Major findings published this week in the Proceedings of the National Academy of Science. : A so-called “me-too” beta-blocker works best for people with a particular genetic mutation. The drug, called bucindolol doesn’t have much benefit to most people with high blood pressure. But for people whose blood pressure is channeled through a specific pathway affected by the Arg 389 gene and have a specific mutation also have a 40 percent higher reduction in mortality from heart failure. People who carry an entirely different gene would do worse on the drug.
The research — carried out and sustained over a decade by Mike Bristow of the University of Colorado and Steve Liggett, now of the University of Maryland — has been translated into both a drug and diagnostic. Media reports (The Washington Post) have stated that “it is unknown, for example, whether even those patients with the responsive gene would do better on bucindolol than on the two beta blockers already on the market for heart failure — a serious disease that kills half its victims within five years.” In fact, to the extent that the expression of the gene and disease is pathway specific — and the Bristow-Liggett research suggests that it is — no other drug would work better. Thus, CV treatments would follow the path taken by targeted cancer drugs.
So much for the effort to shove everyone into the cheapest drug based upon average response. Sometimes an older drug will have spectacular benefits for specific patients as a result of combining it with a diagnostic and sometimes the new medicine designed with a diagnostic in tandem will work better for another group. Evidence based medicine is being replaced by genomic-based medicine. The problem is policymakers and pundits still act and think as if the technology and informatics of healthcare is mired in the 20th century. It’s changing. And if ways of paying for and organizing and choosing healthcare don’t change in response, they become obstacles to better health.
You can read the publication online at the PNAS website: “A polymorphism within a conserved B1-adrenergic receptor motif alters cardiac function and a B-blocker response in human heart failure.