Crestor, CRP, and Inflammation
November 10th, 2008 by The Doc
Not surprisingly, another study has demonstrated a connection between inflammation and symptomatic coronary artery disease.
Even less surprisingly, the study supports the use of statins—namely, Crestor—to invoke a 50% reduction in the risk of heart attack for people who exhibit signs of inflammation in their arteries.
I say, “…less surprisingly,” because the study was funded by AstraZeneca (the company that manufactures Crestor) and the principal investigator, Dr. Paul Ridker, has stated financial ties to the company. Dr. Ridker is also co-holder of a patent on the test that measures inflammation (high-sensitivity C-reactive protein, or CRP). Though he states he has no conflicts of interest, Dr. Ridker stands to profit handsomely from the sweeping recommendations that will likely emanate from his research.
Thankfully, in spite of the excitement surrounding the study’s results, cooler heads are calling for temperance. After all, even though Crestor showed clear benefit in this trial, smart people are pointing out that 120 individuals would have to be treated for two years to prevent a single heart attack. And, with Crestor costing $1200 per year, treating everyone in the US who has a high CRP could cost up to $9 billion.
Furthermore, the study only lasted for two years before it was terminated because of “clear benefit” to those in the test group. Many of those individuals had normal cholesterol levels prior to taking Crestor; the drug will lower their cholesterols even further. The clear implication of this study is that patients will receive therapy for life, but no one has the foggiest notion about the long-term adverse effects of subnormal cholesterol levels. Past research has raised some serious concerns about this.
Additionally, test subjects in this trial showed a slightly higher incidence of diabetes than control subjects did. Would we be trading one problem for another? Would we just add the costs of diabetes management to the life-long costs of a statin drug?
I feel compelled to toss one more pebble into the pond: Does anyone remember the studies of the mid-90’s that revealed bacteria in the inflamed cholesterol plaques in the coronary arteries of heart attack victims?
It seems to me that we are once more using a big gun to shoot at a little tiny target…a big, expensive gun, loaded with silver bullets. I may be wrong, but it would seem prudent—indeed, it would be good science—to chase down the source of the inflammation that jacks up the CRPs in all of these people with normal cholesterol levels who are still having heart attacks.
Once again, as we did ten years ago, someone needs to ask the question: “Is coronary artery disease an infectious disease?”
I think it would be fascinating to conduct another study. Let’s go ahead and measure those CRPs (you’re welcome, Dr. Ridker); for those who exhibit high CRPs, let’s also collect titers or PCRs for, say, Chlamydia pneumoniae and Mycoplasma pneumoniae and maybe a few other ubiquitous bugs. For those with signs of bacterial colonization and high CRPs, let’s consider a course of antibiotics and successive measurement of CRPs.
If nothing useful tumbled out of a study like that, I’d still keep looking for an underlying cause of that inflammation. We might just find a really cheap way—maybe even a lifestyle recommendation (free!)—to prevent all those heart attacks and strokes.
Perish the thought.