Fouremm wrote: "I think "attenuated" plaque is referring to plaque that is changed to a more stable form of plaque which is thought to be less prone to rupture thus causing a cardiovascular event. ie the plaque has been attenuated."

The abstract referenced in my previous post points out that: 1) Attenuated plaque is a measure of vulnerability and 2) apabetalone is reducing markers of attenuated plaque. Although it seems contradictory, attenuated plaque is more vulnerable, not less vulnerable. So apabetalone is reducing markers of vulnerable, attenuated plaque.

In my previous post today, I put together a definition of attenuated plaque from couple different literature sources: "Attenuated plaque seems to be an unusual IVUS finding (hypoechoic or mixed atheroma plaque with deep ultrasound attenuation but without calcification) that is more common in patients with acute coronary syndrome and seems to be associated with a higher inflammatory status, more severe and complex lesion morphology, high rate of transient deterioration in coronary flow during percutaneous coronary intervention (PCI), no-reflow after PCI, and a larger infarct size."

Fourem wrote: "If I recall correctly, after some of the post hoc analysis was revealed RVX had some IVUS slides in the presentations that showed a positive change in the plaque composition in the Apabetalone treated trial population. Positive because, we were told at the time, these changes made the plaque more stable." 

You recall correctly. Here is the news release from few years back on this.

Koo wrote: "Bear would you know if a statin would normally be prescribed for "attenuated coronary atherosclerotic plaque."

Standard of care for those at high risk for acute coronary syndrome and cardiovascular diseases is to lower LDL. Statins are one of a few options for lowering LDL (others include ezetimibe, statin/ezetimibe combo, PCSK9 antibodies). So if a patient is diagnosed by IVUS to have attenuated plaque, then this patient would very likely be prescribed LDL-lowering therapy. If a patient is even having an IVUS done.....it is probably because they have an elevated risk of cardiovascular disease and should be placed on a standard of care LDL lowering therapy. 

Koo wrote: "In other words can Apabetalone become another form of an improved statin?"

You are comparing apples to oranges here. The main target of statins is to inhibit HMG-CoA reductase and indirectly cause an increase in LDL-receptor expression to increase LDL clearance from the circulation and lower LDL levels. We all know that main targets of apabetalone, and it has nothing to do with HMG-CoA reductase and LDL lowering. Apabetalone will never become an improved statin because apabetalone is not a statin and has very little if anything to do with LDL metabolism. One of apabetalone's effects (but not its only one) is to raise apoaI and HDL.....statins don't do that. Although both apabetalone and statins lower hsCRP, reduce plaque and reduce MACE to varying degrees, they act via different targets and different pathways.

LDL lowering therapies have been and will continue to be around for a long, long time as a standard of care for reducing risk of cardiovascular disease. However, LDL-lowering alone has its limitations on how much it can reduce cardiovascular disease risk. This is the opportunity for apabetalone and other non-LDL lowering therapies......to hit other targets/pathways to further reduce risk for cardiovascular diseases.

BearDownAZ