Abstract
Subendothelial accumulation of apo-lipoprotein B with high content of lipoproteins in the predisposed sections of the artery with diffuse intimal thickening is the main mechanism of the development of coronary atherosclerosis. A local biological response to these stored and subsequently modified lipoproteins is a chronic inflammation mediated primarily by macrophages and T cells.
Lipid lowering by high intensity statin treatment leads to the stabilization of coronary plaques and reduction of the occurrences of clinical episodes of destabilisation of coronary disease. Using the newer high precision imaging techniques such as intracoronary ultrasound, virtual histology, optical coherence tomography and NMR showed that the reduction of LDL-cholesterol using high intensity statin therapy leads to demonstrable regression of coronary plaques.
Just completed GLAGOV study demonstrated the possibility of further lowering of LDL cholesterol by combination therapy of high intensity statins with PCSK9 inhibitor evolocumab. Further decline in LDL levels as compared to previous studies was observed with corresponding regression of the plaque volume as demonstrated by intracoronary ultrasound.