Walking the walk: Day #5

This may be a startling admission to some of you, but the last time I did any sort of regular physical exercise was nearly 15 years ago, during my first two years of medical school. Back then, to relieve stress brought on by anatomy, pathology, and life in general, I would jog up First Avenue in Manhattan from my dormitory on 30th Street into the tony neighborhoods of the Upper East Side, then reverse course around 82nd Street and retrace my route home. During my third and fourth years of medical school; family medicine residency and fellowship; clinical, government, and academic careers; and a recently completed Master of Public Health degree, my running for fitness became increasingly sporadic, then ceased entirely.

Until now.

I can't pinpoint exactly what inspired me to start exercising regularly again after so long. Certainly, I'm not a spring chicken anymore, and there are limits to relying on my abundant genetic fortune (both of my paternal grandparents are going strong well into their 90s) to prevent future health problems. Maybe it's because half of my Facebook friends are doing 10Ks, or at least it seems that way. Maybe because my sister-in-law and her husband, both several years older, just completed Ironman triathlons. Maybe I'm tired of counseling patients my age or younger to make time for exercise when I'm not walking the walk myself. (And since it's day #5 after more than 5000 days of physical inactivity, I am mostly walking, though my goal is to slowly but surely get myself back into running shape.)

The fastest I've ever been was at age 14, when I clocked personal records for the mile (5:25) and 3 miles (18:39). I don't expect to approach these again. But this time I'm not aiming for fast - I'm aiming for slow and steady and keeping it up for years and years. I won't turn this blog into a runner's diary, but I thought I'd give you a heads up about what I'm doing amid my posts on clinical and policy issues and broadsides against too much medicine.

Low-value care for acute chest pain in the ED

Last week, the family medicine residency inpatient service that I supervise admitted several patients from the emergency department with acute chest pain that had resolved. Most of them had no history of cardiovascular disease, but were deemed to have enough risk factors to undergo pre-discharge cardiac stress testing after they had "ruled out" for acute coronary syndrome with normal cardiac enzymes. Rationales for the American Heart Association's recommendation for routine stress testing in patients with resolved chest pain include reducing malpractice liability, improving cardiac risk stratification, and initiating appropriate interventions earlier in high-risk patients. Although this practice is widely accepted, there is no evidence that it improves patient-oriented outcomes compared to outpatient management, and some researchers have argued that randomized trials are needed to prove that the benefits actually exceed the harms.

A recent study published in JAMA Internal Medicine adds fuel to this debate by presenting prospectively collected outcomes of adult patients evaluated in the emergency department chest pain unit of Mount Sinai Medical Center from 2004 to 2010. A total of 4181 patients underwent stress testing (512 with exercise ECG tests and the rest with nuclear perfusion imaging), and 470 tests suggested potential myocardial ischemia. 123 patients underwent cardiac catheterizations; 60 of these patients were found to have normal coronary arteries. Of the 63 patients whose catheterizations showed obstructive coronary artery disease, only 28 had lesions that warranted stenting or coronary artery bypass grafting according to expert consensus guidelines.

There are at least two ways to view this study's results. A positive interpretation is that cardiac stress testing led to in the presumptive diagnosis of coronary artery disease in more than 10 percent of patients, who could then have received medical interventions shown to improve outcomes. On the other hand, the high false positive rates on coronary angiography suggest that up to half of these diagnoses were incorrect (and, consequently, that more than 150 patients would have received therapy inappropriately). Nearly 90 percent of patients were exposed to significant radiation doses through nuclear imaging, but less than 1 percent had coronary artery lesions that warranted revascularization. So are the benefits of routine pre-discharge stress testing in patients with resolved chest pain worth the harms? If not, is reducing medical liability risk enough reason to continue a low-value practice?

**

The above post was first published on the AFP Community Blog.

Biased research, aggressive sales, harmful drugs

Approval from the U.S. Food and Drug Administration to market a new drug is a critical waypoint along the path to profits for pharmaceutical manufacturers. Unfortunately, recent case studies have illustrated that FDA approval does not necessarily provide assurances of effectiveness and safety. In last month's Georgetown University Health Policy seminar, we discussed two examples, anemia drugs and the diabetes drug rosiglitazone (Avandia), which were prominently featured in recent articles by Peter Whoriskey in The Washington Post.

Image courtesy of scienceblogs.com

The original impetus for the development of the anemia drugs Epogen, Procrit, and Aranesp, which mimic the  actions of the hormone erythropoietin, was to spare dialysis patients with severe anemia the inconvenience and risks associated with periodic blood transfusions. However, noted Whoriskey, pharmaceutical companies moved aggressively to market these drugs to a far larger patient population who were much less likely to benefit from them:

The trouble would arise as the drugmakers won FDA approval for vastly expanded uses, pushing it in larger doses, for milder anemia and for patients with a wider array of illnesses. Very quickly, the market included nearly all dialysis patients, not just the roughly 16 percent who required blood transfusions. The size of average doses would more than triple. And over the next five years, the FDA would approve it to treat anemia in patients with cancer and AIDS, as well as those getting hip and knee surgery.

Doctors were motivated to give more doses of these drugs due to generous financial incentives (estimated at between $100,000 and $300,000 annually for a typical oncologist) and the seductive thinking that if some drug was good, more was better. Even the publication of a 1998 study in the New England Journal of Medicine showing no survival advantage to boosting hematocrit levels to normal ranges in cardiac patients did little to discourage overprescribing. Not until 14 years later did an independent researcher obtain access to the complete study report from the FDA and conclude that the NEJM authors had used statistical slight-of-hand to obscure an increased risk of heart attacks and death in the normal-hematocrit group. In the meantime, lobbyists working for the drug manufacturers successfully blocked efforts by Medicare administrators to stop paying for the higher (harmful) doses.

Similarly, the evidence that rosiglitazone (Avandia) increased the risk of heart attacks was slow to come to light, due in part to the drugmaker's research emphasis on the surrogate outcome of glycemic control. Although a 2007 meta-analysis first sounded the alarm about rosiglitazone's cardiovascular risks, the manufacturer successfully stalled regulatory action in the U.S. for three more years, during which thousands of new patients were prescribed the drug.

Could the FDA and other U.S. government agencies do more to protect patients from the effects of biased research and aggressive sales tactics for newly marketed drugs? What concrete steps could health policymakers take to encourage research to identify unexpected harms earlier in the drug approval process?

**

The above post first appeared on The Health Policy Exchange.