Peter:
There was a very interesting and illuminating point-counterpoint at the 2000 ACC meeting, which I was able to access online long ago when I asked myself about why alxn had not measured troponin in the Circulation study. The ACC debate was not on the subject of anti-C5, but on the usefullness of CK-MB vs. troponin as clinical measurements. (Abciximab was mentioned briefly, basically to the point that it both reduces CK-MB elevations and reduces mortality in patients undergoing intervention.) I'm trying to recover it but my browser times out.
There is little doubt I guess that troponin release is a more sensitive measurement of necrosis, and maybe it is a better predictor of MI. But the TSC article implies that CK-MB is an invalid measurement for heart damage, and I think that is just wrong. In the acc debate, the two experts agreed that during an MI event elevations of CK-MB represent myocardial necrosis. That's all I need to know. Patients with CK-MB elevation apparently also have more complex coronary lesions, and there is recent evidence that they are more likely to have active thrombus in the lesion. Furthermore, I believe CK-MB has been the measurement of choice, as part of a composite, in the most recent studies forming the basis for approval of other heart drugs like reopro and aggravast.
It may very well be that measuring troponin will be required in trials from here on out, and so much the better--I sure don't think alxn will shrink from it--given what I suspect is the correlation between the two (many heart patients begin with elevated CK-MB) that likely occurs during an induced infarction event.
Would love to hear from the interventional cardiologists if I'm wrong.
--Wilder |
