Visualization of the human coronary vasa vasorum in vivo.

The role of the VV in the pathogenesis of atherosclerosis has been studied using animal models of atherosclerosis and human autopsy samples. Histological analyses and micro-CT studies of the pig coronary artery have revealed that inflammatory cells accumulate in the adventitia with proliferation of the VV prior to arterial wall thickening.6 In a mouse model of hypert is a generally accepted view that the atherosclerosis process is triggered by endothelial damage induced by lifestyle-related diseases such as hypertension, diabetes and dyslipidemia.1 Thus, it is believed that atherosclerosis progresses ‘inside-out’ from the endothelium to the adventitia. On the other hand, it has been reported that growth of atherosclerotic plaques is accompanied by neovascularization from the vasa vasorum (VV) extending through the tunica media into the base of the plaque.2 The VV consist of small arteries that are distributed to the outer and middle coats of the larger blood vessels. VV invasion can be observed when the vessel wall exceeds a certain thickness, which in mammals is 0.5 mm or 29 lamellar units.3 It is assumed that the VV serve as a conduit for nutrients and oxygen, which can not be supplied to the adventitial and outer medial layers of the larger vessels by diffusion I