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?
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