Hemodynamics of Abdominal Aortic Aneurysm and its Clinical Relevance in Patients With Infrarenal Stent-Graft Implantation

2013 ◽  
Author(s):  
Y.-H. Lu ◽  
G.-T. Liu ◽  
S.-H. Lin ◽  
C.-Y. Chen
Keyword(s):  
Cardiovascular Disease ◽  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Cell Loss ◽  
Rate Data ◽  
Abdominal Aortic ◽  
Normal Diameter ◽  
The Media ◽  
Stent Graft Implantation ◽  
Graft Implantation

In 2008 the overall rate of death attributable to cardiovascular disease, or CVD, is 244.8 per 100,000. On the basis of these mortality rate data, one American dies due to CVD on an average of every 39 seconds. Of these deaths, abdominal aortic aneurysm (AAA) accounts for 11,079 [1]. Although an estimate of the total economic burden of AAA is not available, the average cost per discharge for a ruptured AAA exceeded $93,000 in 2003 [2]. Generally, an abdominal aortic aneurysm (AAA) is an irreversible focal dilation of an artery to 1.5 times its normal diameter [3]. AAAs are characterized by the destruction of elastin and collagen in the media and adventitia, smooth muscle cell loss with thinning of the medial wall, infiltration of lymphocytes and macrophages, and neovascularization [4, 5].

Hemodynamic impact of abdominal aortic aneurysm stent-graft implantation-induced stenosis

2015 ◽  
Vol 54 (10) ◽  
pp. 1523-1532 ◽  
Author(s):  
Nicolas Aristokleous ◽  
Nikolaos G. Kontopodis ◽  
Konstantinos Tzirakis ◽  
Christos V. Ioannou ◽  
Yannis Papaharilaou
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Stent Graft ◽  
Abdominal Aortic ◽  
Stent Graft Implantation ◽  
Graft Implantation

scholarly journals Abdominal aortic aneurysm neck remodeling after Anaconda stent graft implantation

2018 ◽  
Vol 68 (5) ◽  
pp. 1354-1359.e2 ◽  
Author(s):  
Elisabeth Vukovic ◽  
Martin Czerny ◽  
Friedhelm Beyersdorf ◽  
Martin Wolkewitz ◽  
Mikolaj Berezowski ◽  
...  
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Stent Graft ◽  
Aneurysm Neck ◽  
Abdominal Aortic ◽  
Stent Graft Implantation ◽  
Graft Implantation

scholarly journals Swedish snuff (snus) and risk of cardiovascular disease and mortality: prospective cohort study of middle-aged and older individuals

BMC Medicine ◽  
2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Olga E. Titova ◽  
John A. Baron ◽  
Karl Michaëlsson ◽  
Susanna C. Larsson
Keyword(s):  
Cardiovascular Disease ◽  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Older Individuals ◽  
Middle Aged ◽  
Entire Study ◽  
Abdominal Aortic ◽  
Increased Risk ◽  
Never Smokers ◽  
Cvd Mortality

Abstract Background Cigarette smoking is a well-known risk factor for cardiovascular disease (CVD), but whether smokeless tobacco such as snuff is associated with the risk of CVD is still unclear. We investigated the association of the use of Swedish oral moist snuff (snus) with a broad range of CVDs and CVD mortality. Methods We used data from a population-based cohort of 41,162 Swedish adults with a mean baseline age of 70 (56–94) years who completed questionnaires regarding snus use and other lifestyle habits and health characteristics. Participants were followed up for incident cardiovascular outcomes and death over 8 years through linkage to the Swedish National Patient and Death Registers. Hazard ratios (HR) were estimated by Cox proportional hazards regression. We conducted analyses among all subjects as well as among never smokers to reduce residual confounding from smoking. Results After adjustment for smoking and other confounders, snus use was not associated with myocardial infarction, heart failure, atrial fibrillation, aortic valve stenosis, abdominal aortic aneurysm, stroke, or CVD mortality. However, in never smokers, snus use was associated with a statistically significant increased risk of total and ischemic stroke (HRs [95% confidence intervals] = 1.52 [1.01–2.30] and 1.63 [1.05–2.54], respectively) and non-significantly positively associated with some other CVDs. Conclusions In this middle-aged and elderly Swedish population, current Swedish snus use was not associated with the risk of major heart and valvular diseases, abdominal aortic aneurysm, or CVD mortality in the entire study population, but was linked to an increased risk of stroke in never smokers.

Abstract 286: Loss of Smad3 Exacerbates Abdominal Aortic Aneurysm Formation With Enhanced Inflammation in an Experimental Mouse Model

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Xiaohua Dai ◽  
Anandita Arora ◽  
Jianbin Shen ◽  
Hong Jiang ◽  
Li Li
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Calcium Chloride ◽  
The United States ◽  
Protective Role ◽  
Elastic Fibers ◽  
Aneurysm Formation ◽  
Abdominal Aortic ◽  
The Media ◽  
Chloride Treatment

Introduction Abdominal aortic aneurysm (AAA) is a complex vascular disease that causes more than 10,000 deaths each year in the United States. Extensive studies have been performed in search of pharmaceutical treatment but surgical repair still remains the most effective treatment. TGF-β signaling is an important mechanism in the pathogenesis of aneurysms; however, there is debate as to whether its role is protective or destructive. Smad3 is a major intracellular mediator of the canonical pathway of TGF-β signaling. Hypothesis We hypothesize that Smad3-mediated TGF-β signal pathway plays important roles in the pathogenesis of AAA. Methods To test this hypothesis, we analyze the effects of loss of Smad3 on aneurysm formation in the calcium chloride induced AAA model using Smad3 knockout mice. Results Three weeks after calcium chloride treatment, the abdominal aorta displayed increased dilation, forming aneurysms. Histology and immunohistochemistry analyses show increased cell proliferation and enhanced inflammatory cell infiltration in the media and adventitia of the vessel wall. This was accompanied by elastic fibers degradation, increased MMPs expression and reduced expression of smooth muscle markers. Further analysis showed that the expression and nuclear localization of Smad2 and Smad4 was significantly increased. Conclusions These results demonstrate that Smad3-mediated TGF-β signaling plays a protective role in the pathogenesis of AAA and Smad2/Smad4 upregulation is not sufficient to compensate for the loss of Smad3 in this experimental model.

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