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The vascular system consists of a complex network of vessels designed to distribute oxygen, fluid, and nutrients to all tissues of the body and remove waste products from the tissue to be excreted from the body. When any component of the vascular system fails, the normal homeostasis is disrupted. Diseases of the arterial system can be particularly catastrophic and constitute the majority of many vascular surgeons’ clinical practice. The most common arterial pathologies treated by vascular surgeons include atherosclerotic disease, aneurysmal disease, aortic dissections, and intimal hyperplasia. While distinct entities, each of these pathologies shares similar underlying pathobiological mechanisms, and they often occur synchronously. Optimal preoperative, intraoperative, and postoperative care for arterial disease requires an intimate understanding of arterial wall anatomy and hemodynamics as most arterial diseases progress in generally predictable patterns directly linked to changes in wall anatomy and subsequent alterations in hemodynamics. Knowledge of the basic anatomy and pathophysiology is important for the consideration of therapies (Table 24-1).

TABLE 24-1Factors That Contribute to the Development and Progression of Atherosclerotic and Aneurysmal Arterial Disease


Each artery wall consists of three tunicae, or layers—the tunica intima, tunica media, and the tunica adventitia. Each layer is structurally distinct and has a unique role in vessel physiology.

On the luminal surface of the tunica intima is the endothelium—a continuous monolayer of endothelial cells. These cells play critical roles in vessel hemostasis, vasomotor tone, vascular thrombosis, and immunity.1,2 Endothelial cells respond to both physical and chemical stresses at the vessel’s luminal surface. They realign parallel to the shear stress on the vessel wall created by constant blood flow.3 Shear stress also increases production of stress fibers and release of vasodilators by the endothelial cells. In contrast, circumferential stress on the vessel wall due to blood pressure oscillation with each heartbeat induces endothelial cell proliferation. The endothelial cell surface is coated with an antithrombogenic glycocalyx to prevent intraluminal thrombus in intact vessels.4 The basal lamina of the intima contains significant amounts of collagen, laminin, and fibronectin, providing strength and distributing mechanical stress throughout the artery wall.5–7 The internal elastic laminal, which separates the tunica intima from the tunica media is comprised primarily of elastic fibers. The internal elastic lamina serves as a barrier ...

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