From the research done as part of the Human Genome Project over the past 10 years, patients, physicians and policymakers will increasingly see scientific studies exploring the relationship between genes, diseases and drugs.
This particular article refers to a study of an experimental beta blocker drug called bucindolol that was originally published in 2001 for patients with symptoms from heart failure at rest or with less than ordinary activity. Over about 2 years, 30% of the patients receiving bucindolol died and 33% of those receiving placebo died, so the drug did not provide any statistically significant advantage. Using genetic material samples from a subset of the original patients, Dr Liggett and colleagues found that a particular genetic marker identified a group of patients who appeared to benefit from bucindolol. Neither the genetic test nor the drug is currently available. Moreover, there are many other drugs known to be effective in heart failure. Thus, this article is an attempt to highlight the future potential of genetic sequencing individuals and using that information to identify drugs that may be beneficial as in this case or harmful in other cases for a particular person. In general, because of the many genes being tested, some of these relationships may occur just by chance alone. So these may be falsely positive tests. In addition, in some cases, genes may identify diseases or potential harms that may never occur or may never become apparent – “false diagnoses” that could lead to additional tests, harms from treatment or worry. While genetic sequencing holds great promise, patients, physicians and policymakers will need to evaluate carefully the risks and benefits of such tests in the future and the science upon which the rationale for the test rests.
These are some of the issues that a story like this could have explored, rather than merely relying on researchers’ hopes for FDA approval of an experimental drug and researchers’ predictions that a genetic test will be approved soon.
There was no mention of cost.
The article reports that “patients with two copies of the arginine variant lived an average 38 percent longer than patients with the glycine variant. Patients with glycine variant didn’t respond to the beta blocker.” Did they live longer whether or not they received bucindolol or not? It is not possible to tell whether the increased mortality in the glycine variant group is due to the effect of having two copies of this allele or whether having two copies of this allele renders a person resistant to the benefits (if any) conferred by bucindolol. And 38% longer is only a relative term. What was the absolute time lived longer?
Although side effects of beta-blockers (depression, fatigue, and asthma-related lung problems) were mentioned, it is not clear what the list of side effects found specifically with bucindolol might be. Since the article also discussed an imminent genetic test that might suggest greater risk of death, it could have also discussed the possible impact this sort of information might have on an individual or family.
Other than mentioning where the study is published, the article does not provide any information about the nature of the clinical evidence supporting the claims reported.
The story says “… heart failure can kill quickly. One in five chronic heart failure patients is dead within a year of being diagnosed and less than half live for more than five years, researchers say. ‘You have a very narrow window before the progression of the disease gets out of hand,’ Liggett said.”
The choice of words provides a negative frame: “kill quickly” and “narrow window” convey a sense of urgency that does NOT apply to all patients with heart failure. Some patients with heart failure are asymptomatic and have a much much better prognosis. These numbers really apply only to those with severe symptomatic heart failure.
Although the article included a comment from Dr. Blumenthal who was mentioned as “not involved in the study”, he was an investigator on the “Beta-blocker evaluation in survival trial” from which data were reportedly used for the current study. Another clinician, Dr. Mehra, cited as not involved in the current study, is the chairman of the department from which the work originated. Thus it appears that the article does not include comments from researchers who did not have a stake in the findings.
The story failed to put the new idea into the context of other currently approved beta-blocker drugs for heart failure, or of other drugs of other classes.
The article discusses two unapproved medical interventions: a genetic test and a particular drug for heart failure. The genetic test needed to determine whether bucindolol might be effective is reported as not approved by the FDA but that such approval could be obtained in the next year or two. In reality, it is not possible to predict whether this test will be approved or when. Secondly, the article mentions that researchers hope that drug, bucindolol, will be approved by the FDA. The application for FDA approval has not even been filed yet.
The story promotes researchers’ hopes that the FDA will approve the experimental beta blocker (bucindolol) and promotes researchers predictions that a genetic test could be approved by the FDA in the next year or two without any justification for that prediction. The true novelty of either idea is still uNPRoven.
There is no evidence that the story relied solely or largely on a news release. However no truly independent sources were interviewed in the story.