<b>Arteries</b>
 
Late radiation symptoms at most sites are caused by widespread, premature blood vessel aging, radiation-induced arteriosclerosis, and radiation-induced blood vessel obliteration, leading to tissue death and scarring. <b>Compromise of tissue circulation can occur wherever the blood vessels were exposed to radiation</b>. It is established that small and medium sized arteries undergo extensive radiation damage. Larger artery stenosis [e.g. carotid, axillary, subclavian] may also present in patients who have undergone radiotherapy.
 
The arterial changes resemble chronic, progressive arteriosclerosis. This may be due to a combination of scarring around the artery, direct damage to the arterial wall, severe damage to and obliteration of the tiny arteries that nourish the larger arteries' walls, and acceleration of naturally occurring arteriosclerosis. Factors that may predispose to arterial occlusion that relate to radiotherapy include maximum tissue dose, beam energy and field size. The time interval between radiotherapy because of malignancy and onset of symptoms due to radiation-induced arteriosclerosis ranged from 1 month to 29 years in one study. 

A typical finding at angiography was the well-localized vascular lesion in the previous radiation area, its localisation clearly distinguishable from typical arteriosclerosis. Due to absence of multifocal arteriosclerotic lesions, long-term results of vascular reconstruction are good and will certainly contribute to further improvement of life quality after curative therapy for malignant disease. Aneurysms of arteries also can occur in association with radiation treatment. An aneurysm occurs when an artery wall is very weak in an area, and the wall bulges out. 

<b>Irradiation of large blood vessels in the course of tumor therapy represents a long-term local risk factor for development of arteriosclerosis</b>. Inclusion of major arteries into the radiation field is often inevitable: in a series of clinical studies, a consistent 3- to 4-fold increase in carotid stenoses is observed following radiation therapy of head and neck tumors. The majority of clinically symptomatic stenoses, however, is not observed earlier than 8 years post irradiation. Although observations in other peripheral arteries do not allow estimating incidences, they do confirm, however, the finding of a very long latent time. Following mediastinal or thoracic wall irradiation, the risk of coronary artery disease is significantly increased after 10 years or more. Radiation related arterial injury is sharply limited to arterial segments included in the treatment field and is often observed in unusual locations. The histological appearance and development however, is not fundamentally different from lesions observed in cases of generalized arteriosclerosis. Experimental observations indicate that patients with general arteriosclerosis risk factors might have a particularly increased risk of developing arterial injury following therapeutic irradiation. 

The studies of late radiation effects upon Skin, Brain, Bone, Heart, Lung, Eye, Spinal Cord and Muscle, <b>all seem to reinforce the concept of the blood vessel wall being the prime site of radiation damage</b>. Most, even all, of the subsequent damage is due to the loss of blood supply to these tissues, and consequent cell death. The tissues then show widespread fibrosis [a kind of scarring.] The effect of radiation can be an on-going process; the percentage of small arteries with cell wall damage increasing with the time after radiotherapy. 

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