The development of atherosclerotic plaques can be thought of as a variable side-effect responsive to the onset dynamics of blood flow and endothelial injury in particular. Endothelial dysfunction marks the extent of atherosclerosis.¹ The response to injury of the endothelium seems to be a reappraisal of dynamics of a process in terms of increased permeability to lipids. Hypercholesterolaemia can induce a variable degree of injury to endothelial cells that is associated with, in particular, the increased permeability of these cells. Chemokines are an essential response mechanism relative to the entry of lipids to the subintima that further progresses as macrophage receptivity and secretory activity. Vascular inflammation induced by the proinflammatory cytokine/nuclear factor κBpathway is important in atherogenesis.²

The localisation of individual plaques demonstrates the evolving nature of a lesion that implicates a primary proliferative response of the medial smooth muscle cells in the first instance and subsequent injury to the endothelium. The circulating endothelial progenitor cells are implicated in angiogenesis, and the smooth muscle progenitor cells promote atherogenesis.³

The concurrently evolving consequences of endothelial injury in parallel with further proliferation and ingrowth of smooth muscle cells within an incipient focus of lipid deposition and of foam cells demonstrates the ongoing processes of receptivity, centred particularly on the endothelial surface. Arterial thrombosis is the principal complication of atherosclerosis leading to stroke and myocardial infarction.⁴

THE MACROPHAGE

The macrophage is an exquisitely sensitive system in the development of parallel pathways in the evolution of both increased endothelial damage and proliferation of smooth muscle cells.⁵ Neutrophil activation is linked to progression of atherosclerosis.⁶

The chemotactic attraction of monocytes by monocyte chemoattractant protein-1,⁷ can self-propagate as a system of amplified effect that …