Abstract

After an acute coronary syndrome (ACS), the risk of major adverse cardiovascular events (MACE) persists despite the reperfusion of the culprit lesion. The addition of proprotein convertase subtilisin/kexin type 9 inhibitors (PCSK9i) to standard lipid-lowering therapies has been demonstrated to effectively reduce the levels of low-density lipoprotein cholesterol (LDL-C), with a consistent decrease of MACE in large, randomized clinical trials enrolling patients at high risk of cardiovascular events. There is a strong rationale for an immediate and aggressive LDL-C lowering with the use of PCSK9i in ACS patients. The PACMAN-AMI trial tested this hypothesis demonstrating that in ACS patients, the addition of subcutaneous biweekly alirocumab, compared with placebo, to high-intensity statin therapy resulted in significantly greater coronary plaque regression in non-infarct-related arteries after 52 weeks, as assessed by novel intra-coronary imaging modalities. These findings might provide the mechanistic rationale in favour of early initiation of very intensive LDL-C-lowering therapy in the acute setting of ACS, potentially modifying the actual common pattern of treatment.

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