Friday, December 25, 2009


The Dec 21st online edition of Lancet carried an interesting long term prospective meta-analysis of 54 clinical trial, across 18 countries, involving 160,000 patients, on whether hs-CRP ( a C-reactive protein found in the blood ), affects outcomes in patients with Coronary Artery Disease ( CAD ). This study, with the acronymn of ERFC ( Emerging Risk Factor Collaboration ), was led by the group at Cambridge and published in the Lancet. Basically what they found, after going through prospective records of the 160,000 patients was that there was no co-relation between hs-CRP levels and incidence of heart attacks, angina, strokes in patients with CAD. This finding was of course in sharp contrast to the work of Dr Paul Ridker at Bringham and Women's at Boston, Mass.. Dr Ridker is the hs-CRP guru and lead investigator of the Jupiter trial on the role of rosuvastatin in the prevention and management of patients with coronary artery disease. He represents the US and new thinking. The inflammation theorist.
There are many us, myself included who thought that the old coronary risk factors would go towards suporting the basic, degenerative theory of coronary artery disease ( the old British School ), has limitations and that clincal events are in some way related to inflammation.hs-CRP measurement in the serum, is a measure of the degree of inflammation present, especially in patients with diabetes. We also know that the measurement of hs-CRP is technically difficult and unless the technicians are well trained, can be full of errors. It is not a simple test, even with kits. We have found widely differing readings from different labs and even from the same lab at different times. I suppose being a high selective and highly sensitive test have this inherent challenge. Maybe that is why the data from both sides of the big pond, is different.
I wonder what this new set of data will do to rosuvastatin, the money spinner for astra-zeneca. Rosuvastatin has been marketed as an agent that will reduce inflammation, reduce CVS events and regress plaques. It also reduces hs-CRP and the theory is that because of its efficacy in reducing hs-CRP, it is so good for management of CAD. Now that selling point may have to be re-considered.
Interesting. But as always, we must remember that this is a prospective, meta-analysis of 54 clinical trial, and not a head to head, interventional study. So that data, and conclusion must be taken in that light. It is cheaper and the Cambridge boys have given us a useful hint that all is not so simple. Something as complex as coronary artery disease cannot be so simple to understand and even to treat.

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