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Inflammatory aneurysms

Atherothromboembolism ntracranial small vessel disease Leukoaraiosis Dissection (Table 6.4) Fibromuscular dysplasia Congenital arterial anomalies Moyamoya syndrome Embolism from arterial aneurysms Inflammatory vascular diseases Irradiation... [Pg.56]

Gavish L, Perez LS, Reissman P, Gertz SD (2008) Irradiation with 780 nm diode laser attenuates inflammatory cytokines but upregulates nitric oxide in lipopolysaccharide-stimulated macrophages implications for the prevention of aneurysm progression. Lasers Surg Med 40(5) 371-378... [Pg.274]

Artwork Description Top Left Panel Neuronal Immunocytochemistry Composite. Top Right Panel Magnetic Resonance Image of an Adult Human Brain. Bottom Left Panel Cerebral Angiogram Highlighting an Aneurysm. Bottom Right Panel Immunocytochemistry Highlighting Blood Vessels and Inflammatory Cells in an Ischemic Brain. Created by Elizabeth Hoyte and Carolina Maier. [Pg.194]

Spinal subarachnoid hemorrhage is very rare. It is caused by a vascular malformation, hemostatic failure, coarctation of the aorta, inflammatory vascular disease, mycotic aneurysm or a vascular tumor such as ependymoma. Accumulating hematoma may compress the spinal cord. Suspicion is aroused if the cerebral angiogram is negative and the patient develops spinal cord signs. [Pg.354]

For subarachnoid hemorrhage surgical clipping of the causative aneurysm or resection of the arteriovenous malformation is the mainstay of treatment. Endovascular coiling of the aneurysm can also be performed. Post-operative infection (either brain or respiratory) is an uncommon complication and not believed to be any more common than after other invasive surgical procedures. Hypervolemic-hemodilution and hypertensive (HHH) therapy is used to prevent spasm. There may be a role for anti-inflammatory measures for the prevention of vasospasm and delayed cerebral ischemia, as shown in a recent pilot study of patients treated with statins (Lynch et al., 2005). [Pg.439]

Fig. 32.12 PSC periductal fibrosis and inflammatory infiltration aneurysmal bile-duct ectasia (HE)... Fig. 32.12 PSC periductal fibrosis and inflammatory infiltration aneurysmal bile-duct ectasia (HE)...
Congenital anomalies and aneurysms in the hepatic arteries are very rare. (129) Acquired aneurysms are the result of vessel wall damage, injuries or inflammatory processes. (I3l, 133, 136) Pseudoaneurysms may occur after acute pancreatitis and the formation of pseudocysts. (135) (s. tab. 39.5)... [Pg.837]

A 71-year-old man with bladder carcinoma in situ received six instillations of BCG at weekly intervals followed 3 months later by three booster instillations at weekly intervals. Four months later an inflammatory aortic aneurysm, which had ruptured into a pseudoaneurysm, was diagnosed and excised. Mycobacterium bovis was found. After treatment with isoniazid and rifampicin he recovered. There was no sign of tumor in the bladder at cystocopy 8 months after the last BCG instillation. [Pg.399]

A 48-year-old man with an inflammatory aneurysm of the ascending aorta and severe heart failure due to massive aortic regurgitation was given a continuous intravenous infusion of milrinone O.Smicrograms/kg/ minute (1). His pulmonary arterial pressure fell and his symptoms improved over 7 weeks while he was taking corticosteroids. The diseased tissue was successfully replaced at operation and the milrinone was tapered uneventfully. [Pg.2346]

Atrial fibrillation with mitral valve disease has long been considered a stroke risk factor. Recurrent embolism occurs in 30-65% of patients with rheumatic mitral valve disease who have a history of a previous embolic event. Most of these recurrences (around 60%) develop within the first year. Mechanical prosthetic valves are a prime site for thrombus formation and patients with these valves require anticoagulation [7, 38]. Bacterial endocarditis can cause stroke as well as intracerebral mycotic aneurysms. Because mycotic aneurysms are inflammatory defects in the vessel wall, treatment with systemic thrombolysis or anticoagulation can lead to rupture with subsequent lobar hemorrhage. Nonbacterial, or marantic, endocarditis is also associated with multiple embolic strokes. This condition is most common in patients with mucinous carcinoma and may be associated with a low-grade disseminated intravascular coagulation. A nonbacterial endocarditis, called Libman-Sacks endocarditis, occurs in patients with systemic lupus erythematosus (SLE) [42],... [Pg.32]

There has been a long-standing interest in the role of MMPs in cardiovascular disease (D2). Numerous studies have demonstrated increased levels of MMPs, especially MMP-9, at sites of atherosclerosis and aneurysms (G3, V2). The current opinion that the inflammatory process may play a leading role in the development of vascular atherosclerotic plaques has led to the suggestion that secretion and activation of MMPs by macrophages induces degradation of extracellular matrix in the atherosclerotic plaque leading to plaque rupture. Based on these concepts, MMPs have been proposed to represent sensitive markers of inflammation in patients with coronary artery disease. [Pg.43]

Chronic infection with C burnetii is usually manifested by infective endocarditis, which is also the most severe complication of Q fever. In addition, a report73 from France of 92 cases published in 1993 also listed hepatitis, infected vascular prostheses and aneurysms, osteomyelitis, pulmonary infection, cutaneous infection, and an asymptomatic form. In addition, 7 of the 92 patients described in this report experienced fever only. Also noted was the observation that although 81% of patients had an identifiable risk factor, only 31% lived in a rural area. In addition, some form of immunodeficiency was observed in 20% of the patients, raising the possibility that chronic Q fever occurs as a result of reactivation of latent infection.73 Inflammatory pseudotumor of the lung as a chronic complication of Q fever has also been reported.74,75... [Pg.530]

Inflammatory transmural angiitis in systemic lupus erythematosus, polyarteritis nodosa, or giant cell arteritis causes focal fibrinoid necrosis and elastic tissue disruption. Subacute or chronic changes usually produce ectasia and may facilitate aneurysm formation. Aneurysms in acute arteritis tend to be multiple, peripheral and non side-wall in configuration. [Pg.174]

The third approach is in the implantation of functional tissue that is developed ex vivo. This approach attempts to create a biological substitute made from synthetic materials to be used as grafts or cardiac patches for treating HF. Clinically used materials include synthetic woven Dacron, extended polytetrafluoroethylene (ePTFE), and natural glutaraldehyde-fixed pericardium. These materials, however, have limited success rates due to thrombosis, inflammatory response, mechanical mismatch between native tissue and implants, aneurysm, and lack of remodeling for natural materials. ... [Pg.3448]

Clinical Applications 300 Aortic Aneurysm 300 Thoracic Aortic Aneurysm 300 Abdominal Aortic Aneurysm 302 Inflammatory Aortic Aneurysm 303 Aortic Dissection 304 Stanford A Dissection 305 Stanford B Dissection 305 Penetrating Aortic Ulcer 306 IMH 306 Aortitis 307 Injury of the Aorta 307 CTA in Endovascular Aortic Reconstruction 308... [Pg.297]

The inflammatory AAA is a variant of an AAA accompanied by a thickened aneurysm wall and a periaortic or retroperitoneal fibrosis. They are associated with increased morbidities. Some authors describe that they represent between 3 and 10% of AAAs (Tang et al. 2005), while others report between 10 and 30% (Theisen et al. 2007). The inflammatory components show increased enhancement of contrast... [Pg.303]

Takayasu s arteritis can affect the whole aorta and its side branches. In the acute stage of the disease, CT and MRI show an inflammatory thickening of the aortic waU, with increased contrast enhancement. This enables the differentiation from atherosclerotic transformations of the aortic wall. In MRI, edema of the waU can additionally be detectable (Yamada et al. 1998). In chronic stages of the disease (weeks to months), long-segment stenosis of occlusion with the formation of collateral circulation, intraluminal thrombi, and calcifications of the aortic wall can be seen. The incidence of aortic aneurysms in Takayasu s arteritis lies between 30 and 50%... [Pg.307]

Takahashi K, Stanford W (2005) Multidetector CT of the thoracic aorta. Int J Cardiovasc Imaging 21 141-153 Tang T, Boyle JR, Dixon AK, Varty K (2005) Inflammatory abdominal aortic aneurysms. Eur J Vase Endovasc Surg... [Pg.310]

Wallis F, Roditi GH, Redpath TW, Weir J, Cross KS, Smith FW (2000) Inflammatory abdominal aortic aneurysms diagnosis with gadolinium enhanced Tl-weighted imaging. Clin Radiol 55 136-139... [Pg.310]

Generally, SMA aneurysms are mycotic, celiac aneurysms develop from cystic medial degeneration, GDA pseudoaneurysms occur in the presence of duodenal ulceration, and gastroepiploic and pancreaticoduodenal aneurysms arise secondary to inflammatory changes from pancreatitis. Other causes include polyarteritis nodosa, amphetamine abuse, and connective tissue disorders. [Pg.111]

Involvement of medium-sized or large arteries is rare in WG. However, case reports of WG with aneurysms or macroscopic inflammatory lesions involving... [Pg.616]


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See also in sourсe #XX -- [ Pg.174 ]




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