14 Atherosclerosis Introduction

Authors: Maria Radu & Klaus Bendtzen, IIR 2005.

Atherosclerosis has long been thought of as a condition caused by the accumulation of lipid-rich plaques in artery walls that physically block the vascular flow, eventually leading to ischemia and later infarction of downstream tissues and organs. It is now widely recognized that atherosclerosis is a chronic inflammatory response to different risk factors, e.g. high plasma cholesterol levels, in particular low-desity lipoprotein (LDL) cholesterol, which is considered one of the culprits for atherosclerosis (1, 2).
Inflammation results from a complex interaction between cells and soluble factors that can arise in any vascularized tissue in response to infectious and noxious stimuli (3, 4). Normally, inflammation leads to recovery and healing with or without scar formation, but if dysregulated, inflammation may by itself cause structural and/or functional tissue damage.


	Atherosclerosis and inflammation
*Authors: Maria Radu & Klaus Bendtzen, IIR 2005.* Atherosclerosis has long been thought of as a condition caused by the accumulation of lipid-rich plaques in artery walls that physically block the vascular flow, eventually leading to ischemia and later infarction of downstream tissues and organs. It is now widely recognized that atherosclerosis is a chronic inflammatory response to different risk factors, e.g. high plasma cholesterol levels, in particular low-desity lipoprotein (LDL) cholesterol, which is considered one of the culprits for atherosclerosis (1, 2). Inflammation results from a complex interaction between cells and soluble factors that can arise in any vascularized tissue in response to infectious and noxious stimuli (3, 4). Normally, inflammation leads to recovery and healing with or without scar formation, but if dysregulated, inflammation may by itself cause structural and/or functional tissue damage.

Figure 1 The normal human large- and middle-sized elastic artery has a trilaminar structure. In contact with the blood are endothelial cells (ECs) that rest upon a basement membrane. Underneath is the intimal layer, consisting of smooth muscle cells (SMCs) scattered within the intimal extracellular matrix. The barrier between the tunica intima and media is formed by the internal elastic lamina. Tunica media consists of multiple layers of tightly packed SMCs embedded in a matrix rich in elastin and collagen. Finally, the external elastic lamina makes up the transition to the outermost layer, the adventitia. The inner two thirds of the artery wall are supplied with blood from the lumen, whereas the outer one third is nourished by the vasa vasorum. The state of contraction is controlled by the autonomic nervous system but also by the local release of hormones and nitric oxide from ECs (5).