Impact of shear stress and atherosclerosis on entrance-tear formation in patients with acute aortic syndromes

Abstract

Weak aortic media layers can lead to intimal tear (IT) in patients with overt aortic dissection (AD), and aortic plaque rupture is thought to progress to penetrating atherosclerotic ulcer (PAU) with intramural hematoma (IMH). However, the influences of shear stress and atherosclerosis on IT and PAU have not been fully examined. Ninety-eight patients with overt AD and 30 patients with IMH and PAU admitted to our hospital from 2002 to 2007 were enrolled. The greater curvatures of the aorta, including the anterior and right portions of the ascending aorta and anterior portion of the aortic arch, were defined as sites of high shear stress. The other portions of the aorta were defined as sites of low shear stress based on anatomic and hydrodynamic theories. Aortic calcified points (ACPs) were manually counted on computed tomography slices of the whole aorta every 10 mm from the top of the arch to the abdominal bifurcation point. IT was more often observed at sites of high shear stress in overt AD than in PAU (73.5 vs 20.0 %, P < 0.0001). Significantly more ACPs were present in PAU than in overt AD (18.6 ± 8 vs 13.3 ± 10, P = 0.007). The present study suggests that high shear stress and less severe atherosclerosis could induce the occurrence of an IT, thereafter progressing to overt AD, and that low shear stress and more severe atherosclerosis could proceed to PAU with IMH. These findings may help to identify the entrance-tear site.

Clinicopathological study on penetrating atherosclerotic ulcers and aortic dissection: distinct pattern of development of initial event

“…On clinical examination, the patients with AD showed a high prevalence of hypertension, but low prevalence of hypercholesterolemia, diabetes mellitus, and obesity. These findings suggest that atherosclerosis may not be a risk factor for AD, which is consistent with previous reports [5,7,12].…”

“…In contrast, severe atherosclerosis was not associated with AD, but with PAU, also consistent with previous reports [5,7]. Hypertension has always been considered the mechanical force that finally leads to aortic wall rupture [14].…”

“…Twenty-five (92.6 %) of the 27 patients in the AD group and 4 (40 %) of the 10 patients in the PAU group were clinically diagnosed with The role of atherosclerosis in the progression of AD is controversial. Some investigators do not consider atherosclerosis as a risk factor of AD [5,7,12]. On the other hand, a few reports suggest that rupture of ulcerocalcific aortic atheromas may have initiated the intimal tear in AD, particularly in type III dissection [13].…”

“…In contrast, the entrance tear was considered as plaque ulcer in 8 (80.0 %) of the 10 patients with PAU. The patients with PAU showed a significantly higher prevalence of soft plaque, complicated lesions, and medial fibrosis than those with AD, whereas the underlying diseased medial layer to the driving force of intraluminal blood [7]. PAU has been thought to originate from plaque ruptures on the aortic wall and to cause medial hemorrhage and pseudoaneurysm [2,9].…”

“…AD and PAU progress with biochemical and biomechanical changes, and consequently rupture as mechanical events [7,8]. AD has been believed to begin with the formation of a tear in the aortic intima that directly exposes Abstract An intimal tear is responsible for the development of aortic dissection (AD).…”