Diagnosis and management issues in thoracic aortic aneurysm

Thoracic aortic enlargement is an increasingly recognized condition that is often diagnosed on imaging studies performed for unrelated indications. The risk of unrecognized and untreated aortic enlargement and aneurysm includes aortic rupture and dissection which carry a high burden of morbidity and mortality. The etiologies underlying thoracic aortic enlargement are diverse and can range from degenerative or hypertension associated aortic enlargement to more rare genetic disorders. Therefore, the evaluation and management of these patients can be complex and requires knowledge of the pathophysiology associated with thoracic aortic dilation and aneurysm. Additionally, there have been important advances in the treatment available to patients with thoracic aortic disease, including an increased role of endovascular therapy. Given the risk of mortality, increased clinical recognition and advances in therapeutics, the American College of Cardiology, American Heart Association and related professional societies have recently published guidelines on the management of thoracic aortic disease. This review focuses on the pathophysiology and various etiologies that lead to thoracic aortic aneurysm along with the diagnostic modalities and management of asymptomatic patients with thoracic aortic disease.     

Abdominal aortic aneurysm: pathogenesis and implications for management

Abdominal aortic aneurysm (AAA) affects approximately 5% of elderly men and is responsible for a significant number of deaths in Western Countries. At present surgery by open or endovascular means is the only widely used therapy for this condition. In this review we examine the risk factors, serum, and genetic associations of AAA. Epidemiology studies suggest that smoking cessation and control of cholesterol and blood pressure should reduce the number of patients developing AAA. Natural history studies suggest that smoking cessation should reduce the rate of progression of AAA. Clear level 1 evidence for drug treatments of AAA are presently lacking; however, animal and human in vitro studies suggest that medication targeted at reducing inflammation and proteolysis are most likely to be beneficial, with limited data to support the use of statins, Angiotensin II inhibitors, and macrolides. Work has commenced in understanding which patients, identified by clinical, serum, and genotype, are more at risk of AAA progression and thus should be selected out for aggressive treatment. Well designed large multicenter randomized controlled trials are required to examine the medical treatment of AAA.     

Transforming growth factor-beta signaling in thoracic aortic aneurysm development: a paradox in pathogenesis

Thoracic aortic aneurysms (TAAs) are potentially devastating, and due to their asymptomatic behavior, pose a serious health risk characterized by the lack of medical treatment options and high rates of surgical morbidity and mortality. Independent of the inciting stimuli (biochemical/mechanical), TAA development proceeds by a multifactorial process influenced by both cellular and extracellular mechanisms, resulting in alterations of the structure and composition of the vascular extracellular matrix (ECM). While the role of enhanced ECM proteolysis in TAA formation remains undisputed, little attention has been focused on the upstream signaling events that drive the remodeling process. Recent evidence highlighting the dysregulation of transforming growth factor-beta (TGF-beta) signaling in ascending TAAs from Marfan syndrome patients has stimulated an interest in this intracellular signaling pathway. However, paradoxical discoveries have implicated both enhanced TGF-beta signaling and loss of function TGF-beta receptor mutations, in aneurysm formation; obfuscating a clear functional role for TGF-beta in aneurysm development. In an effort to elucidate this subject, TGF-beta signaling and its role in vascular remodeling and pathology will be reviewed, with the aim of identifying potential mechanisms of how TGF-beta signaling may contribute to the formation and progression of TAA.     

Successful management of esophageal necrosis after thoracic endovascular aortic repair for ruptured traumatic aortic aneurysm

A 65-year-old man reported nausea and anorexia after falling down a flight of stairs. Computed tomography (CT) showed a ruptured descending thoracic aortic aneurysm, and emergency thoracic endovascular aortic repair (TEVAR) was performed. However, after resuming food intake, the patient developed a fever. CT scan showed severe pneumomediastinum and a mediastinal abscess, and the patient was diagnosed with esophageal perforation. Emergency esophagectomy was performed, with an esophageal fistula made at the cervix. Jejunostomy was then performed to enable enteral nutrition. Histological examination showed substantial necrosis at the middle intrathoracic esophagus, and the patient was diagnosed with esophageal necrosis leading to perforation. Five months after the esophagectomy, gastric conduit reconstruction through the retrosternal route was performed. The patient was able to resume food intake, and survived more than 1 year after this surgery. Here, we describe the successful management of this rare case of esophageal necrosis after TEVAR for ruptured traumatic aortic aneurysm.     

Percutaneous thoracic aortic aneurysm repair through transcaval aortic access

Transcaval aortic access has been used for deployment of transcatheter aortic valves in patients in whom conventional arterial approaches are not feasible. This access can be vital in other situation when large bore access is needed. We described a case of 65‐year‐old man who had large thoracic descending aortic aneurysm with diffuse bilateral iliac disease precluding the arterial access required for the procedure. The patient underwent successful transcaval access with placement of 22‐Fr balloon expandable sheath followed with successful deployments of 32 mm × 32 mm × 150 mm Valiant stent graft (Medtronic, Minneapolis, MN). The aorto‐vena cava tract was closed successfully using 12 × 10 PDA occluder device with no residual flow at the end of the case, which was confirmed on repeated CT next day.     

覆膜支架植入术治疗胸主动脉夹层动脉瘤的麻醉及围术期处理（附6例报告）

报告6例Debakdy Ⅲ型胸主动脉夹层动脉瘤患者,均在全麻和控制性低血压下完成股动脉覆膜支架植入术。结果：6例内支架植入位置准确,主动脉内膜瘘口被封堵,狭窄的主动脉真腔基本恢复正常。麻醉平稳,无严重心脑血管并发症。认为全麻、 直接动脉压监测下的控制性低血压是保护手术顺利进行的关键。     

Natural history, pathogenesis, and etiology of thoracic aortic aneurysms and dissections

The natural history of thoracic aortic aneurysms and dissections is diverse, reflecting a broad spectrum of etiologies which include increasing aortic size, hypertension, and genetic factors. The pathogenesis is related to defects or degeneration in structural integrity of the adventitia, not the media, which is required for aneurysm formation. The ascending and descending aorta appear to have separate underlying disease processor that lead to a weakened vessel wall and an increased susceptibility for dissection. Etiologic factors for aortic aneurysms and dissections are multifactorial, reflecting genetic, environmental, and physiologic influences.     

Etiology, pathogenesis and management of senile inflammatory pulmonary diseases]

We studied the etiology, pathogenesis and management of therapy-resistant inflammatory pulmonary diseases. First, to understand the pathogenesis of rhinovirus (RV) infection-induced exacerbation of bronchial asthma, we infected cultured human tracheal epithelial cells with RV. The epithelial cells produced a variety of proinflammatory cytokines, intercellular adhesion molecules (ICAM-1) and low-density lipoprotein receptor, and increased the permeability across the epithelial cells. These findings suggest that these factors and the increased permeability may cause airway inflammation, resulting in the exacerbation of asthma. Glucocorticoid and bafilomycin inhibited RV infection in the epithelial cells by reducing ICAM-1 expression and RV RNA entry from the acidic endosomes to the cytoplasm. Second, we revealed the mechanisms of aspiration pneumonia induced by silent aspiration in patients with cerebral infarction. We also developed a pharmacologic treatment for preventing aspiration pneumonia with amantadine, which stimulates the dopaminergic neurons; the angiotensin-converting enzyme inhibitors, which decrease substance P catabolism; and cilostazol, which inhibits platelet aggregation and induces cerebral vasodilation. Third, we demonstrated that exhaled carbon monoxide concentrations caused by heme oxygenase-1 upregulation, may be a useful noninvasive means of monitoring airway inflammation and of controlling elderly patients with bronchial asthma. Finally, we demonstrated that microsatellite polymorphism in the heme oxygenase-1 gene promoter is associated with susceptibility to emphysema caused by cigarette smoke in Japanese patients with chronic pulmonary emphysema.     

An alternative for descending thoracic aortic aneurysm repair

A simple technique termed "clamp test and spinal cord-plegia" for descending thoracic aortic aneurysm surgery is described. The clamp test is a passive method of creating ischemic conditions, whereas spinal cord-plegia is an active method of decreasing metabolism. This technique is a practical test that double-checks for critical feeding arteries and seems to have an excellent spinal cord-preserving effect.