Expression of annexin II in experimental abdominal aortic aneurysms

Annexin II is a receptor of tissue-type plasminogen activator (t-PA). We have previously identified annexin II by immunolocalization in human atherosclerotic abdominal aortic aneurysms (AAAs). To investigate possible interactions between annexin II and AAA development, we examined annexin II mRNA and protein expression in a rat model of experimental AAA. AAAs were induced in rats by transient aortic infusion of elastase. The rats were divided into three groups: a saline-treated control group, a group with 15-min elastase infusion, and a group with 30-min elastase infusion. The 15-min elastase-infused group had smaller aneurysms and more preserved media than the 30-min elastase-infused group. Immunohistochemistry showed that annexin II expression was increased in the thickened intima and media of AAA rats as compared with the media of control rats. Furthermore, annexin II was colocalized with macrophages and smooth muscle cells. Quantitative real-time polymerase chain reaction showed that annexin II mRNA levels were up-regulated only in the smaller aneurysm group compared with the control group. In contrast, t-PA mRNA levels were increased in both the 15- and 30-min elastase-infused groups as compared with the control group. These results demonstrate various levels of annexin II expression within the aortic wall of rats with experimental AAAs. It has been suggested that alteration of fibrinolytic activity regulated by annexin II within the aortic wall may be associated with aneurysm formation.     

Infrarenal abdominal aortic aneurysms

Opinion statement Screening programs should be instituted to identify patients with small asymptomatic abdominal aortic aneurysms (AAAs) in the community. Screening for AAAs reduces the rate of aneurysm rupture and reduces death from aneurysmal disease in the population. The indications for aneurysm surgery have been defined by two recent randomized clinical trials. Patients with symptomatic or ruptured AAAs should be treated by urgent or emergency surgery. Patients with asymptomatic AAAs should not undergo surgical repair until the aneurysm exceeds 5.4 cm in maximum diameter. The most appropriate surgical option for the majority of patients with AAAs is conventional inlay grafting. This may be approached transperitoneally, although the retroperitoneal approach is favored for inflammatory or juxtarenal aneurysms. Conventional aneurysm repair may be performed with acceptable mortality and good long-term durability in specialized centers with a high volume of cases. The place of endovascular aneurysm repair remains to be defined. Endovascular repair is the best option in high-risk patients with suitable aneurysm morphology. The questions over the long-term durability of endovascular aneurysm surgery in preventing aneurysm rupture make it unsuitable for young patients. Randomized trials will define the indications for this technique. Endovascular surgery is likely to become the most appropriate treatment for ruptured aneurysms in the next decade.     

Peptic ulcers and abdominal aortic aneurysms

Upper gastrointestinal endoscopy was performed in 106 of 204 Chinese patients with intact abdominal aortic aneurysms, ninety-seven for screening and nine for gastrointestinal bleeding or pain. Peptic disease was discovered in 38 patients: 12 duodenal ulcers, 12 gastric ulcers, four duodenal and gastric ulcers, three duodenitis, three gastritis and four previously operated for ulcers. The eight patients who bled before aneurysmectomy all had gastric ulcers; four required emergency operation and two died. Only two patients bled from duodenal ulcers, both after aneurysmectomy and one died. Excluding gastritis and duodenitis, peptic ulcer was found in 26.4% of patients with abdominal aortic aneurysms. Half of these ulcers were gastric ulcers and 50% of them bled before aneurysmectomy. Duodenal ulcers tend to remain asymptomatic before operation and two of 12 (16.7%) bled postoperatively. The risk of bleeding for ulcers associated with aneurysms was 10 of 28 (35.7%) ulcers. The result of this uncontrolled study suggests that routine endoscopic screening should be used in all patients with aortic aneurysms and early surgery should be offered for gastric ulcers.     

Management of abdominal aortic aneurysms

Optional statement Abdominal aortic aneurysms (AAAs) are a lethal disease. Ultrasound is the modality of choice for screening patients for AAAs. It is reasonable to screen patients over age 60, particularly men, women with cardiovascular risk factors, smokers, and patients with a family history of AAAs. Patients with small (< 5.5 cm) AAAs should be followed with serial ultrasound. Medical management should focus on treating comorbidities, particularly those that put patients at risk for other cardiovascular diseases. Smoking cessation is mandatory in these patients. Patients with large or symptomatic AAAs should be evaluated for surgery; this includes careful imaging of the abdomen, aggressive treatment of comorbidities, and perioperative β blockade. Endovascular repair has lower short-term morbidity compared with conventional open repair. Trials assessing long-term results are in progress. Basic science and translational research focusing on the underlying pathogenesis of AAAs will likely pave the way for medical therapies in the future.     

A family with abdominal aortic aneurysms

This investigation focused on 7 siblings to 2 brothers with abdominal aortic aneurysm (AAA), with respect to AAA, Chlamydia pneumoniae (CP) serology, serum cholesterol, and smoking habits. Five male and 4 female siblings were included. All siblings underwent ultrasonography, and surgical specimens from the aorta were prepared for immunohistochemical (IHC) analysis. Blood was obtained from all living siblings and serum cholesterol level was analyzed. Serologic analysis was done by microimmunofluorescence (MIF). Smoking habits were recorded. In addition to the 2 known siblings with AAA, 2 other brothers with AAA were found. Four of 8 siblings had IgG 1/512 or greater and 7 of 8 had IgA 1/64 or greater. Two of 3 were positive for CP in IHC obtained from aortic specimens. Two of 8 had hypercholesterolemia; 7 of 9 were smokers. C. pneumoniae as well as smoking seems to be important in the pathogenesis of AAA in this small cohort; however, larger patient cohorts are needed.     

Mouse models of abdominal aortic aneurysms

Many mouse models of abdominal aortic aneurysms have been developed that use a diverse array of methods for producing the disease, including genetic manipulation and chemical induction. These models could provide insight into potential mechanisms in the development of this disease. Although experimental studies on abdominal aortic aneurysms (AAAs) have used a variety of mammalian and avian approaches, there is an increasing reliance on the use of mice. The models recapitulate some facets of the human disease including medial degeneration, inflammation, thrombus formation, and rupture. Most of the mouse models of AAA are evoked either by genetically defined approaches or by chemical means. The genetic approaches are spontaneous and engineered mutations. These include defects in extracellular matrix maturation, increased degradation of elastin and collagen, aberrant cholesterol homeostasis, and enhanced production of angiotensin peptides. The chemical approaches include the intraluminal infusion of elastase, periaortic incubations of calcium chloride, and subcutaneous infusion of AngII. A common feature of these models is the reduction of AAA incidence and severity by the prophylactic administration of matrix metalloproteinase (MMP) inhibitors or genetically engineered deficiencies of specific members of this proteolytic protein family. The validation of mouse models of AAAs will provide insight into the mechanisms of progression of the human disease.     

Ultrasonographic screening for abdominal aortic aneurysms

Abdominal aortic aneurysms (AAAs) occur in 1 of 20 older men, remain asymptomatic for many years, and, if left untreated, cause death from rupture in about one third of patients. Ultrasonography is a suitable screening test for AAA, and elective repair can prevent rupture. Although these features suggest a promising target for a screening program, evidence of benefit from AAA screening has only recently become available. Four randomized trials of ultrasonographic screening involving more than 125 000 men have been reported, and each trial observed a reduction in AAA-related mortality (which was statistically significant in 2 trials), ranging from 21% to 68%. One trial in women found no benefit. Other studies indicate that screening can begin in men older than 65 years of age and does not need to be repeated if results are negative. An AAA larger than 5.5 cm in diameter should be considered for elective open or endovascular repair. Most aneurysms detected at screening are smaller and should be kept under surveillance with periodic imaging measurement. Widespread elective repair of small AAAs could reduce the benefits and increase the costs of screening. No medical treatments have been proven to reduce the enlargement rate. If elective repair is reserved for larger AAAs, one-time ultrasonographic screening for AAA can be recommended for men 65 to 79 years of age who have ever smoked [correction].     

Elastin degradation in abdominal aortic aneurysms

Histological sections through the walls of abdominal aortic aneurysms showed scarce and disrupted elastic tissue. The elastin content of the aneurysmal aortic media was only 8.1 +/- 3.2% dry defatted weight (n = 11). The elastin content of grossly normal age and anatomically matched aortic media was 35.0 +/- 3.2% dry weight (n = 4) and the elastin content of severely atherosclerotic, stenosed infrarenal aortic media was 22.0 +/- 7.2% dry weight (n = 6). There was an inverse correlation of elastin content with the elastinolytic activity of aortic media homogenates, r = -0.78. Elastase activity, measured by the hydrolysis of [3H]elastin, was highest in aneurysmal aortic homogenates, 92.1 +/- 43.7 U/mg protein (n = 18), falling to 46.9 +/- 13.3 U/mg protein (n = 13) in severely stenosed atherosclerotic aortic homogenates and 35.5 +/- 11.9 U/mg (n = 6) in grossly normal aortic homogenates. The elastinolytic activity of stenotic aorta contained leukocyte elastase as an important component. In aneurysmal homogenates leukocyte elastase was also found but the increased elastase activity resulted from a protease(s) (Mr 95,000) extracted in 2 M urea, having minimal specificity for alanyl bonds and no immunological cross-reactivity with leukocyte elastase.     

Surgical treatment of pararenal abdominal aortic aneurysms

Thirty patients with juxtarenal infrarenal and 16 patients with suprarenal abdominal aortic aneurysms underwent elective (58%) or urgent (42%) repair. Twenty-three patients were hypertensive and 20 had impaired renal function preoperatively. Nineteen patients required combined aortic and renal artery reconstruction, in which reimplantation was the most common technique used. The perioperative mortality rate was 7.4% in the elective group and 36.8% in the urgent group. Rupture of the aneurysm and a preoperative high serum creatinine level were risk factors correlating to early mortality. Among survivors, 61% showed a rise in serum creatinine in the early postoperative period. In all but one the transient renal insufficiency was resolved within one month. Of the hypertensive patients 64% were cured or under control with medication following combined reconstruction. These results demonstrate that surgical repair of pararenal abdominal aortic aneurysms can be performed with an acceptable mortality and morbidity.     

Influence of periodontitis on abdominal aortic aneurysms

Periodontitis is known to be a risk factor for abdominal aortic aneurysm (AAA). However, the influence of periodontitis on AAA development is to be elucidated. This article is to review the relationship between periodontitis and AAA. We focused on the roles of specific periodontopathic bacteria in AAA, matrix metalloproteinases and toll-like receptors in the pathophysiology in the section of experimental analysis. Furthermore, we showed clinical data of periodontitis in patients with AAA. We concluded that periodontal pathogens play a critical role in the AAA development.