Despite technological advances, the long-term outcomes of endovascular aorticaneurysm repair (EVAR) are still debatable. Although most endograft failures after EVAR can be corrected with endovascular techniques, open conversion may still be required. A 70-year-old male patient presented at the emergency unit with abdominal pain. Twice, in the third and fourth years after the first repair, a stent graft had been placed over a non-adhesive portion of the stent graft due to type Ia endoleaks. In the most recent admission, a CT scan showed type III endoleak and ruptured aneurysm sac. On this occasion the patient underwent late open conversion. The failure was repaired with total preservation of the main endovascular graft body and interposition of a bifurcated dacron graft. This case demonstrates that lifelong radiographic surveillance should be considered in this subset of patients. Late open conversion following EVAR of ruptured abdominal aortic aneurysms can be performed safely.
Physical interconnections between components of tunica media are important in maintaining structural integrity and physicomechanical properties of the aortic wall (Dingemans et al., 2000; Silver and Siperko, 2003). It confers plasticity, adaptability and flexibility to the aortic wall enabling it to function as a mechanically homogenous structure (O geng’o et al., 2010). It ensures the efficient functioning of the aorta in dampening out pulsatile flow and blood pressure delivered by the heart, thus limiting distal shear stress and allowing regular irrigation of peripheral organs (Faury, 2001). Disruptions of these linkages implicate disease processes such as atherosclerosis (Lavezzi et al., 2005) and aneurysm formation (Hayashi et al., 2009). In this case, the presence of abscess caused by C. pseudotuberculosis disturbed vascular integrity, disrupted these linkages and determined the formation of an aorticaneurysm. The aorta rupture triggered the animal’s death.
Abdominal aorticaneurysm (AAA), a common vascular disease in the elderly population, is a degenerative process of the abdominal aorta . Clinically, AAAs can be repaired using open surgery and endovascular technique. However, the two established therapeutic manage- ments are only indicated for patients whose AAA has surpassed 5.5 centimeters in diameter, i.e. a size with a substantially increased risk of lethal rupture [13,14]. Nowadays physicians remain incapable of modifying the natural history of AAA progression. Nevertheless, more and more studies aimed at understanding the underlying events that support AAA develop- ment and developing potential therapeutic strategies that modify the disease course of AAA [13,15]. Over the past 2 decades, researchers have begun to understand the molecular mecha- nisms driving aneurysm formation through studies of human specimens and three mouse AAA models (i.e., angiotensin II [AngII]-infusion model, CaCl 2 -induced model, and elastase-
Introduction. Thoracoabdominal aorticaneurysm (TAAA) type IV represents an aortic dilatation from the level of the diaphragmatic hiatus to the iliac arteries branches, including visceral branches of the aorta. In the traditional procedure of TAAA type IV repair, the body is opened using thorac- tomy and laparotomy in order to provide adequate exposure of the descending thoracic and abdominal aorta for safe aortic reconstruction. Case report. We reported a 71-year- old man with elective reconstruction of the TAAA type IV performed by transabdominal approach. Computed tomog- raphy scans angiography revealed a TAAA type IV with di- ameter of 62 mm in the region of celiac trunk and superior mesenteric artery branching, and the largest diameter of 75
Recent studies have demonstrated a potential synergistic effect of the combination with atorvastatin and amlodipine on the inhibition of vascular inflammation. In a mouse model of femoral artery injury, the combination therapy attenuated leukocyte adhesion and oxidative stress . In a rat ischemic stroke model, pretreatment with atorvastatin and amlodipine ameliorated post-ischemic brain weight increase and induction of MMP-9 . However, the molecular mechanisms of the Figure 9. Working model of the present study. Angiotensin-II induces Rho-kinase activation as well as cyclophilin A expression associated with enhanced apoptosis, increased inflammation and activation of MMP-2, leading to structural weakness, arterial expansion and formation of abdominal aorticaneurysm. Arterial expansion induces decreased endothelial KLF-2 expression (low shear stress) causing further inflammation. In contrast, combination therapy with statin and CCB suppresses angiotensin-II-induced Rho- kinase activation with resultant inhibition of several processes and abdominal aorticaneurysm.
Background. Abdominal compartment syndrome (ACS) is a rapid increase in intra-abdominal pressure asssociated with multi-organs dysfunction. It is caused mostly by abdominal bleeding und massive volume compensation. Case report. We reported a 76-year-old patient admitted to the hospital with aortic abdominal aneurysm, 13.7 cm in diameter, rup- tured in vena cava, which caused intraabdominal hyperten- sion, the liver and kidney dysfunction, as well as circulation, respiration and metabolic disorders. Intraabdominal pres- sure was measured by bladder manometry. Central venous pressure and systemic arterial pressure were monitored continuously. Clinical signs were thrill and typical abdominal bruit. Aorto-caval fistula was diagnosed by the use of con- trast computerized tomography. Caval endoaneurysmatic suture and aortobiiliac bypass with 18 × 9 mm Dacron prothesis were performed. Haemodynamic changes were mostly corrected during the surgery. The complete correc- tion of haemodynamics, liver, kidney, respiration and meta- bolic changes was established in the next few weeks. Con- clusion. The ACS was caused by rupture of abdominal aorticaneurysm in vena cava followed by edema of the ab- dominal organs, retroperitoneum, abdominal wall and asci- tes. Caval endoaneurysmatic suture and aortobiiliac bypass with 18 × 9 mm Dacron prothesis solved aortocaval fistula as well as all the organs and metabolic dysfunctions caused by ACS.
Abdominal aorticaneurysm reconstruction is usually performed in vascular surgical practice. However, the repair of an abdominal aorticaneurysm associated with a pelvic kidney is rare. Our goal is to present a case report of an abdominal aorticaneurysm associated with two congenital pelvic kidneys wich was treated successfully by aneurysmectomy and inclusion of an aortoaortic graft (Rev. Col. Bras. Cir. 2005; 32(1): 54-55).
We believe this to be the first study to examine the association of reported salt intake with aorticaneurysm in humans. The role of high salt intake in aorticaneurysm formation has been previously examined in three rodent model studies [10–12]. Nishijo and colleagues examined the effect of adding 1% sodium chloride to the drinking water of transgenic mice that overproduced angiotensin II . They reported that mice receiving salt loading developed thoracic and abdominal aortic aneurysms which ruptured in 67% of animals during 30 days of salt administration. Nishijo et al. reported that salt loading stimulated an increase in drinking volume and plasma atrial natriuretic peptide associated with loss of aortic vascular smooth muscle cells . Kanematsu and colleagues administered the mineralocorticoid deoxycortico- Table 1. Association of risk factors with reported salt intake in 11742 men.
Abdominal aorticaneurysm (AAA) is a common chronic degenerative disease involving the aortic wall in human. It is estimated that approximately 10% of elderly men show localized structural deterioration of the aortic wall, leading to progressive aortic dilation and rupture [1,2]. Accumulating body of evidence indicate that AAA is influenced by various risk factors including family history, smoking, aging, lifestyle and hypertension [1,3]. Nonetheless, it is also increasingly becoming clear that certain hematological factors also significantly influence the development of AAA . Of note, angiotensin II (Ang II) is one of the key regulatory peptide implicated in the pathogenesis of certain cardiovascular diseases, particularly AAA . Recent lines of evidence suggest that Ang II could trigger intracellular accumu- lation of reactive oxygen species (ROS) culminating in the initiation of lipid peroxidation-mediated oxidative stress . ROS is involved in myriad of downstream signaling pathways viz., transcription factors, tyrosine kinases, protein kinases, ion
Abdominal aorticaneurysm (AAA) is a common, progressive, and life-threatening degenerative vascular disease. AAA is histologically characterized by transmural infiltration of inflam- matory cells, depletion of vascular smooth muscle cells (SMCs), and degradation of arterial extracellular matrix (ECM) [1,2]. Data generated in mouse aneurysm models indicate that macrophage- mediated inflammation is critical for the development and progression of aneurysm [3,4]. Depletion of macrophages  or preventing them from expressing ECM degrading enzymes such as MMPs [6–8] protected mice from developing aneurysm. Mono- cyte chemoattractant protein-1 (MCP-1) has been implicated in the pathogenesis of several cardiovascular diseases including AAA. Elevated MCP-1 mRNA and protein expression has been consistently detected in aneurysmal aortic tissues of human patients as well as animal models [9–12]. Blocking MCP-1 signaling either through genetic deletion or siRNA-mediated knockdown, or through inhibition of its receptor, CCR2,
Despite concerted efforts to understand the pathophysiologic mechanisms, there is still not a definite answer regarding the factors underlying this process (6). There are recognized pathologic processes, such as the increment of proteolytic pathways and programmed cell death, oxidative stress and immune/inflammatory cell infiltration, along with intraluminal thrombus (ILT) formation, together culminating with loss of arterial wall matrix and its compensatory disrupted remodelling. (4, 7) The loss of arterial wall is thought to result from an imbalance between proteases – most consistently matrix metalloproteinases 2 and 9 (8) - and their regulators (9), provoking enzymatic degradation of structural matrix proteins, such as elastin and collagen, as well as decreased vascular smooth muscle cell (VSMC) functions and ultimately its number(7), creating space for immune cell infiltration in the external layers – media and adventitia- rendering it prone to dilation. (7) On the other hand, ILT formation is a common finding and is yet to be clarified its role on the AAA evolution. Indeed, inflammatory activity is present in ILT and can also be a responsible for the degradation of the quality of the aortic wall. Though, from a mechanical view, ILT can function as a protective layer, wherein smaller thrombi are associated with a faster AAA growth. (10)
Hybrid techniques means that after insertion of the stent graft to exclude the aneurysm, laparoscopy is perfor- med to secure the stent graft in the region of a short infrare- nal neck with a band or sutures and to clip lumbar arteries and the inferior mesenteric artery to avoid type 2 endole- aks. Despite encouraging short and mid-term results, pro- blems such as endoleaks, endotension and graft migration are frequently encountered after EVAR. 29-31 With close follow-up, re-interventions after EVAR reveal a signifi- cant number of secondary procedures between 10 to 27% and an annual rate of late rupture at 0.5 to 1.5%. Without intervention, persistent endoleaks are associated with late aneurysm rupture and the subsequent, long-term failure of EVAR. 32-36 Laparoscopic techniques can be used to over- come many of these challenges after EVAR. Laparoscopic adjuncts after EVAR include several options: 1) clipping of the inferior mesenteric artery (IMA) and lumbar arteries to treat type II endoleaks; 2) thrombus removal and tight closure of the sac of the aneurysm to reduce the sac diame- ter; 3) fixation of the endograft to the aortic neck to prevent device migration; 4) banding of the aorta to prevent neck dilatation and; 5) laparoscopic conversion after EVAR fai- lure (Figure 7).
velopment of AAA. These findings indicate that a decline in adventitial decorin may result in the initiation of AAA. Decorin expression in adventitial cells may indirectly result in protection of the aortic media against inflammatory insults by unknown mechanisms. However, we pre- sented another possibility; decorin, which is released from the adventitia of normal and non- aneurysmal aortic walls, can reach the media, affect medial VSMCs, and directly protect the media from proteolytic degradation. Consistent with our results, reduced expression of decorin in the adventitia was associated with a high risk of aortic rupture in another mouse model of AAA induced by angiotensin II . Among human aneurysmal diseases, deficient decorin ex- pression has been associated with lethal forms of Marfan’s syndrome  and aortic dissection [30,31].
Aortotracheal fistula is a rare condition that is invariably fatal if not diagnosed and surgically treated. Patients usually present with small intermittent hemoptysis. The findings using computerized tomography (CT) are usually diagnostic. CT should be considered in the initial investigation of patients suspected to have such a disease. A 62-year-old woman with a aneurysm of the descending thoracic aorta presented with new-onset back pain and hemoptysis. The hemoptysis was thought to be the result of invasion of the bronchial tree by the aneurysm.
From October 2008 to March 2010, consecutive surgical patients for acute type A aortic dissection (20 patients), aorticaneurysm (nine patients) or coronary artery disease (20 patients) who had blood samples and/or surgical specimens of the aortic tissues available were selected randomly into this study, while the Marfan patients were excluded. The surgical patients were comparable in terms of their age and gender. Blood samples (4 ml) were obtained from the right radial arterial indwelling catheter after systemic heparinization prior to the start of cardiopulmonary bypass in the operating room. Twenty-one young healthy volunteers without underlying health issues donated forearm venous blood (4 ml) as control samples. Blood samples were centrifugated at 3000 × g for 5 min, and plasma was collected and stored at -80°C until detection. The surgical specimens of the aortic tissues were obtained immediately after they were severed during the operations of the replacement of the aorta in the patients with aortic dissection or aorticaneurysm. In patients receiving coronary artery bypass grafting, the tiny aortic tissues 0.2~0.4 cm in size were taken when the punch holes of the proximal anastomosis on the anterior wall of the ascending aorta were made. The aortic tissues were stored at -80°C, and were thawed for RNA, protein, or supernatant preparations until detection of TGF-ß 1 mRNA by quantitative real-time reverse transcription polymerase chain reaction (RT-PCR), of TGF-ß 1 , TßRI, Smad2/3, Smad4 and Smad7 by Western blot, and of TGF-ß 1 by enzyme-linked immunosorbent assay (ELISA), respectively. The patients’ demographics were listed in Table 1.
All dissections were conﬁned to the abdominal aorta between the renal arteries and the inferior mesenteric artery without retrograde extension to the thoracic aorta. The mean dissection length was 85 mm (range, 64–114 mm). In three cases the dissection was limited to the abdominal aorta, in another one the aortic dissec- tion extended into the left common iliac artery with a contralateral iliac occlusive disease (3) and in ﬁve another cases the dissection involved both iliac arteries. Five patients (two asymptomatic and three symptom- atic with abdominal pain) were treated medically and put under surveillance: none of them have so far developed either an abdominal aorticaneurysm or an extension of dissection. Four patients were treated endovascularly under spinal anesthesia; in the operat- ing room the common femoral arteries (CFAs) were surgically exposed (two had bilateral cutdown). One patient was treated with a 23 14 mm Excluder bifur- cated stent graft (W.L. GORE & Associates, Flagstaﬀ, AZ, USA) (Fig. 1a–c). In one case, a Talent bifurcated (aortouniiliac) endograft (Medtronic Vascular, Santa Rosa, CA, USA) was positioned through the left CFA. Because the contralateral iliac artery was not suitable for iliac limb deployment, an occluding cov- ered stent was then positioned, and a 8-mm ePTFE
follow-up, we observed abdominal aortic dilation that involved the celiac trunk, the superior mesenteric artery, right and left renal arteries, anastomosed in Dacron graft 11 years ago to correct thoracoabdominal aorticaneurysm (fig. 1). This aortic segment had grown 0.4 cm/year in the previous 2 years, and at the time of surgical indication, it was 5.9 cm in the major transversal diameter. The patient reported scattered episodes of lumbar pain not related to effort. He also had mild left ventricular dysfunction with an ejection fraction of 50%, systemic blood hypertension, chronic obstructive pulmona- ry disease, hypercholesterolemia, peripheral vasculopathy, obstructive carotid disease (left carotid with 50% obstruction in the carotic bulb), atrophic left kidney, and borderline renal function (serum creatinine 1.6 mg/dL).
Heparin-induced thrombocytopenia (HIT) is a transient disorder caused by platelet-activating antibodies against platelet factor 4 (PF4)- heparin complexes. Clinically, it translates into arterial or venous throm- bosis and carries high morbidity and mortality. The use of large doses of heparin during endovascular repair of abdominal aorticaneurysm could increase the incidence of HIT. We report two cases associating the use of heparin during endovascular repair of abdominal aorticaneurysm with the development of HIT.
Introduction: Endovascular aneurysm repair (EVAR) is the therapy of choice in high risk patients with abdominal aorticaneurysm. The good results described are leading to the broadening of clinical indications to younger patients. However, reintervention rates seem higher and even with successful treatment sometimes there is growth of the aneurysm sac and rupture, meaning a failure of the therapeutic goal. This study proposes to analyse the impact of age in patients’ selection and post-EVAR results.