Abstract
With great interest, I read the relevant consensus document led by Konstantin Krychtiuk highlighting the importance of early and aggressive reduction of low-density lipoprotein cholesterol (LDL-C) following acute coronary syndrome (ACS) event to improve clinical outcomes.1 While the ‘strike early and strong’ message is perfectly sound, I would wish to put more emphasis on the window of opportunity for lipid lowering among ACS patients before they receive an invasive management. Authors are to be commended for integrating early lipid lowering in their proposed management pathway; however, the concept of statin ‘pre-loading’ should be put more forward. The mechanisms behind very early statin use in ACS and their translation to clinical benefit are not fully elucidated; however, such effects could be explained by the multifactorial impact of statin treatment on molecular and cellular events that are fundamental to the pathogenesis of ACS. Such mechanisms, independent of the central action on atherogenic lipoproteins, include reduction of inflammation, modulation of thrombogenesis and thrombolysis, improvement of endothelial dysfunction, and amelioration of ischaemia/reperfusion injury.2 It has been previously shown in clinical studies that statin pre-loading before percutaneous coronary intervention (PCI) can limit periprocedural microcirculatory damage, significantly reduce ‘no-reflow’ phenomenon, and can elicit greater endothelial protection in both chronic and acute coronary syndrome populations.3,4,5 These beneficial pharmacodynamic effects of statin pre-loading in patients with ACS might translate to short-term reduction in adverse events, especially those that are coronary-driven.
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