Dear Hassan,

what about  identifying subjects with preclinical atherosclerosis? While waiting for technological and scientific progress, such patients could be treated more aggressively. I'm working for some years now on this topic and my ongoing and yet unpublished data seem to be interesting.  I hope you find my attached rewiev useful.    

Regards, Roberto

What we really need to develop is a simple blood test that relates to coronary artery plaque enlargement, inflammation or,instability, such as a highly specific coronary artery C Reactive protein.Then high risk patients could be checked  every month and appropriate measures taken to forestall the pathological event.

Frankly, I think we are getting carried away with the idea of reducing "residual risk" - we're at the point now of trying to squeeze blood from a stone. The IMPROVE-IT trial is a great example of this. Very high NNT required to prevent 1 nonfatal MI over an extended follow-up period (both the treatment and control groups had significantly elevated residual risk despite LDL levels in the 50's and 70's). We need to be a bit more humble in our approach to this problem, we will never eliminate cardiac risk in a secondary prevention population - it's hubris to expect otherwise.

We need to appreciate that resources are finite and we can't get carried away with therapies with high NNT's in the quest to reduce "residual risk". Instead, we should focus on the fact that 60-80% of coronary heart disease is preventable and redirect resources and efforts toward getting the public to exercise more, eat better, maintain healthy weight, and obviously, quit or never start smoking.  Starting everyone on a statin for primary prevention isn't the answer either; the answer won't be found in a doctor's office.

I have been thinking a lot about this problem. One idea that occurred to me, was to implant a coronary sinus probe, that could detect decreased blood flow, a  drop in oxygen saturation, and possibly an increase in inflammatory markers like the C reactive protein. The other end of the probe would need to  be attached to  a pacemaker- like implantable cannister, that could be interrogated. In this way an impending myocardial ischemic event could be predicted, and appropriate measures taken.

Though reduction of LDL or non-HDL is associated with reduction of atherosclerosis but it is not halted. Raised HDL  was considered protective but it is now termed "chameleon" as in conditions where inflammatory markers are raised, raised HDL is associated with accelerated atherosclerosis. Similarly high TG has adverse effects but yet to be defined. Thus we have to have more understanding about the risk factors.