment). Further, if clinical guideline goals have continued to be elusive, the diagnosis of refractory hypertension is added and the process is reinitiated with a different combination of drugs, different classes of drugs, different drug options within a given class of drugs, different dosages, or all of the above.
Thus, from the time of initial diagnosis and the start of treatment to the point in which blood pressure is adequately controlled may take anywhere from three months to well over one year. This trial-and-error standard of care is clearly not optimal.