Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0162871 (abdominal aortic aneurysm)
 8,664 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The abdominal compartment syndrome (ACS) is a clinical entity that develops after sustained and uncontrolled intra-abdominal hypertension. ACS has been demonstrated to affect multiple organ systems including the cardiovascular, respiratory, gastrointestinal, genitourinary, and neurologic systems. To date most descriptions of ACS are found in the trauma literature, but the development of ACS in the general surgical population is being increasingly observed. In this study the development of ACS in a nontrauma surgical population is described and examined. The records of 18 surgical intensive care unit patients with documented ACS were reviewed retrospectively. Data acquired included demographics, urine output in mL/hour, cardiac index in L/m2/min: systemic vascular resistance index in mm Hg/L/m2/min: and pulmonary artery occlusion pressure, peak inspiratory pressure, partial pressure of oxygen in arterial blood, pH, partial pressure of carbon dioxide, and intra-abdominal pressure (all in mm Hg). When they were available values were obtained before and after decompression. Data are presented as mean +/- standard deviation and are analyzed by Student's t-test; significance was accepted to correspond to a P value <0.05. Nineteen episodes of ACS were identified in 18 patients. The average age was 69.2 years, and the observed mortality of the group was 61.1 per cent (11 of 18). Diagnoses included abdominal aortic aneurysm (eight), postoperative laparotomy (six), pancreatitis (three), and cerebral aneurysm (one). Of the parameters examined urine output, peak inspiratory pressure, and cardiac index demonstrated a significant change before and after decompression. The average intra-abdominal pressure was 43.4 mm Hg. Five of 18 patients (two with abdominal aortic aneurysm, two with postoperative laparotomy, and one with pancreatitis) were found to have necrotic bowel on decompressive laparotomy. The development of ACS is described in a surgical intensive care unit. ACS is the end result of uncontrolled intra-abdominal hypertension and results in systemic derangements. Surgical decompression of ACS significantly reduces peak inspiratory pressure while increasing urine output and cardiac index. The observed association between ACS and ischemic bowel may result from decreased mucosal perfusion as a direct result of abdominal hypertension. In our patient population ACS resulted in a 61.1 per cent mortality.
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PMID:Abdominal compartment syndrome in the surgical intensive care unit. 1246 11

Therapeutic planning for patients with concomitant thoracic aortic aneurysm (TAA) or abdominal aortic aneurysm (AAA) and noncardiovascular disease such as cerebral aneurysm, carotid artery stenosis, or lung, intraabdominal or urologic tumor should be considered based on the combination of the two different conditions, the size of aneurysm, or the severity of noncardiovascular disease. The aims of this paper are to review the therapeutic plans for concomitant TAA or AAA and noncardiovascular disease. In patients with concomitant TAA or AAA and cerebral aneurysm, carotid artery stenosis, and concomitant TAA and intraabdominal or urologic tumor, the surgical procedures have usually been staged with the repair of cerebral aneurysm, or carotid artery stenosis, the resection of intraabdominal or urologic tumor performed first, followed by the repair of TAA or AAA. Simultaneous surgical treatment has been performed for most patients with concomitant TAA and lung tumor, and concomitant AAA and intraabdominal or urologic tumor. The issue of performing simultaneous pulmonary resection and repair of AAA in patients with concomitant lung tumor and AAA remains controversial. Endovascular grafting of TAA and AAA can be performed with relatively low procedure-related morbidity and mortality rates in selected patients.
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PMID:[Treatment strategy for patients with concomitant thoracic or abdominal aortic aneurysm and noncardiovascular disease]. 1593 51

Over-degradation of extracellular components by matrix metalloproteinases (MMPs) has been implicated as an important characteristic during the pathological evolution of the abdominal aortic aneurysm (AAA) and cerebral aneurysm (CA), which contribute to progressive dilation of vascular wall. However, mRNA and protein expression of local rennin-angiotensin system (RAS) components are found down-regulated in CA walls, which is contrary to long-holding concept that local RAS will be activated in response to increased hemodynamic stress and contributes to thickening of arterial wall. Similarly, MMPs inhibition by doxycycline effectively ameliorate AAA expansion in basic and clinical researches, but can not reduce the incidence of CA formation in rat. These evidences may suggest that suppression of RAS favors the regression of AAA, but at an increased risk of CA rupture. As the strategies of RAS blockade have became the optimal antihypertensive drugs of choice in clinical arena, the discrepant responses to pharmacologic intervention of AAA and CA should be received considerable attentions, due to their high prevalence in hypertensive population. Here we proposed that AAA and CA, outward remodeling of elastic and muscular arteries respectively, presented with different pathological evolutions and distinct responses to drug intervention, i.e., RAS and MMPs inhibition. It can not be excluded that the potentially deleterious effects of RAS inhibition on CA may be masked by the beneficial action of controlled blood pressure, and the propagation of CA will be exacerbated once suboptimal dose have been prescribed, or under the condition of stress, even drug withdrawal. If the paradoxical outcomes of these two kinds of arterial remodeling were proven true in basic research, clinical use of RAS blockade should be prudent in hypertensive patients, and routine procedures to detect the existence of CA should be considered. Therefore, in depth investigation in their responses to pharmacological approaches will provide us with more insights into the pathogenesis of arterial aneurysm.
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PMID:Abdominal aortic aneurysm and cerebral aneurysm present different pathological evolutions and responses to pharmacological therapy. 1703 Jan

Fasudil (a Rho-kinase inhibitor) has been shown to attenuate abdominal aortic aneurysm development, but any preventive effect against development of cerebral aneurysms is unclear. The effect of fasudil on the development of cerebral aneurysms was investigated in 55 female Sprague-Dawley rats divided into 4 groups: Group 1 (n=10) was the control group without treatment. Groups 2-4 (n=15 each) were subjected to cerebral aneurysm induction procedures plus 1% NaCl in the drinking water. Groups 3 and 4 were also treated with 0.5 or 1.0mg/mL of fasudil in the drinking water, respectively. Vascular corrosion casts of the cerebral arteries were prepared and examined using a scanning electron microscope after 2 months. No significant differences were observed in the degree of induced hypertension between Groups 2, 3 and 4. No aneurysms were found in Group 1. Examination of the left anterior cerebral-olfactory artery junction, which is the most susceptible site for aneurysm development, found significantly fewer aneurysmal lesions in Groups 3 (60%) and 4 (53%) compared to Group 2 (100%) (P<0.02). This study suggests that fasudil attenuated induction of cerebral aneurysms in the rat model.
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PMID:Fasudil, a Rho-kinase inhibitor, attenuates induction and progression of cerebral aneurysms: experimental study in rats using vascular corrosion casts. 2004 78

An 80-year-old woman with subarachnoid hemorrhage underwent emergency neck clipping of a cerebral aneurysm. She had previously undergone surgery for an abdominal aortic aneurysm 10 years before. Anesthesia was induced with propofol and maintained with a combination of fentanyl and sevoflurane (0.5-1.5%) in air and oxygen. Ventricular fibrillation occurred immediately before clipping of the aneurysm, in the absence of preexisting myocardial ischemia, and recurred 4 times thereafter during the surgery. The ventricular fibrillation was successfully treated with cardioversion. We administered catecholamines, nitrates, calcium antagonists, nicorandil and heparin, following which the patient's hemodynamics gradually improved. After the operation, the patient was transferred to the cardiovascular center of a neighboring university where she successfully underwent emergency percutaneous transluminal coronary angioplasty. The patient was discharged from hospital 10 days later without any complications. Patients undergoing vascular surgical procedures or having a preoperative history of prior vascular surgery are at high risk for perioperative myocardial infarction. It is necessary to perform cardiac examination, including coronary angiography, preoperatively in such patients, even in those who are otherwise asymptomatic.
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PMID:[Case of myocardial infarction during emergency clipping surgery of a cerebral aneurysm]. 2005 3

Self-healing phenomenon was found in the periarterial elastase-induced abdominal aortic aneurysm (AAA) in rabbit. This kind of aneurysm model does not progress and heals spontaneously in the long term, which is quite different from the performance of AAA disease in human. In order to better mimic human AAA and overcome this shortcoming of traditional AAA model in rabbit, we studied the pathogenesis of cerebral aneurysm (CA) model in small animal, which shows an excellent long-term patency and progressive enlargement. We found that hemodynamic conditions, such as turbulence flow, high blood flow, and shear stress, play an important role in the formation and progression of CA. So, we hypothesize that hemodynamic change may also play an essential role in the initiation and progression of rabbit AAA, and self-healing will be overcome if hemodynamic condition changes by coarctation of infra-renal aorta after elastase incubation.
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PMID:Different long-term outcomes of abdominal aortic aneurysm and intracranial aneurysm models: hemodynamic change may also play an essential role in the initiation and progression of abdominal aortic aneurysm in rabbits. 2480 72

Statins have been suggested in previous studies to play a protective role in experimental cerebral aneurysm (CA) models; however, no evidence supports that the application of statins can protect against aneurysm rupture in humans, and the risks of lipid levels and aneurysms remain unknown. Therefore, this meta-analysis aimed to summarize and update the epidemiological evidence to systematically assess the relationships of statin therapy and hyperlipidemia with the incidence, rupture, postrepair mortality, and all-cause mortality of abdominal aortic aneurysm (AAA) and CA. Related studies were initially retrieved from the electronic databases PubMed, Embase, and Cochrane Library from inception to August 4, 2018. Subsequently, 33 studies were enrolled into this meta-analysis, and the maximum adjusted risk ratios (RRs) as well as the corresponding 95% confidence intervals were extracted. Finally, a total of 32 observational studies involving 150,134 participants were enrolled into this meta-analysis. The RRs of statin therapy for AAA incidence, AAA rupture, CA rupture, postrepair mortality, all-cause mortality, and adverse events were 1.83 (0.56-5.98), 0.67 (0.47-0.97), 0.50 (0.18-1.36), 0.60 (0.48-0.74), 0.66 (0.58-0.75), and 0.58 (0.47-0.71), respectively. Besides, the RR of hyperlipidemia for CA rupture was 0.79 (0.67-0.93). Our findings suggested that statin therapy could reduce the risks of AAA rupture, postrepair mortality, all-cause mortality, and adverse events, without inducing the risk of AAA incidence or CA rupture, and that hyperlipidemia was associated with a lower risk of CA rupture.
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PMID:Relationships of Statin Therapy and Hyperlipidemia With the Incidence, Rupture, Postrepair Mortality, and All-Cause Mortality of Abdominal Aortic Aneurysm and Cerebral Aneurysm: A Meta-analysis and Systematic Review. 3068 98

Flow stagnation and residence time (RT) are important features of diseased arterial flows that influence biochemical transport processes and thrombosis. RT calculation methods are classified into Eulerian and Lagrangian approaches where several measures have been proposed to quantify RT. Each of these methods has a different definition of RT, and it is not clear how they are related. In this study, image-based computational models of blood flow in an abdominal aortic aneurysm and a cerebral aneurysm were considered and RT was calculated using different methods. In the Lagrangian methods, discrete particle tracking of massless tracers was used to calculate particle residence time and mean exposure time. In the Eulerian methods, continuum transport models were used to quantify RT using Eulerian RT and virtual ink approaches. Point-wise RT and Eulerian indicator RT were also computed based on measures derived from velocity. A comparison of these methods is presented and the implications of each method are discussed. Our results highlight that most RT methods have a conceptually distinct definition of RT and therefore should be utilized depending on the specific application of interest.
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PMID:A critical comparison of different residence time measures in aneurysms. 3095 50