Elastin metabolism of the infrarenal aorta

Abstract

Aortic tissue elastase and alpha 1-antitrypsin were assayed in 67 patients with different types of infrarenal aortic disease; occlusive disease, elective abdominal aortic aneurysms (AAAs), multiple aneurysms, and ruptured aneurysms. Elastase modified by alpha 1-antitrypsin (elastase/alpha 1-antitrypsin) increased significantly as the type of aortic disease changed from occlusive to aneurysmal disease. Aortic elastase was significantly higher in patients with AAAs, multiple aneurysms, and ruptured AAAs compared with occlusive disease. The alpha 1-antitrypsin, was significantly lower in patients with multiple aneurysms and ruptured AAAs. These data suggest that the ratio between elastase and its major serum inhibitor, alpha 1-antitrypsin, is significantly altered in the aortic wall in different types of infrarenal aortic disease. In addition, the ratio between these two enzyme systems changes in favor of more proteolytic activity as the type of infrarenal disease changes from occlusive to aneurysmal.

Etiology and Pathogenisis of Aortic Aneurysm

“…Dobrin et al concluded that both elastin and collagen are possibly critical in AA dilatation with collagen failure resulting in gross expansion and rupture . This work confirmed experimental studies demonstrating that treatment with elastase leads to arterial dilatation and stiffening at physiologic pressures, whereas treatment with collagenase leads to arterial rupture without dilatation (Cohen et al, 1988). Cohen suggested that elastin degradation is a key step in the development of aneurysms, but that collagen degradation is ultimately required for aneurysm rupture.…”

“…This reflects in experimental studies that suggest that aortic elastase is significantly higher in patients with AAAs, multiple aneurysms, and ruptured AAAs compared with AOD. Also elastase and its major serum inhibitor, alpha 1-antitrypsin, are significantly altered in the aortic wall in different types of infrarenal aortic disease (Cohen et al, 1988). AA development is characterised by intial elastin fragmentation responsible for aneurysmal elongation and tortuosity.…”

“…Other studies confirmed that both elastin and collagen content is decreased in AA walls with increased collagen cross-links (Carmo et al, 2002) and an increased collagen to elastin ratio. (Cohen et al, 1988) Loss of elastin appears to be accompanied by an increase in the collagen content of the arterial wall, resulting in an overall decrease in the elastin to collagen ratio (Halloran & Baxter, 1995). This reflects in experimental studies that suggest that aortic elastase is significantly higher in patients with AAAs, multiple aneurysms, and ruptured AAAs compared with AOD.…”

Critical role of dipeptidyl peptidase I in neutrophil recruitment during the development of experimental abdominal aortic aneurysms

“…While abundant evidence has implicated matrix metalloproteinases in the elastin degradation that accompanies AAAs (4,(6)(7)(8)(9)(10)(11), the role of serine proteases has received much less attention (12). Early studies, however, indicated that human AAA tissues express a higher amount of elastase activity compared with normal or atherosclerotic aortas and that elastase activity is highest in patients with ruptured AAAs (13)(14)(15). Immunoreactive neutrophils are also evident within the adventitia and mural thrombus of AAAs, suggesting that release of neutrophil serine proteases might play an important but poorly understood role in aneurysmal degeneration (16,17).…”

Splenic artery aneurysm and orthotopic liver transplantation

“…Ruptured splenic artery aneurysm has also been reported in a patient with cirrhosis secondary to alpha-l-antitrypsin deficiency [17], as well as in a patient with iliac artery dissection [4]. Alpha-1 -antitrypsin content in the aortic wall has been found to be significantly lower in patients with multiple infra-renal aneurysms and ruptured abdominal aortic aneurysms [5]. Alpha-l-antitrypsin deficiency has also been associated with rupture of a middle colic artery aneurysm in a patient with multiple visceral aneurysms [12] and with rupture of an intra-cranial aneurysm and spontaneous dissection of the internal carotid artery [15].…”