APOA1 and myocardial infarction: The elevation of cholesterol efflux caused by CSL112 has been shown to be transient and recedes to baseline with clearance of the apoA-I.26 It is not known how a transient enhancement of cholesterol efflux capacity immediately after acute MI will affect clinical outcomes compared with the sustained or long-term measures of cholesterol efflux assessed in the Dallas Heart Study.18 Although MACE end points were not reduced in AEGIS-I, this phase 2b study was designed as a safety trial and was not sufficiently powered to assess efficacy (Table VII in the online-only Data Supplement).