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Atherosclerosis derives from the Greek word for “gruel” or “porridge”, demonstrating the manifestation of the lipid material found in the core of the typical atherosclerotic plague [7]. Though the exact initiator of atherosclerotic plaque formation is still debatable, there is a general consensus that the endothelial denuding injury, which could be triggered by multiple causes, such as smoking, hypertension, hyperglycaemia, immune injury, infection, sets a complex pathogenic sequence into motion [7–9]. From this point on, an inflammatory response leads to the development of the plaque. Endothelial cell dysfunction leads to platelet aggregation and release of platelet factors which subsequently recruit circulating monocytes from the blood into the intima, where they differentiate into macrophages and induce the proliferation of smooth muscle cells in an attempt to restore endothelial function. These cells will expand the extracellular matrix that would entrap and modify lipoproteins to become lipid‐rich foam cells, forming a fibromuscular plaque [7,8].