Patients With Peripheral Arterial Disease (Lower Extremity, Renal, Mesenteric, and Abdominal Aortic) A Collaborative Report from the American Association for Vascular Surgery/Society for Vascular Surgery,* Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology, and the ACC/AHA Task Force on Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Peripheral Arterial Disease) Endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation; National Heart, Lung, and Blood Institute; Society for Vascular Nursing; TransAtlantic Inter-Society Consensus; and Vascular Disease Foundation

/pdf/acc-aha-2005-practice-guidelines-for-the-management-of-4ltfid6e9i.pdf

ACC/AHA 2005 Practice Guidelines for the Management of Patients With Peripheral Arterial Disease (Lower Extremity, Renal, Mesenteric, and Abdominal Aortic)

Background—Great arteries in congenital heart disease (CHD) may dilate, become aneurysmal, or rupture. Little is known about medial abnormalities in these arterial walls. Accordingly, we studied 18...

Structural abnormalities of great arterial walls in congenital heart disease: light and electron microscopic analyses.

The histologic changes that occur in the media of the normal aorta at various ages were studied in 100 normal aortas. These changes encompassed (1) cystic medial necrosis, defined as pooling of mucoid material; (2) elastin fragmentation, characterized by disruption of elastin lamellae; (3) fibrosis, defined as an increase in collagen at the expense of smooth muscle cells; and (4) medionecrosis, defined as areas with apparent loss of nuclei. The changes showed a striking correlation with age and may represent the normal aging process for the aorta as determined histologically. The alterations showed a close relation in onset and location within the media, suggesting a phenomenon of injury and repair caused by hemodynamic events. These findings in the normal aging aorta reveal that none of the histologic changes observed can be regarded as the specific structural alteration responsible for the development of dissecting aneurysm.

Histologic changes in the normal aging aorta: Implications for dissecting aortic aneurysm

Natural history, pathogenesis, and etiology of thoracic aortic aneurysms and dissections

Characterization of the inflammatory and apoptotic cells in the aortas of patients with ascending thoracic aortic aneurysms and dissections.

Einleitung (S. 186). I. Vorgesehichte und Leiehen6ffnung eines neuen Falles (S. 189). II . Das Bild tier Greisenaort~ (S. 190). I II . Medionecrosis idiopathiea cystiea (S. 194). 1. Kernausfall und Nekrose (S. 194). 2. Mucoide Entartung und Cystenbildung (S. 197). 3. Umbau zur neuen Media (S. 201). 4. Intima, Adventitia (S. 208). 5. Bauehaorta, Iliacae, Pulmonalis, tterz (S. 210). 6. Stellung des neuen Falles zu den bisherigen (S. 211). IV. Einige Einzelfragen (S. 212). 1. Vergleich zwisehen Medianekrose und muscoider Entartung (S. 212). 2. Art des Krankheitsverlaufes (S. 212). 3. Uber Stoffabfuhr (S. 213). 4. Vergleich mit der Aortenlues (S. 214). V. Leistungsunf~higkeit der kranken Aorta (S. 215). VI. Ursaehe tier /YIedionecrosis idiopathica aortae (S. 219). VII. Atherosklerose (S. 223). 1. Das Bild der fortschreitenden Atheromh6hle (S. 224). 2. Nmcbige Heilung der Atheromh6hle (S. 225). 3. Folgen der Atheromatose fiir die Media (S. 227).

Medionecrosis aortae idiopathica cystica

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Medionecrosis aortae idiopathica cystica