Effects of Statins on Coronary Atherosclerotic Plaques

Abstract

Statins were associated with slower progression of overall coronary atherosclerosis volume, with increased plaque calcification and reduction of high-risk plaque features. Statins did not affect the progression of percentage of stenosis severity of coronary artery lesions but induced phenotypic plaque transformation. (Progression of AtheRosclerotic PlAque DetermIned by Computed TomoGraphic Angiography Imaging [PARADIGM]; NCT02803411).

PCSK9 inhibition and inflammation: A narrative review

“…In the virtual histology evaluation of the GLAGOV study with evolocumab, this did not lead to meaningful reductions in hs-CRP levels [89]. Interpretation of findings from the GLAGOV study, however, should consider that coronary patients were on statin background, and that HMGCo-A reductase inhibitors are associated per se with a slower progression of coronary atheromas, with increased plaque calcification and reduction of high-risk plaque features [143]. In the near future, findings from other ongoing RCTs will certainly shed light on the correlation between PCSK9 inhibition and plaque regression.…”

Quantitative coronary computed tomography angiography for the detection of cardiac allograft vasculopathy

“…While the long-term efficacy of these lastnamed medications remains unclear [44], quantitative CTA may represent a novel tool to monitor not only the progression of CAV but also the effects of immunosuppressive drugs. In fact, quantitative coronary CTA has been successfully utilized for monitoring of coronary plaques in patients receiving statins [40,45,46] in contrast to earlier studies, such as the SATURN trial [47], which traditionally relayed on IVUS.…”

Statin-Induced Nitric Oxide Signaling: Mechanisms and Therapeutic Implications

“…Secondly, statins improve stability of the plaques, thereby making them less prone to rupture. Although the mechanism for this effect is yet unclear, it has been hypothesized that statins induce plaque calcification [79,80]. By restoring the NO/ONOO− balance and preventing the progression of atherosclerosis, statins activate eNOS, increase NO bioavailability, reduce the release of ONOO− from the endothelium, and increase HO-1 expression and total HO activity [81].…”