What is a characteristic of atherosclerosis is a deposit of plaque on or within the arterial wall?

Main Arteries, Veins, and Branches Around the Shoulder

axillary artery: a continuum of the subclavian artery in the axillary area that branches into highest thoracic, lateral thoracic, anterior humeral circumflex, posterior humeral circumflex, thoracoacromial, and subscapularis.

brachial artery: a continuum of the axillary artery and main artery of the arm. The branches are listed in “Surgery of the Arm and Forearm” later in this chapter.

cephalic vein: large vein between the deltoid and pectoralis muscles.

subclavian and axillary vein: the continuous vessel running alongside the subclavian and axillary arteries. The branches are not consistent and are rarely described in orthopaedic procedures.

subclavian artery: main artery from the chest leading down through the arm that branches into internal thoracic, vertebral, thyrocervical, transcervical, superior intercostal, and suprascapular.

Abstract

Transplant arteriosclerosis (TA) is a vascular condition characterized by concentric arteriosclerotic thickening of the intima of arteries within transplanted organs and also involves functional abnormalities that prevent proper vasodilation. It occurs in all solid organ transplants and is established in heart transplantation to be a main cause of late graft failure. The structural and functional changes that occur in TA compromise blood flow and lead to ischemic damage of the graft. The pathogenesis of TA involves immune targeting of vascular cells, which results in vascular cell damage and dysfunction. The resultant response of blood vessels to these immune-driven alterations leads to arteriosclerotic thickening and vasomotor dysfunction. Here, we discuss the immunopathological mechanisms underlying the development of TA and current therapeutic strategies for its prevention.

Arteriosclerosis.

Arteriosclerosis is characterized by intimal fibrosis of large elastic arteries, atherosclerosis is characterized by intimal and medial lipid deposits in elastic and muscular arteries, and arterial medial calcification has characteristic mineralization of the walls of elastic and muscular arteries.

Arteriosclerosis is an age-related disease that occurs frequently in many animal species but rarely causes clinical signs. The disease develops as chronic degenerative and proliferative responses in the arterial wall and results in loss of elasticity (“hardening of the arteries”) and, less often, luminal narrowing. The abdominal aorta is most frequently affected, but other elastic arteries and peripheral large muscular vessels may be involved. Lesions are often localized around the orifices of arterial branches. Etiologic factors in the development of arteriosclerosis are not well defined, but the significant role of hemodynamic influences is suggested by the frequent involvement at arterial branching sites, in which blood flow is turbulent. Grossly, the lesions are seen as slightly raised, firm, white plaques. Microscopically, initially the intima is thickened by accumulation of mucopolysaccharides and later by the proliferation of smooth muscle cells in the tunica media and fibrous tissue infiltration into the intima. Splitting and fragmentation of the internal elastic lamina are common

Arteriosclerosis

Arteriosclerosis is characterized by conduit artery dilatation and diffuse, non-occlusive medial and intimal wall hypertrophy. The oscillatory component of blood pressure is determined by the pattern of LV ejection, the viscoelastic properties of the large conduit arteries and the reflection of pulse waves.36 Faster pulse wave velocity is associated with arterial stiffness resulting from arteriosclerosis. Consequently, early rebound of pressure waves from the distal vessels increases systolic pressure and predisposes to LVH, and low diastolic pressure predisposes to diminished coronary flow during diastole. In both CKD and non-CKD patients, faster pulse wave velocity is correlated with shortened stature, male gender, smoking, hypertension, diabetes, volume overload, humoral imbalance and age. In CKD increased prolactin levels significantly and independently contribute to the variance of both flow-mediated dilation and pulse wave velocity, but not in intima-media thickness. In addition to this association with endothelial dysfunction and arterial stiffness, prolactin levels were associated with increased risk of cardiovascular events and mortality.37

Vascular pathology

Arteriosclerosis, infarcts of various sizes, and hypoxic-ischemic cell alterations are common changes that are observed in the brains of aged subjects (Fig. 10.6). No consensus has been reached in the community regarding how these alterations should be assessed and graded (Alafuzoff et al., 2012). The clinical relevance of these alterations is also unclear. It is however recommended to register the vascular alteration, as they have been reported as being of significance in age-related cognitive decline (Qiu and Fratiglioni, 2015). Vascular tissue alterations should be registered while assessing the brain by the naked eye but also in the sampled tissue stained by histochemical stains such as hematoxylin and eosin (Fig. 10.1 and Table 10.1).

Vascular Cells

Vascular sclerosis is an integral feature of the renal scarring process. Renal arteriolar hyalinosis is present in CKD at an early stage, even in the absence of severe hypertension. Furthermore, these vascular changes are often out of proportion to the severity of systemic hypertension. Vascular sclerosis is associated with progressive kidney failure in glomerulonephritis. Hyalinosis of afferent arterioles has been implicated in the pathogenesis of diabetic glomerulosclerosis. Changes in postglomerular arterioles and damage to peritubular capillaries may further exacerbate interstitial ischemia and fibrosis. Ischemia and the ensuing hypoxia are fibrogenic influences that stimulate tubular cells and kidney fibroblasts to produce ECM components and to reduce their collagenolytic activity.46

Loss of peritubular capillaries with the associated impaired angiogenesis has been linked in experimental models of renal scarring to a fall in the renal expression of the proangiogenic VEGF. Together with an overexpression by scarred kidneys of thrombospondin, an antiangiogenic factor, this would perpetuate microvascular deletion and ischemia.47 The administration of VEGF preserves peritubular capillaries and improves scarring and functional outcome. Finally, the vascular endothelium, adventitia, and pericytes may be a source of interstitial myofibroblasts, contributing to the development of interstitial renal fibrosis.48

Recent evidence also points to lymphatic neoangiogenesis in association with interstitial inflammation and progressive renal fibrosis.49 Such a process appears to be driven by macrophages that express the lymphangiotropic growth factor VEGF-C. It may play a role in interstitial remodeling as it provides an exit route for inflammatory cells involved in interstitial inflammation.

ARTERIOSCLEROSIS

Abstract

Arteriosclerosis is a group of conditions characterized by thickening and stiffening of the arterial wall. Atherosclerosis is characterized by the formation of atheromas (lipid-laden plaques) in medium to large arteries. These are associated with calcifications of the arterial wall along with other changes. Atherosclerosis can cause clinically important vascular pathology by slow encroachment on the lumen as in occlusive coronary artery disease. Alternatively, because the endothelium overlying atheromata is abnormal, platelet aggregation occurs, and this promotes occlusive clot formation. Lastly, rupture of the plaque can also lead to rapid vascular occlusion with clot. Over the years there have been a variety of hypotheses seeking to explain the development of arterial lesions; these hypotheses have become increasingly complex as our biochemical and molecular biological skills and knowledge increase.

Arteriosclerosis

Arteriosclerosis is the progressive replacement of smooth muscle cells with proteinaceous material (predominantly collagen) within the media of small arteries and arterioles (40 to 400 μm in diameter). The microscopic appearance is of concentric layers of a hyaline substance in the same location where smooth muscle normally occurs. The most strongly associated risk factors are hypertension and diabetes. As the process continues, the lumen constricts, which results in progressive tissue hypoperfusion. The latter is exacerbated during periods of hypotension, because the loss of smooth muscle prevents vasodilation. In certain cases, especially with accelerated hypertension, the same vessels develop a more disorganized process, which results in patchy fibrinoid accumulation, necrosis, and foam cell formation. When this accumulation is rapid, the end result may be acute small-vessel or lacunar infarction. From a therapeutic point of view, this knowledge is important, because it explains why anticoagulation and thrombolysis have no effect on stroke from this cause.

8.9 Arteriosclerosis and Blood Flow

Arteriosclerosis is the most common of cardiovascular diseases. In the United States, an estimated 200,000 people die annually as a consequence of this disease. In arteriosclerosis, the arterial wall becomes thickened, and the artery is narrowed by deposits called plaque. This condition may seriously impair the functioning of the circulatory system. A 50 % narrowing (stenosis) of the arterial area is considered moderate. Sixty to seventy percent is considered severe, and a narrowing above 80% is deemed critical. One problem caused by stenosis is made clear by Bernoulli’s equation. The blood flow through the region of constriction is speeded up. If, for example, the radius of the artery is narrowed by a factor of 3, the cross-sectional area decreases by a factor of 9, which results in a nine-fold increase in velocity. In the constriction, the kinetic energy increases by 92, or 81. The increased kinetic energy is at the expense of the blood pressure; that is, in order to maintain the flow rate at the higher velocity, the potential energy due to pressure is converted to kinetic energy. As a result, the blood pressure in the constricted region drops. For example, if in the unobstructed artery the flow velocity is 50 cm/sec, then in the constricted region, where the area is reduced by a factor of 9, the velocity is 450 cm/sec. Correspondingly, the pressure is decreased by about 80 torr (see Exercise 8-8). Because of the low pressure inside the artery, the external pressure may actually close off the artery and block the flow of blood. When such a blockage occurs in the coronary artery, which supplies blood to the heart muscle, the heart stops functioning.

Stenosis above 80% is considered critical because at this point the blood flow usually becomes turbulent with inherently larger energy dissipation than is associated with laminar flow. As a result, the pressure drop in the situation presented earlier is even larger than calculated using Bernoulli’s equation. Further, turbulent flow can damage the circulatory system because parts of the flow are directed toward the artery wall rather than parallel to it, as in laminar flow. The blood impinging on the arterial wall may dislodge some of the plaque deposit which downstream may clog a narrower part of the artery. If such clogging occurs in a cervical artery, blood flow to some part of the brain is interrupted causing an ischemic stroke.

There is another problem associated with arterial plaque deposit. The artery has a specific elasticity; therefore, it exhibits certain springlike properties. Specifically, in analogy with a spring, the artery has a natural frequency at which it can be readily set into vibrational motion. (See Chapter 5, Eq. 5.6.) The natural frequency of a healthy artery is in the range 1 to 2 kilohertz. Deposits of plaque cause an increase in the mass of the arterial wall and a decrease in its elasticity. As a result, the natural frequency of the artery is significantly decreased, often down to a few hundred hertz. Pulsating blood flow contains frequency components in the range of 450 hertz. The plaque-coated artery with its lowered natural frequency may now be set into resonant vibrational motion, which may dislodge plaque deposits or cause further damage to the arterial wall.