12-05-2011, 03:22 PM
Imaging Case : Aortic Dissection
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PATHOGENESIS — etiologies for a thoracic aneurysm.
Association with atherosclerosis — The vast majority of thoracic aneurysms are associated with atherosclerosis and the risk factors for aneurysm formation are the same as those for atherosclerosis (eg, hypertension, hypercholesterolemia, smoking) . However, it remains unclear whether atherosclerosis is actually responsible for aneurysm formation [6]. It seems likely that there is a multifactorial, systemic, nonatherosclerotic causal process, such as a defect in vascular structural proteins, with atherosclerosis occurring secondarily.
Most theories emphasize the primary role of breakdown of the extracellular matrix proteins elastin and collagen by proteases such as collagenase, elastase, various matrix metalloproteinases, and plasmin (formed from plasminogen by urokinase plasminogen activator and tissue type plasminogen activator) [8]. These proteolytic factors are derived from endothelial and smooth muscle cells and from inflammatory cells infiltrating the media and adventitia [8].
The combination of protein degradation and mechanical factors are thought to cause cystic medial necrosis, which has the appearance of smooth muscle cell necrosis and elastic fiber degeneration with cystic spaces in the media filled with mucoid material. These changes result in vessel dilatation and subsequent aneurysm formation and possible rupture.
The following observations in animal models are consistent with the importance of plasmin and metalloproteinases in aortic aneurysm formation:
• Blockade of plasmin formation by overexpression of plasminogen activator inhibitor-1 prevents the formation of aneurysms and rupture by inhibiting metalloproteinase activation [9].
• Aneurysm rupture correlates with an increase in metalloproteinase (gelatinase A and B) levels; local overexpression of tissue inhibitor of matrix metalloproteinases, produced by retrovirally infected smooth muscle cells, can prevent aneurysmal degeneration and rupture
http://cmbi.bjmu.edu.cn/uptodate/picture...ortic4.gif
http://cmbi.bjmu.edu.cn/uptodate/Valvula...eurysm.htm
http://cardiologycases.files.wordpress.c...ion-1b.png
http://cardiologycases.wordpress.com/201...issection/
PATHOGENESIS — etiologies for a thoracic aneurysm.
Association with atherosclerosis — The vast majority of thoracic aneurysms are associated with atherosclerosis and the risk factors for aneurysm formation are the same as those for atherosclerosis (eg, hypertension, hypercholesterolemia, smoking) . However, it remains unclear whether atherosclerosis is actually responsible for aneurysm formation [6]. It seems likely that there is a multifactorial, systemic, nonatherosclerotic causal process, such as a defect in vascular structural proteins, with atherosclerosis occurring secondarily.
Most theories emphasize the primary role of breakdown of the extracellular matrix proteins elastin and collagen by proteases such as collagenase, elastase, various matrix metalloproteinases, and plasmin (formed from plasminogen by urokinase plasminogen activator and tissue type plasminogen activator) [8]. These proteolytic factors are derived from endothelial and smooth muscle cells and from inflammatory cells infiltrating the media and adventitia [8].
The combination of protein degradation and mechanical factors are thought to cause cystic medial necrosis, which has the appearance of smooth muscle cell necrosis and elastic fiber degeneration with cystic spaces in the media filled with mucoid material. These changes result in vessel dilatation and subsequent aneurysm formation and possible rupture.
The following observations in animal models are consistent with the importance of plasmin and metalloproteinases in aortic aneurysm formation:
• Blockade of plasmin formation by overexpression of plasminogen activator inhibitor-1 prevents the formation of aneurysms and rupture by inhibiting metalloproteinase activation [9].
• Aneurysm rupture correlates with an increase in metalloproteinase (gelatinase A and B) levels; local overexpression of tissue inhibitor of matrix metalloproteinases, produced by retrovirally infected smooth muscle cells, can prevent aneurysmal degeneration and rupture
http://cmbi.bjmu.edu.cn/uptodate/picture...ortic4.gif
http://cmbi.bjmu.edu.cn/uptodate/Valvula...eurysm.htm