Question special
Lead Moderator

In post hoc analysis (see Table 2), canakinumab did not have an impact on cardiovascular deaths. The primary driver of the significant difference in primary end point was reduction in non-fatal MI. We don't know the range in severity of these events. Was the study underpowered to detect a difference in fatal MIs, or does canakinumab only protect against certain subtypes of MI? Is it possible that canakinumab slows progression of CAD / plaque burden but does not protect against acute plaque rupture?