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Aortic aneurysm and dissection of descending aorta have to be rapidly diagnosed and treated. The treatment frequently includes surgery. The natural history, indications of surgical treatment and surgical technique are reviewed.

Intravesical application of bacillus of Calmette-Guérin (BCG) has proved to be an effective form of treatment for some stages of bladder cancer. Infrequent, serious complications of this treatment have become apparent as its use has become more widespread. We report a case of Mycobacterium bovis mycotic abdominal aortic aneurysm and a case of M. bovis mycobacteremia that developed as complications of intravesical BCG therapy. These cases are discussed in the context of a review of reported complications of intravesical BCG therapy and a review of measures currently advocated to prevent them.

Traumatic injury to the descending thoracic and abdominal aorta is uncommon in children and is usually secondary to recognized blunt trauma. Child abuse has not been previously reported as a cause. We report a 3-year-old boy who was kicked in the abdomen by his father. A resulting pseudoaneurysm was successfully resected.

We report a rare case of 76-year-old man who developed ruptured thoracoabdominal aortic aneurysm complicated with abdominal high aortic occlusion. His left limb was amputated due to Buerger's disease. CT showed that the aneurysm extended from the descending thoracic aorta to the upper part of the abdominal aorta and its had a maximum width of 68 x 83 mm. Angiogram revealed the aortic occlusion at the level of the left renal pelvis. We performed emergency operation, which was aneurysmectomy and replacement with artificial vascular graft, under femoro-femoral and subrenal aortic extracorporeal bypass. Because of the severe calcification at the subrenal aorta and the weak pulsation of the left renal artery, the bypass was placed from the aortic graft to the right lower limb and the left renal artery was reconstructed. Abdominal aortic occlusion might increase his hypertension and might cause aneurysmal change on the proximal aortic wall.

Purpose: The pathogenesis of abdominal aortic aneurysm (AAA) involves many factors; elastin degradation is believed to lead to initial dilation, whereas changes in the collagen structure predispose the aneurysm to rupture. The major collagens in the aortic wall are types I and III. We set out here to determine whether changes in serum propeptide of type III procollagen (PIIINP), a biologically relevant marker of type III collagen turnover, could be associated with the characteristics of AAA., Methods: The aminoterminal PIIINP and the carboxyterminal propeptide of type I collagen were measured by radioimmunoassay in 87 patients with AAA and 90 control subjects with aortodistal arteriosclerosis. The samples were taken from the peripheral blood and from the abdominal aorta at the levels of the diaphragm and the common iliac artery., Results: Mean PIIINP concentrations were higher in patients with AAA than in control subjects (3.47 micrograms/L vs 2.73 micrograms/L, p < 0.0001), correlating positively with aneurysm diameter in the former (r = 0.27, p = 0.04) and with the maximum thickness of the intraluminal thrombus (r = 0.39, p = 0.003). The gradient in PIIINP between the upper and lower end of the abdominal aorta was significant in the AAA group (-0.30 microgram/L, range -0.20 to -0.50 vs -0.10 micrograms/L, range -0.20 to 0.30, p = 0.002)., Conclusions: These studies indicate that the turnover of type III collagen is increased in patients with AAA.

Seasonality in ischaemic coronary artery disease is well documented with a winter/summer variation the commonest pattern. The influence of seasonal variation on events in other vascular territories is less well documented. The incidence of ruptured abdominal aortic aneurysm and emergency lower-limb ischaemia was analysed on a monthly basis over a 5-year period. A total of 372 ruptured abdominal aortic aneurysms occurred with a peak incidence in spring and autumn; however, no seasonal pattern was seen in the rate of emergency admissions with lower-limb ischaemia (n = 606). The explanation for this seasonal pattern in ruptured aneurysms is unknown. The haemodynamic adjustments to changes in climate require further study.

Abdominal aortic aneurysms (AAAs) have traditionally been attributed to atherosclerosis, although there is increasing epidemiological, biochemical and genetic evidence that aneurysmal arterial disease is different from occlusive atherosclerosis. One of the most consistent biochemical findings in the aneurysmal aorta is a significant reduction in elastin protein; the cause, for this remains unclear. There is in vitro evidence that vitamin D3 (1,25 dihydrocholecalciferol) inhibits the production of elastin by smooth muscle cells. On the basis of this observation and the possibility that some subjects may be exposed to excess vitamin D3, the hypothesis that vitamin D3 may be a previously unrecognized aetiological factor in the pathogenesis of AAA is developed.

We now know our past concepts of AAA pathogenesis to be oversimplified and inaccurate. In fact, the metabolic activity of the aneurysm wall is markedly increased in comparison with normal aorta. It has become clear that AAAs result not from passive dilatation, but from a complex remodeling process involving both the synthesis and degradation of matrix proteins. Our understanding of this process has been advanced by applying molecular biology techniques. Although elastin fragmentation and medial attenuation remain the most striking histological features of AAA tissue, experimental and clinical evidence suggests that the adventitia, which is predominantly collagen, is capable of maintaining the dimensional stability of the aorta in the absence of the medial elastin network. Thus, although factors that result in fragmentation and attenuation of elastin may be important in the etiology of AAA, factors regulating the balance of collagen synthesis and degradation likely determine the rate of AAA progression. The resident inflammatory cells in AAA undoubtedly play an important pathological role in aortic dilatation. Thus, understanding the interaction between aortic mesenchymal cells (smooth muscle cells and fibroblasts) and inflammatory cells (lymphocytes and macrophages) should allow for the identification of genetic factors that predispose to AAA. In addition to the possibility of early identification of patients at risk for AAA, new insights into AAA pathogenesis might allow for development of pharmacological strategies for inhibiting expansion of small AAA.

Between 1983 and 1993, a total of 110 patients underwent elective repair of thoracoabdominal aortic aneurysm. Mortality rate varied with the extent of repair: 26 per cent (five of 19) after type I repair, 42 per cent (eight of 19) after type II repair, 24 per cent (four of 17) after type III repair and 15 per cent (eight of 55) after type IV repair. A further 20 patients underwent urgent operation for suspected rupture in nine and true rupture in 11. The mortality rate was 73 per cent for those with true rupture and 33 per cent for those with threatened or contained rupture. Death was most commonly due to coagulopathy and bleeding (39 per cent) or myocardial ischaemia (19 per cent). Preoperative risk factors for death included type II repair, urgent or emergency operation, aortic dissection, impaired renal function and abnormal spirometry (P < 0.05). Postoperative risk factors included reoperation, dialysis or prolonged ventilation (P < 0.05). Twenty patients required dialysis; ten died, five recovered normal renal function and five were discharged on dialysis. Eight patients developed paraplegia and four of them died. Thoracoabdominal aneurysm remains a formidable surgical challenge, but 90 per cent of survivors are free of major morbidity.

Patients with testicular carcinoma frequently present with advanced disease and symptoms resulting from metastatic lesions. We report an unusual case of successful emergency management of a massive rupturing aortic pseudoaneurysm midway through systemic chemotherapy for stage III germ cell tumor by percutaneous trans-luminal placement of an aortic bypass stent-graft. Unstable hemorrhage was controlled, allowing our patient to complete chemotherapy and undergo elective retroperitoneal lymph node dissection with resection of the pseudoaneurysm and residual disease after normalization of tumor markers. Final pathological evaluation revealed only fibrosis in the resected tissue. Followup angiography demonstrated a patent stent-graft and the patient was without evidence of disease 1 year after retroperitoneal lymph node dissection.

We report a case of retrograde aortic dissection after bilateral iliac artery stenting. A 63-year-old black woman underwent aortography with balloon angioplasty of bilateral common iliac artery lesions and subsequent vascular stent placement. The patient developed an acute aortic dissection from the level of the aortic bifurcation to the left subclavian artery. This case is presented to call attention to the previously unreported complication of retrograde aortic dissection after bilateral iliac artery angioplasty and stent placement presenting as acute chest pain.

Objective: To determine the frequency of aneurysm and dissection of the aorta in patients with giant cell arteritis and to assess the effects of these events on these patients., Design: Population-based cohort study., Setting: A multispecialty and a primary care clinic in southern Minnesota., Patients: 96 residents of Olmsted County, Minnesota, who developed giant cell arteritis between 1950 and 1985. The presence of aortic aneurysm, dissection, or both was confirmed using computed tomography, ultrasonography, angiography, or autopsy., Results: 11 of the 96 patients were found to have thoracic aortic aneurysms. In 2 of these patients, the aneurysms were detected when giant cell arteritis was diagnosed. In the remaining 9 patients, the aneurysms occurred a median of 5.8 years after giant cell arteritis was diagnosed. Six of the 11 died suddenly of acute thoracic aortic dissection. Five patients who did not have thoracic aortic aneurysms developed isolated abdominal aortic aneurysms a median of 2.5 years after giant cell arteritis was diagnosed. The incidence of thoracic aortic aneurysm in patients with giant cell arteritis was 999 per 100,000 person-years; the incidence of abdominal aortic aneurysm in these patients was 555 per 100,000 person-years. Compared with all persons of the same age and sex living in Olmsted County, patients with giant cell arteritis were 17.3 times (95% Cl, 7.9 to 33.0) more likely to develop thoracic aortic aneurysm and 2.4 times (Cl, 0.8 to 5.5) more likely to develop isolated abdominal aortic aneurysm., Conclusions: Giant cell arteritis is associated with a markedly increased risk for the development of aortic aneurysm, which is often a late complication and may cause death.

A traumatic pseudoaneurysm of the abdominal aorta eluded detection at initial laparotomy, but was later detected serendipitously. Early abdominal x-ray film and appreciation of paraspinal bullet fragments could have led to its earlier detection. A portable abdominal x-ray film should be a routine part of the preoperative resuscitation of abdominal gunshot wounds.

We created a simple experimental aneurysm by a minimal operative trauma performing the balloon-dilatation and the rupture of the abdominal aorta of animals. The aorta of minipigs was dilated under angiographic control until the rupture became visible. The abdominal aorta and its branches were mapped out and measured. The angiographics were calculated using a planimetric device. The dilatation of the aorta was increased up to 3.5 times the initial diameter when rupture occurred. The microscopical examination showed lesions in all three layers of the vessel only at the rupture site and some focal lesions of the tunica intima. This one-step procedure of producing an experimental aneurysm is done using a low operative trauma and allows testing of endovascular systems using only one anaesthetic.

Decision analysis is an explicit and quantitative technique which is particularly well suited for medical problems involving multiple complex clinical features. In this article, a decision analysis model was used to measure the risks and benefits between different therapeutic options, for a patient with a 4 cm diameter asymptomatic abdominal aortic aneurysm and concomitant end-stage renal failure. A Markov model was built to stimulate the natural history of abdominal aortic aneurysm, its risk of rupture, and the age-dependent dialysis-related mortality. Despite end-stage renal disease that limits life expectancy and increases the surgical risk, the model suggests that surgical resection of the aneurysm (immediate, or delayed if the diameter exceeds 5 cm in diameter) would result in greater life expectancy compared with therapeutic abstention unless the surgical risk exceeds 8.5% and 22%, respectively. Moreover, the gain in life expectancy between immediate and delayed surgery is not significant, and individual decision-making between these two options should include additional elements representing patients' preference. In conclusion, this model emphasizes the usefulness of decision analysis as a decision aid to medical problem-solving. The Markov simulation, which represents in a realistic manner the natural history of aortic aneurysm, and sensitivity analyses reinforce the credibility of this approach.

Background: A study in old patients on the incidence of aneurysms in abdominal arteries (AAA) and on the maximum diameter of the aorta below the renal arteries in those patients without arterial dilatation., Material and Methods: The study comprised 411 individuals, 218 women and 153 men with an average age of 74.4 years. Physical examination of the abdomen (EF) and abdominal ultrasonography (US) were done, and the latter was considered the "golden standard" of reference. In relation to the aorta, it was considered as an aneurysm the maximum artery diameter larger than 30 mm and for the iliac arteries, the maximum diameter larger than 15 mm., Results: The US showed the presence of aneurysm in the aortic-iliac territory in nine patients, one woman and eight men, corresponding to a prevalence of 2.1%, 4.1% in men and 0.4% in women. Two such aneurysms were in the iliac arteries (one aneurysm in a common iliac artery) and the other seven in the aorta below the renal arteries. The bearers of iliac aneurysm are men. The prevalence of the AAA was of 1.7% (7/411), 3.1% in men and 0.4% in women. The EF showed suspicion of the presence of aneurysm in 3 of these patients. The other 6 patients had no aneurysm. Considering all the aneurysms of the aortic-iliac territory, the EF had a sensitivity of 33.3%, a specificity of 99% and a positive prediction value of 33.3%. Considering only AAA, the sensitivity of the EF was 42.8%, the specificity 98.5%, and the positive prediction value, 33%. In the 402 patients without arterial aneurysm the maximum diameter of the aorta varied from 11 to 29 mm, with an average value of 16-21 mm., Conclusions: US is a non-invasive diagnostic procedure that should be used for the old age population.

Pseudoaneurysm formation is an uncommon complication of simultaneous aortic and renal artery revascularization procedures that has been noted to occur primarily at sites of anastomosis. We present the computed tomographic and angiographic findings of an unusual case of contained leak arising from the proximal renal artery stump with associated inferior vena caval compression and thrombosis in a patient who had had abdominal aortic aneurysmectomy and bilateral aortorenal bypass.

The walls of human abdominal aortas and atherosclerosis-induced aneurysms contain similar amounts of collagen. The quantitative ratio between collagens of various types of this protein does not differ significantly either, whereas solubility of the collagen in aneurysmal wall and its susceptibility to the action of EDTA are distinctly decreased. In contrast with collagen, the amount of elastin in aneurysms is significantly lower. Total amount of glycosaminoglycans slightly decreased as compared with that of normal tissue, but the ratio of particular compounds varies. The percentage of chondroitin sulphate is increased and that of heparan sulphate significantly decreased. The significance of these changes in pathogenesis of aneurysms is discussed.

Historically the most common cause of abdominal aortic aneurysms has been attributed to atherosclerotic degeneration of the vessel wall. However, over the last decade this widely accepted theory has been challenged by a substantial body of research that proposes that atherosclerosis is more likely to be an associated finding rather than an instigating factor. Arguments against an atherosclerotic theory are supported by differences in the characteristics of atherosclerotic occlusive disease and aneurysmal disease. Emerging theories propose that development of abdominal aortic aneurysms involves genetic factors and fundamental structural changes in the aorta. The purpose of this article is to review these emerging theories and discuss their implications on patient treatment.

Anastomotic false aneurysm (AFA) of the aorta is a potentially lethal complication after prosthetic grafting. Nineteen aneurysms were encountered in 18 patients within a 30-year period (1960-1991). There were 10 men and 8 women, aged 27-80 years (mean 58 years). In 14 patients, the prostheses were made of silk, in 2 were PTFE, and in 1 each Dacron or silk-Dacron cross-weaved. Patients with an intact AFA had a pulsatile abdominal mass, abdominal pain, an occluded graft and peripheral emboli. Five patients were asymptomatic. Clinical onset of AFA varied from 2 weeks to 12 years (mean 5 years). The accurate rate of diagnosis of single plane angiography was 75% (3 of 4), and computed tomography 100% (ten of ten). Ultrasound was used only once and suggested an AFA. Four AFAs were less than 5cm in diameter. Five patients refused operation and died in 2 years from rupture. Operative mortality was 11% (1 of 9). Treatment was resection of AFA and replacement with a new graft. Life-long follow-up is required for patients with an aortic aneurysm. All ratroperitoneal AFAs should be resected, since the outcome of rupture is poor.

Predisposing factors for aortic dissection are well known from necropsy series. To evaluate the frequency of aortic and aortic valve disease in aortic dissection in vivo, 139 patients with acute aortic dissection (96 men, 43 women, mean age 60.5 +/- 15.7 years) were studied by transoesophageal echocardiography (TEE) using 3.5 and 5.0 MHz transducers. Left ventricular hypertrophy by TEE, defined as an end-diastolic wall thickness of the left ventricular septal wall over 1.5 cm, was found in 42 (67.7%) of 62 patients with type I, in 10 (58.8%) of 17 patients with type II and in 46 (76.7%) of 60 patients with type III dissection. The mean value for the aortic root diameter was 3.2 +/- 1.3 cm.m-2 in type I dissection and 2.8 +/- 0.9 cm.m-2(ns) in type II dissection. In the patient group with type III dissection this diameter was significantly smaller (1.8 +/- 0.9 cm.m-2; P < 0.001). Thickening of aortic valve leaflets was demonstrated in six (9.7%) of 62 patients with aortic dissection type I (two of them with mild aortic stenosis), in two (11.8%) of 17 patients with aortic dissection type II and in 15 (25.0%) of 60 patients with aortic dissection type III. A bicuspid aortic valve was diagnosed in five (6.3%) of 79 patients with aortic dissection types I and II and in one (1.7%) of 60 patients with type III dissection. By colour coded Doppler echocardiography, aortic regurgitation was found in 46 (74.2%) of 62 patients with type I, 13 (76.5%) of 17 patients with type II and 23 (38.3%) of 60 patients with type III dissection.(ABSTRACT TRUNCATED AT 250 WORDS)

Ehlers-Danlos syndrome (EDS) type IV results in a high incidence of vascular lesions. The extreme fragility of arteries is associated with multiple aneurysm formation, spontaneous rupture, and dissection. Surgical management of patients with this disorder is hazardous and often unrewarding. In this report we describe the difficulties encountered in the management of three patients with EDS-related vascular lesions. Three patients presented with pain and exhibited characteristic features of EDS. Diagnostic modalities included computerized tomography, transesophageal echocardiography, and magnetic resonance. Aortography was performed only in specific situations. One patient with pericardial and mediastinal hemorrhage was stabilized and treated conservatively, with a good outcome. An adolescent with a ruptured aortic pseudoaneurysm died at surgery. The third patient underwent successful surgical correction of multiple aortic and renal aneurysms. In view of the increased risk of fatal vascular complications, surgeons should identify patients with EDS before performing invasive procedures. Arteriography should be used only when necessary. Although operative mortality remains at a high level due to the tendency of vessels to tear with even minimal manipulation, mortality from hemorrhage without surgical intervention is even greater. The key to favorable outcomes lies in identification of the syndrome preoperatively, surgical intervention only in life- or limb-threatening situations, and appropriate modification of surgical technique.

The etiology of infrarenal, "nonspecific" aortic aneurysms was previously believed to be degenerative arteriosclerosis, but recent studies of the components of the aortic wall have shown that complicated disturbances primarily concerning the synthesis and degradation of elastin and collagen are major pathogenetic components. Non-invasive measurements of the biomechanical properties of the aneurysms and determinations of the directions and forces of local flow velocity vectors within the aneurysmatic sac have provided new knowledge of the abnormal physical factors that follow dilatation. Detailed studies on the biochemical and physiological factors will make it possible to identify patients at risk and provide the foundations for interventions that will prevent development of the disease.

A 53-year-old woman presented with abdominal discomfort and was diagnosed using ultrasonography to have an abdominal aortic aneurysm. Aortography revealed a saccular aneurysm 4 cm in diameter of the infrarenal aorta with a 'string of beads' appearance. The renal and other visceral arteries appeared to be normal. Resection and graft replacement was performed because of the possibility of rupture. Histological examination of the specimen revealed the most common type of fibromuscular dysplasia, namely medial fibroplasia. Fibromuscular dysplasia should be considered as a potential cause of abdominal aortic aneurysm in female patients with no atherosclerosis risk factors.

Acute type IIIb dissection of the aorta was observed in a patient who had undergone kidney transplantation 5 years previously. Arteriograms showed that the true channel was compressed by the false channel, excluding the right common iliac artery to which the renal artery of the transplanted kidney had been anastomosed. The patient was treated successfully by fenestration of the abdominal aorta.

Six cases of arterial aneurysms, due to "Behçet's disease" located in various arteries are presented. Surgical reconstruction included: Resection of the lesions and replacement with corresponding grafts with satisfactory results. In spite of the macroscopic similarity of the aneurysms found in "Behçet's disease" as compared to those of mycotic origin, the presence of any microorganism could not be detected in various cultures or pathological specimens. Meticulous diagnosis on the nature of the aneurysm, close follow-up and careful postoperative anticoagulant treatment, is imperative for satisfactory immediate and late results.

Between March 1991 and April 1993, 1188 subjects aged 65-75 years, out of 2734 invited, underwent abdominal ultrasound for screening of asymptomatic abdominal aortic aneurysms (AAA). For each patient the maximal anteroposterior and transverse diameters of the suprarenal and infrarenal aorta were measured. According to the literature data an AAA is defined as an aortic dilatation > 29 mm. AAA < 40 mm are followed by ultrasound every 6 months and the AAA > 39 mm are considered for surgical repair after complete clinical work-up. In addition any aortic dilatation ranging 26-29 mm is followed too, using the same criteria. The aorta was normal in 1112 patients (95.12%), an infrarenal aortic dilatation was found in 21 patients (1.79%), an AAA < 40 mm in 15 patients (1.28%) and an AAA > 39 mm in 21 patients (1.79%). The global prevalence of AAA > 29 mm was 3.07% (0.3% for the females and 6.8% for the males), similar to that reported by other authors. The statistically significant (p < 0.01) risk factors were: smoking, alcohol consumption, coronary disease and chronic lung obstruction. Hypertension and dyslipidaemia were not significant (but HDL-cholesterol and Apo-B), according to a different etiology of the aneurysms. In addition 38.5% of the patients had total cholesterol > 240 mg/dl but only 34.9% of these was under medical treatment and/or on a diet. Our preliminary data confirm the results of similar studies in other countries: screening for AAA is worthwhile on the general population and, looking to a better cost-benefit rate, it might be focused only on males.

Background: Activation of proteolysis is characteristic of abdominal aortic aneurysm (AAA) disease, and by substrate gel enzymography with casein the most conspicuous proteinase of AAA wall has a molecular weight of approximately 80 kd. This activity has been resolved into separate metalloproteinase and serine proteinase (SP) components, by binding out the metalloproteinase by affinity to tissue inhibitor of metalloproteinases. Because plasmin plays a key role in activating members of the metalloproteinase family, the following experiments were done to test the hypothesis that the unknown SP is plasmin., Methods: Immunoblots, immunoprecipitations, and immunohistochemistry were performed by conventional methods with a specific polyclonal antibody to plasminogen., Results: Immunoblot analysis of extracts from AAA specimens (n = 7) revealed dense bands corresponding to known molecular forms of plasmin. Only trace amounts were detected in control aortic extracts (n = 4). When samples were equalized for total protein, the mean amount of immunoreactive material in the 80 kd band (in densitometric units) was 216 +/- 44 (SEM) for AAAs versus 27 +/- 15 (SEM) for controls (p < 0.01). The residual 80 kd SP activity on casein substrate gel enzymography was quenched by immunoprecipitation with the specific antibody. Immunohistochemistry revealed strong reactivity of the AAA wall., Conclusions: Because plasmin plays a key role in the cascade for activation of the matrix metalloproteinase (including collagenase and the metalloelastases), the present results suggest that plasmin may be important in the sequence of events leading to the destruction of aortic matrix in AAA.

Purpose: Perfusion of the isolated aorta of the rat with a saline solution containing pancreatic elastase induces an abdominal aortic aneurysm (AAA). An interesting feature of this model is the phenomenon of latency, suggesting that additional steps beyond the initial injury are required for AAA formation. This study was performed to determine whether the latency period for aortic dilation to aneurysmal proportions is correlated with the appearance of proteinases of endogenous origin and the interval for infiltration of inflammatory cells., Methods: Twenty Wistar rat aortas were perfused with the test solution, and 20 with normal saline solution. Laparotomy was performed on days 1, 2, 3, and 6 for measurement and harvest of the aorta. Histochemical studies were performed to analyze changes in matrix proteins, and substrate gel enzymography was used to determine the appearance of endogenous proteinases. Immunohistochemical studies were performed with monoclonal antibodies to T cells (CD-4, -5, and -8), monocytes/macrophages (ED-2), B cells (LC-A), immunoglobulin G, and immunoglobulin M., Results: The exogenously administered elastase was not detectable beyond day 2, but the aortic diameter did not progress to aneurysmal dimensions until the interval between days 3 and 6. During the period from day 3 to day 6, multiple endogenous matrix proteinases became detectable in the aortic tissue preparations. Immunohistochemical study revealed progressive infiltration of the aorta with various subsets of inflammatory cells., Conclusion: The results suggest that the latency in AAA formation in this model corresponds with a complex sequence of biochemical and cellular events. The model provides an "early window" into these interesting early phases leading to aneurysm formation.

The pathogenesis of abdominal aortic aneurysm involves many factors acting over time. However, destruction of elastin in the aortic wall is a key event that shifts the load produced by blood pressure on to collagen. This is exacerbated in the presence of hypertension. Smoking and age are further important factors, as is the site; elastic lamellae are relatively less common in the abdominal aorta. Once the shielding effect of elastin is lost, further dilatation and rupture of the aorta depend on the physical properties of the collagen present.

Aortic aneurysms have been induced in the rat by combining the chemotactic property of cotton for inflammatory cells and the resulting granuloma formation with the mechanical and haemodynamic stress of aortic coarctation. A stenosing cotton ligature was placed around the aorta, between the renal arteries, in male Wistar rats under standardized conditions. Three months later, 7 out of 12 rats (58%) had developed saccular aneurysms of the inter-renal aorta. The aneurysmal wall consisted of a collagenous shell with a few newly formed elastic fibrils on its luminal side. Detailed histological studies of the inter-renal aorta at different times after placing stenosing or non-stenosing cotton or nylon ligatures between the renal arteries, together with studies using anti-hypertensive therapy (cilazapril) and immunohistochemical studies using an anti-macrophage antibody (ED1) were performed to try to establish cellular events involved in this aneurysmal remodelling. We conclude that in this model aneurysm formation requires (i) deep mechanical injury to the aortic wall, (ii) the presence of hypertension upstream to the stenosis and (iii) an inflammatory response to the cotton ligature. The early inflammatory reaction was less in the case of nylon and although macrophages were present in both cases the most striking difference was the greater incidence of PMNs in the case of cotton.

A patient with mild hypothyroidism underwent a repair of abdominal aortic aneurysm. Although the serum TSH level of this patient was very high and T4, free T4 levels were low, T3 level remained within normal ranges. Inhalation anesthesia with continuous epidural block was selected and there was no complication such as hypotension or hypothermia during perioperative period. Recently, several reports demonstrate that the preoperative supplemental therapy of the thyroid hormone should not be necessary in the case of mild hypothyroidism. Moreover, the biological potency of T3 is higher than that of T4. Thus, in patients whose T3 level is kept within normal ranges even if serum T4 level is low and serum TSH level is high, we may say that they are in euthyroid state. We think these patients can be anesthetized safely.

Purpose and Methods: Aortic aneurysms are characterized by the destruction of the extracellular matrix of the media, whereas occlusive disease involves excess matrix accumulation within the intima. Plasmin degrades extracellular matrix directly and indirectly by activation of latent metalloenzymes. To determine the expression of tissue- and urokinase-type plasminogen activators, immunoassay, fibrin autography, Northern analysis, and immunohistochemistry were performed on specimens of aneurysmal (n = 12), occlusive (n = 8), and healthy (n = 6) aorta., Results: Immunoassay of tissue-type plasminogen activator revealed 8.7 +/- 0.9 ng tissue-type plasminogen activator/mg extracted protein in aneurysmal aorta, 5.7 +/- 0.3 ng/mg in normal aorta, and 2.5 +/- 0.3 ng/mg in occlusive aorta (p < 0.05 for comparisons between all groups). No urokinase-type plasminogen activator antigen was detected by urokinase-type plasminogen activator immunoassay. Fibrin autography exhibited lytic activity at 64 kDa and 54 kDa attributable to tissue-type plasminogen activator and urokinase-type plasminogen activator. The vast majority of fibrinolysis was secondary to free tissue-type plasminogen activator and was greatest in aneurysmal disease and least in occlusive disease. There was only a small amount of lysis secondary to urokinase-type plasminogen activator. Expression of tissue-type plasminogen activator and urokinase-type plasminogen activators mRNA was comparable in aneurysmal and occlusive aortas. In contrast to occlusive disease, aneurysms had an inflammatory cell infiltrate characterized by the expression of urokinase-type plasminogen activator by specific mononuclear cells. Tissue-type plasminogen activator expression was evident in the intima of normal and diseased aorta and in the media of diseased aorta., Conclusion: Differential expression of plasminogen activators within the arterial wall may contribute to the unique pathogenesis of aneurysmal and occlusive aortic disease.

Tobacco use represents the most powerful chemical addiction, which has been defined as "the inability to discontinue smoking" and it is one of the main cardiovascular risk factors. It produces alterations in platelet activity, blood viscosity and vascular wall and clinical signs related to the different vascular districts. The probability of carotid lesions increases up to 32% for 10 years/smoking and the progression of the disease is proportional to tobacco consumption; on the contrary smoking cessation may be helpful. Furthermore the risk of PAOD increases 2 to 9-fold, irrespective the number of cigarettes and these modify significantly the long-term patency of the femoro-distal reconstructions (57% vs 78% at 2 years). Very impressive indeed the data concerning major amputations (21% vs 2%) and the mortality rate for cardiovascular diseases (83% vs 33%) between smokers and non-smokers. For the abdominal aortic aneurysm too smoking represents the main independent risk factor and the mortality rate rises 6 to 25-fold compared to the normal population. The conclusions are obvious and can be shortly summarized in the following sentence: "Stop smoking and keep walking".

Purpose: To describe findings in, and the clinical course and outcome of, aortic dissection (dissecting aneurysm) caused by angiographic procedures., Materials and Methods: The records of approximately 15,500 angiographic procedures performed between 1985 and 1991 were reviewed. In the six cases of iatrogenic aortic dissection identified, computed tomography (CT) was performed for diagnosis, follow-up, or both., Results: The type of aortic dissection was Stanford type A in three patients and Stanford type B in three patients. The sites of injury were the abdominal aorta (n = 2), right brachiocephalic artery (n = 2), middle of the thoracic aorta (n = 1), and right common iliac artery (n = 1). One patient had anterograde dissection from the site of injury; two patients, retrograde dissection; and three patients, extensive dissection that extended in both anterograde and retrograde directions. Retrograde dissections decreased in size or disappeared in 1-3 months due to the absence of reentry, whereas anterograde dissections persisted during follow-up (15-27 months). All patient were treated without surgery., Conclusion: Angiographers should be aware of this potentially serious complication. The extent and type of the aortic dissection can be determined with CT.

The natural history and the factors determining the expansion of aneurysms have not been elucidated. To study the respective roles of elastolysis, collagenolysis, inflammatory cells, and hypertension in the pathogenesis of aneurysms, two previously described in vivo experimental models were used. An isolated segment of the abdominal aorta was infused with 15 units of pancreatic elastase. The maximal diameter of the aorta was measured before and after infusion and the isolated aorta was excised for classic histologic and immunohistologic studies. Twelve hours after the infusion of elastase the mean diameter of the aorta increased by 30%. The aorta had a cylindric form and only collagen fibers remained. Two and a half days after the infusion the aorta was spherical in shape and the diameter increased by 300% (3.09 +/- 0.08 mm) (p < 0.05). The entire aortic wall was invested by inflammatory cells. Six days after infusion the diameter increased by 421% (4.38 +/- 0.03 mm) (p < 0.05), and immunohistochemical staining showed numerous T lymphocytes and macrophages. Between 6 and 12 days, after perfusion inflammation decreased, the final diameter was 4.23 +/- 0.14 mm (not significant). Sixteen rats had thioglycollate and plasmin infusion, which are nonspecific activators of inflammation. Nine days after infusion the diameter of the aorta had increased by 288%; the elastic fibers of the media were fragmented and rare and the entire aortic wall was invaded by inflammatory cells, predominantly macrophages. The diameter of the aorta increased progressively. Two groups of 17 hypertensive rats (renovascular and spontaneous hypertension) received an aortic infusion of 15 units of pancreatic elastase. Elastolysis overlapped the limits of the infusion and inflammation persisted after 2 weeks. The mean diameter of the aorta (F = 11, p < 0.01) and the mean length of the aneurysms (F = 11.2, p < 0.001) were significantly increased. This study demonstrates that elastolysis and especially collagenolysis are determinants of aneurysmal expansion. Inflammation may be a promoting factor in the degradation of the aortic wall. Hypertension increases the hemodynamic stress to the aorta and activates mural inflammation.