Value of Routine Flexible Sigmoidoscopy and Potential Predictive Factors for Colonic Ischemia after Open Ruptured Abdominal Aortic Aneurysm Repair.

Background and Objectives: colonic ischemia (CI) after ruptured abdominal aortic aneurysm (rAAA) repair is associated with increased morbidity and mortality. CI may be detected by using flexible sigmoidoscopy, but routine use of flexible sigmoidoscopy after rAAA is not clearly proven. The objective of this study was to evaluate the efficacy of routine flexible sigmoidoscopy in detecting CI after rAAA repair, and to identify potential hemodynamic, biochemical, and clinical variables that can predict the development of CI in the patients who underwent rAAA surgery. Materials and Methods: we retrospectively included all rAAA cases treated in Viborg hospital from 1 April 2014 until 31 August 2017, recorded the findings on flexible sigmoidoscopy, and the incidence of CI. We collected specific hemodynamic, biochemical, and clinical variables, measured pre- and perioperatively, and the first three postoperative days. The association between CI and possible predictors was analyzed in a logistic regression model. Results: a total of 80 patients underwent open rAAA repair during the study period. Flexible sigmoidoscopy was performed in 58 of 80 patients (73.5%) who survived at least 24 h after open rAAA surgery. Perioperative variables lowest arterial pH (p = 0.02) and types of operations-aortobifemoral bypass vs. straight graft (p = 0.04) showed statistically significant differences between CI groups. The analysis of the postoperative variables showed statistically significant difference in highest lactate on postoperative day 1 (p = 0.01), and lowest hemoglobin on postoperative day 2 (p = 0.04) comparing CI groups. Logistic regression model revealed that postoperative hemoglobin and lactate turned out to be independent risk factors for the development of CI (respectively OR = 0.44 (95% CI = 0.29-0.67) and OR = 1.91 (95% CI = 1.2-3.05)). Conclusions: flexible sigmoidoscopy can identify patients being at higher risk of mortality after open rAAA repair. The postoperative lactate and hemoglobin were found to be independent risk factors for the development of CI after open rAAA repair. Further larger studies are warranted to demonstrate these findings.

Abdominal Aortic Aneurysms Growth Is Associated With High Concentrations of Plasma Proteins in the Intraluminal Thrombus and Diseased Arterial Tissue.

Objective- Porosity of the intraluminal thrombus (ILT) is believed to convey biologically active components from the bloodstream toward the aneurismal wall. Accumulation of molecules in the abdominal aortic aneurysmatic tissue may influence vascular protein turnover and regulate abdominal aortic aneurysm growth. We sought to identify proteins with concentrations in the ILT and the abdominal aortic aneurysm wall which associate with aneurysmal expansion rate. Approach and Results- Proteomic analysis by liquid chromatography tandem-mass spectrometry of separated wall and ILT samples was correlated with preoperative aneurysmal growth rate in 24 individuals operated electively for infrarenal abdominal aortic aneurysm. The median preoperative growth rate was 3.8 mm/y (interquartile range, 3) and the mean observational time was 3.3±1.7 years. Plasma components dominated the group of proteins with tissue concentrations, which correlate positively with growth rates ( P<0.001, Fisher exact test, both in the ILT and the wall). In contrast, in the wall and thrombus samples, ECM (extracellular matrix) proteins were significantly more prevalent in the group of proteins with negative correlations to growth rates ( P<0.05, Fisher exact test). Similarly, a long series of proteins, related to cellular functions correlated negatively to growth rates. Conclusions- When the preoperative aneurysmatic growth rate has been high, the concentration of many plasma proteins residing in the ILT and the aneurysmatic tissue is also high, compatible with the hypothesis of increased tissue porosity and accumulation of plasma components as a driver of aneurysm expansion. Moreover, many matrix and cellular proteins which are found in high concentrations in slower-growing aneurysms provides new knowledge about potential treatment targets.

Peripheral artery disease patients are poorly aware of their disease.

Objectives. We hypothesized, that patients with peripheral arterial disease (PAD) are less aware of risk factors and possible outcomes of the disease compared to patients with coronary artery disease (CAD), which are similar. Hence, the aim of this study was to evaluate awareness of and attitudes towards PAD and CAD among patients, who are already diagnosed with either disease. Design. A cross-sectional descriptive study was performed. Basic demographics, the presence and awareness of risk factors for PAD and CAD; perceived systemic and limb consequences, severity of PAD and CAD, self-reported knowledge about other non-vascular illnesses were assessed using an anonymous questionnaire. Results. 203 were invited and 157 (77%), 63 with PAD and 94 with CAD, patients agreed to take part in and completed the survey. Basic demographic characteristics were similar in both groups, except for the level of education: PAD patients were less educated compared to CAD patients (p = .002). Only 35% of PAD patients were familiar with the definition of PAD (key words were registered) in contrast to 52% CAD definition awareness among CAD patients (p = .034). PAD patients were significantly less familiar with other common diseases (p = .002) and risk factors for both PAD (p < .001) and CAD (p = .003) in comparison to equivalent CAD group parameters. Conclusions. PAD patients are less aware of risk factors for PAD and atherosclerosis in general, other illnesses and have lower level of education, which may negatively affect overall management of this complex disease.

IGF-I and IGFBP2 in peripheral artery disease: results of a prospective study.

BACKGROUND AND OBJECTIVES: The search for novel risk factors of cardiovascular disease (CVD) has provided valuable clinical data concerning underlying mechanism of disease. Increasing evidence indicates a possible involvement of insulin-like growth factor-I (IGF-I) and its binding protein 2 (IGFBP-2) in the pathogenesis of CVD disorders. The aim of this study was to examine the relationship between levels of IGF-I and IGFBP-2 with all-cause and CVD mortality in a prospective study of patients with lower-extremity peripheral artery disease (PAD). METHODS AND MATERIAL: Serum IGF-I and IGFBP-2 levels were obtained in 440 patients (257 males) with symptomatic PAD. Patients were followed for a median of 6.1 (IQ 5.1-7.2) years. The relationship between times to lethal outcome and baseline serum IGF-I and IFGBP-2 levels were examined by Cox proportional hazard analysis. The role of IFGBP-2 for prognosis of CVD death was assessed with c-statistic. RESULTS: During follow-up 115 (26%) patients (48 females and 67 males) died, and 53 (12%) died from CVD-related causes. Cox regression analysis revealed that an increase of 100 µg/l of baseline IFGBP-2 were significantly associated with an increased risk for CVD mortality [crude hazard ratio (HR) 1.14 (95% CI (1.05-1.23)), and adjusted HR 1.12 (95% CI (1.01-1.24))]. The receiver operating characteristic (ROC) analysis yielded area under curve of 0.61 (95% CI: 0.51-0.67, p = 0.022). However, the model including IFGBP-2 did not show a significant improvement in accuracy of CVD death prediction [the area under ROC curve 0.73 (0.66-0.80) vs. 0.75 (0.69-0.82), p = 0.696], and net reclassification improvement was 10.3% (p = 0.23). CONCLUSIONS: Increased IFGBP-2 concentration was significantly and independently associated with long-term CVD mortality in patients with lower-extremity PAD. However, risk prediction of CVD mortality did not improve by adding IFGBP-2 to a model containing conventional CVD risk factors.

A novel view to varicose veins pathogenesis: Proteomic profiling suggests a pivotal role of extracellular matrix degradation.

INTRODUCTION: Although morphological and anatomical studies indicate that venous wall weakening and subendothelial fibrosis characterize varicose veins (VV), the pathogenesis of VV remains poorly understood. The aim of this study is to obtain protein expression profiles in patients with VV and thereby get a step closer to understanding the pathogenesis of VV. METHODS: Specimens were obtained from total of 10 patients, that is, from 5 patients undergoing VV surgical stripping and from 5 non-VV patients undergoing bypass surgery. Specimens were collected from the same layers of venous wall. Proteins were extracted from each specimen and analyzed by ion mobility spectrometry (IMS-MS). In total, 1387 were identified and 486 proteins were identified in all samples. From these, 15 proteins were differentially expressed between VV and non-VV samples (p < .05) and 12 of these showed a fold change >1.5. RESULTS: Interestingly, among the differentially expressed proteins, only two proteins were significantly increased in the VV tissue, that is, GAPDH (p = .028, fold change 2.74), where several proteins involved in maintaining the homeostasis in the extracellular matrix, that is, the CXXC zinc finger protein 5 (CXXC5) and nucleoporin (SEH1) were prominently downregulated (p = .049, fold change 37.8, and p = .040, fold change 3.46). The downregulation in protein expression of CXXC5 and SEH1 as well as upregulation of GAPDH were validated by Western blotting. CONCLUSION: The identified differentially expressed proteins suggest an altered profile of the connective tissue proteins as well as an increased proteolytic enzyme activity which both may be central in the pathophysiology of varicose veins.

Proteomic identification of differentially expressed proteins in aortic wall of patients with ruptured and nonruptured abdominal aortic aneurysms.

OBJECTIVE: To compare the basic proteomic composition of abdominal aortic aneurysm (AAA) wall tissue in patients with nonruptured and ruptured aneurysms. METHODS: A proteomic approach with two-dimensional gel electrophoresis (2D-PAGE) and mass spectrometry (MS) was used to identify differentially expressed proteins in AAA tissue from nine patients with nonruptured and eight patients with ruptured AAA. Computerized image analysis was used to detect protein spots. Differentially expressed protein spots were in-gel digested and identified by liquid chromatography-tandem mass spectrometry (LC-MS/MS). Western blot analysis was used to confirm differential expression. RESULTS: Seven differentially expressed proteins were detected among 745 protein spots, selecting spots whose average relative volumes differed more than twofold between the nonruptured and the ruptured group. Four protein spots were up-regulated in the ruptured group, and three were down-regulated. Five of the spots were identified. Among the upregulated spots, No. 605 was identified as peroxiredoxin-2. The up-regulation was confirmed by Western blotting. No. 381 was identified as an actin fragment. Two spots, Nos. 719 and 499, could not be identified. Among the down-regulated protein spots, No. 130 contained two peptides; one reliably determined peptide, FEDGVLDPDYPR, is found in vitronectin. Another peptide, QIDNPDYK, was borderline significant and found in calreticulin. The down-regulation of vitronectin was confirmed by Western blotting. Spot Nos. 193 and 199 both contained peptides from albumin with actin also present in No. 199. CONCLUSION: The identified proteins suggest that the aortic wall of ruptured aneurysms responds to a stressful condition and that proteolytic degradation of the cytoskeleton and connective tissue may be part of the response.

Proteomic analysis identifies mitochondrial metabolic enzymes as major discriminators between different stages of the failing human myocardium.

OBJECTIVES: Our aim was to identify patterns in differentially regulated proteins associated with the progression of chronic heart failure. We specifically studied proteomics in chronic reversibly (RDM) and irreversibly dysfunctional myocardium (IRDM), as well as end-stage failing myocardium (ESFM). METHODS: We studied biopsies from 9 patients with stable chronic heart failure undergoing coronary artery bypass surgery (CABG) (EF 34% +/- 3%) and from 4 patients with ESFM undergoing heart transplantation (EF 17% +/- 5%). In CABG patients paired echocardiographic studies before and 6 months after revascularization classified dysfunctional myocardium as RDM or IRDM. Regions with preserved contractile function served as control. We used two-dimensional gel electrophoresis (2D-PAGE) and computerized image analysis to investigate myocardial protein expression. Proteins were identified by in-gel digestion and subsequent liquid chromatography-tandem mass spectrometry (LC-MS/MS). RESULTS: Among 3 significantly altered protein spots in RDM we identified 2 up-regulated glycolytic enzymes. In IRDM 15 proteins were signficantly altered of which we identified 10, among these 6 were down-regulated mitochondrial enzymes. In ESFM 9 of 12 significantly altered protein spots were identified. Six were down-regulated mitochondrial enzymes. CONCLUSION: Myocardial metabolism may be involved in the progression of heart failure to irreversible dysfunction and end-stage heart failure.

Evaluation of prognostic clinical and ECG parameters in patients after myocardial infarction by applying logistic regression method.

Noninvasive risk stratification of patients who have suffered myocardial infarction (MI) is one of the greatest challenges in today's cardiology. No single test has sufficient predictive ability. Therefore, a combination of the tests must be applied for better post-MI risk stratification. The purpose of this study was to assess noninvasive predictors of 2 years cardiac mortality in post-MI patients and create a stratification model for identification of high-risk patients. Clinical, electrocardiographic, and echocardiographic parameters were evaluated before hospital discharge in 180 survivors of acute MI (mean age 57.0 +/- 9.9, male 82.2%), followed up for 2 years. A multivariate logistic regression analysis was used to determine informative predictors of cardiac mortality. A clinical score was constructed using the regression coefficient from the multivariate model. During follow-up, 16 deaths (8.8%) occurred. Multivariate analysis identified a combination of six variables that showed the strongest association with cardiac mortality. Based on the coefficients of the logistic regression, six variables were used to create a scoring system: filtered QRS duration (QRSd) >114 ms, coefficient of variation (Cv) or=445 ms, left ventricular ejection fraction (LVEF)

JNK, p38, ERK, and SGK1 Inhibitors in Cancer.

Mitogen-activated protein kinases (MAP kinases) are a family of kinases that regulates a range of biological processes implicated in the response to growth factors like latelet-derived growth factor (PDGF), epidermal growth factor (EGF), vascular endothelial growth factor (VEGF), and stress, such as ultraviolet irradiation, heat shock, and osmotic shock. The MAP kinase family consists of four major subfamilies of related proteins (extracellular regulated kinases 1/2 (ERK1/2), c-Jun N-terminal kinase (JNK), p38, and extracellular regulated kinase 5 (ERK5)) and regulates numerous cellular activities, such as apoptosis, gene expression, mitosis, differentiation, and immune responses. The deregulation of these kinases is shown to be involved in human diseases, such as cancer, immune diseases, inflammation, and neurodegenerative disorders. The awareness of the therapeutic potential of the inhibition of MAP kinases led to a thorough search for small-molecule inhibitors. Here, we discuss some of the most well-known MAP kinase inhibitors and their use in cancer research.

Expression of matrix metalloproteinases, their tissue inhibitors, and osteopontin in the wall of thoracic and abdominal aortas with dilatative pathology.

Matrix metalloproteinases (MMPs) degrade extracellular matrix and may play a central role in the pathogenesis of aortic aneurysms. We studied 2 groups of patients: 15 with dilatative pathology of the ascending thoracic aorta and 17 with aneurysm of the abdominal aortic wall (AAA). We compared the expression of MMPs, tissue inhibitors of matrix metalloproteinases (TIMPs), and osteopontin in the wall of thoracic and abdominal aneurysms. In AAA, MMP-9 and TIMP-1 expression in inflammatory cells was higher than in smooth muscle cells (SMCs) (median score: 3.5 versus 1, P < .0001; 2 versus 1, P < .04, respectively), whereas MMP-2 demonstrated higher expression in SMCs than in inflammatory cells (median score: 0 versus 4, P < .0001). In ATA, MMP-2, MMP-9, TIMP-1, TIMP-2, TIMP-3, and osteopontin expression in SMCs was higher than in inflammatory cells (median score: 3 versus 0, P < .0001; 4 versus 1, P < .0005; 2 versus 0, P < .001; 5 versus 2, P < .0001; 2 versus 0, P < .005; and 5 versus 1.5, P < .0001, respectively), when both inflammatory cells of the media and the adventitia were considered together. The cellular expression of MMP-9 and their tissue inhibitors TIMP-1, TIMP-2, and TIMP-3 differs in the dilatative pathology of abdominal and thoracic aortas, so the hypothetical model of morphogenesis of AAA cannot completely explain the formation of dilatative pathology of the ascending thoracic aorta.

Coronary computed tomography angiography and calcium scoring in routine clinical practice for identification of patients who require revascularization.

BACKGROUND: The predictive value of CCTA to predict coronary artery disease is high in particular in the absence of coronary calcification. However, the consideration of both CCTA and the calcium score, in addition to the risk factors to determine the indication for coronary revascularization, has not been yet studied. MATERIALS AND METHODS: This study included 2302 patients (mean age: 60±9.8 years, 46% men), without known coronary artery disease (CAD), who underwent 320-row CCTA. Logistic regression, c-statistic and net reclassification improvement (NRI) were used to assess the role of coronary artery calcium score (CACS) in predicting revascularization after CCTA. RESULTS: The revascularization rates were 0.75% in patients with a CACS of 0, and there were no adverse events during the follow-up period. The revascularization rates were 3.3% in patients with a CACS of 1-99, 15.4% in patients with a CACS of 100-399, 25.6% in patients with a CACS of 400-999, and 42.4% in patients with a CACS≥1000. The crude and adjusted odds ratios (95% confidence interval) for revascularization per CACS group category were 2.89 (2.53-2.3) and 2.71 (2.33-3.15), respectively; the area under the ROC curve (AUC) was 0.85 (0.83-0.88). The addition of CACS to conventional risk factors improved the accuracy of risk prediction model for revascularization (AUC 0.74 vs 0.63, P=0.001), but it did not reclassify a substantial proportion of patients with positive CACS to risk categories (NRI=-0.023, P=0.66). CONCLUSIONS: The 320-row CCTA might rule out CAD in low- to intermediate-risk patients. However, its accuracy in identifying patients who require revascularization is limited. The CACS added to the conventional risk factors did not improve the identification of patients who require revascularization.

Serum antibodies against Chlamydia pneumoniae outer membrane protein cross-react with the heavy chain of immunoglobulin in the wall of abdominal aortic aneurysms.

BACKGROUND: Chlamydia pneumoniae (Cp) has been demonstrated in arteries and abdominal aortic aneurysms (AAAs). However, the validity of the methods used is questioned, and antibiotic treatment trials have thus far shown disappointing results. Nevertheless, antibodies against the Cp outer membrane proteins (OMPs) have been associated with progression of atherosclerosis and AAAs. The aim of this study was to detect Cp OMPs in the wall of AAA patients by use of purified serum antibodies directed against Cp OMP and to assess potential cross-reacting proteins in AAA walls. METHODS AND RESULTS: Seventeen patients undergoing infrarenal AAA repair were studied. Full AAA thickness tissue was collected from the anterior wall of the aneurysm. Anti-OMP was extracted from seropositive AAA patients by use of an ELISA kit (Labsystems). Analysis was performed by use of 2D polyacrylamide gel electrophoresis, immunoblotting, and mass spectrometric protein identification. OMP antigens were not detected in 16 of 17 AAA walls. However, 3 major AAA proteins cross-reacted with anti-OMP. The proteins were all identified as heavy chains of human immunoglobulin. CONCLUSIONS: We could not find evidence of Cp OMP in 16 of 17 AAA walls, but instead, all samples showed a strong cross-reaction between Cp OMP antibodies and human immunoglobulin. This might indicate that AAA is an autoimmune disease, perhaps triggered by an initial Cp infection.

Markers of inflammation in relation to long-term cardiovascular mortality in patients with lower-extremity peripheral arterial disease.

BACKGROUND: Elevated levels of inflammatory mediators reflect vascular inflammation, and play a significant role in the genesis of atherosclerosis, plaque instability and rupture. METHODS AND MATERIAL: Plasma α-defensin and serum high sensitivity C reactive protein (hs-CRP) levels were examined in 463 patients with lower-extremity peripheral arterial disease (PAD). The relationships between inflammatory markers and lethal outcome were examined by Cox regression, and receiver operating characteristic (ROC) analysis. RESULTS: Overall, 126 patients died, hereof 59 of cardiovascular causes. The patients with chronic critical limb ischemia (CLI) at baseline had significantly higher α-defensin and hs-CRP levels compared with patients with intermittent claudication (IC). For patients with IC, the relative risk for cardiovascular mortality was three times higher in patients within the upper tertile of α-defensin concentration (>162 µg/l), when compared with those in the two lower tertiles (HR 3.04 95% CI 1.26-7.32). The multivariable model revealed that IC-patients with high α-defensin and high hs-CRP concentration had more than 5 times higher risk for cardiovascular mortality than those with either high α-defensin or high hs-CRP alone, and low α-defensin or low hs-CRP concentrations (HR 5.16, 95% CI 1.78-14.8). Area under the ROC curve for combined use of high values of α-defensin and hs-CRP was 0.71 (95% CI 0.57-0.85). The addition of α-defensin or hs-CRP to conventional risk factors significantly improved the accuracy of risk prediction model for cardiovascular mortality. No associations were found among α-defensin, hs-CRP, and lethal outcome for patients with CLI. CONCLUSIONS: Combined analysis of α-defensin and hs-CRP, adds prognostic information with regard to the long-term cardiovascular prognosis among patients with IC.

Higher cystatin C level predicts long-term mortality in patients with peripheral arterial disease.

AIMS: Cystatin C and cathepsins could play a role in different processes and stages of the atherosclerotic disease. We aimed to investigate the relationship of cystatin C, and cathepsins L, and S, to lethal outcome in patients with peripheral arterial disease (PAD). METHODS AND RESULTS: We studied 378 patients with established PAD. Cox regression was used to assess relationships between serum cystatin C or cathepsins L and S, and time to lethal outcome. The role of cystatin for prognosis of cardiovascular death was assessed with c-statistic, and net reclassification improvement (NRI). Patients with cystatin C levels above 1 mg/l (fifth quintile) had a significantly increased adjusted risk for all-cause and cardiovascular mortality compared to patients with cystatin C levels below or equal to 1 mg/l (hazard ratios (HR) 2.2, 95% CI 1.22-4.12, and HR 3.2, 95% CI 1.39-7.59, respectively). Furthermore, high cystatin C levels were related with higher all-cause (adjusted HR 2.99, 95% CI 1.31-6.85) and cardiovascular mortality (adjusted HR 4.36, 95% CI 1.07-18.8) among PAD patients without renal impairment. Although the addition of cystatin C to conventional risk factors improved the accuracy of risk prediction model for cardiovascular mortality (0.72-0.79; p=0.03), it did not reclassify a substantial proportion of patients to risk categories (NRI=0.12, p=0.128). CONCLUSIONS: Higher cystatin C levels independently predicted 5 years all-cause, and cardiovascular death in PAD patients. However, a small improvement in discrimination with the addition of cystatin C to conventional risk factors, and no improvement in reclassification of risk categories suggest that clinical usefulness of cystatin C for predicting cardiovascular mortality in PAD population might be modest.

Impact of soluble TWEAK and CD163/TWEAK ratio on long-term cardiovascular mortality in patients with peripheral arterial disease.

AIM: Soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) has recently been introduced as a potential mediator of cardiovascular disease. We examined the associations between sTWEAK, its scavenger receptor sCD163, sCD163/sTWEAK ratio and risk for long-term all-cause and cardiovascular mortality in patients with lower-extremity peripheral arterial disease (PAD). METHODS: sTWEAK and sCD163 serum levels were measured retrospectively in a cohort of 295 patients with symptomatic PAD followed for 6.1±2.1 years. The endpoints were defined as all-cause or cardiovascular death. The relationship between sTWEAK, sCD163 levels, sCD163/sTWEAK ratio, and times to fatal outcome was examined by Cox proportional hazards analysis. RESULTS: sTWEAK levels were significantly lower (672 (IQR 515; 872)pg/ml vs. 814 (IQR 673; 957)pg/ml, p < 0.0001), and sCD163/sTWEAK ratio significantly higher (0.91 (IQR 0.63; 1.37) vs. 0.77 (IQR 0.55; 1.12), p = 0.008) in patients with critical limb ischemia (CLI) on admission as compared with those with intermittent claudication (IC). During follow-up, 80 (27%) patients died, hereof 33 (11.5%) of cardiovascular causes. Cox regression analysis revealed that an increase of 100 pg/ml of baseline sTWEAK were associated with a decreased risk for all cause [adjusted hazard ratio (HR) 0.89 (95%CI (0.80-0.99)), p = 0.043] and cardiovascular mortality [adjusted HR 0.83 (95% CI (0.69-0.99)), p = 0.038]. The patients with lower sTWEAK concentrations had a higher risk for cardiovascular death being more than two times as great as patients in the two upper tertiles (adjusted HR 2.2, 95% CI (1.06-4.87), p = 0.035). Similarly, the risk of cardiovascular death was 3-fold increased for patients in the upper tertile of sCD163/sTWEAK ratio as comparing with the patients in two lower tertiles (adjusted HR 3.04, 95% CI (1.44-6.43), p = 0.004). The model including sCD163/sTWEAK ratio have shown a significant improvement in accuracy of cardiovascular death prediction (the area under ROC curve 0.79 (0.72-0.86) vs. 0.84 (0.78-0.90), p = 0.019). CONCLUSIONS: Decreased sTWEAK concentration, and increased sCD163/sTWEAK ratio were significantly and independently associated with long-term cardiovascular mortality in patients with lower-extremity PAD.

Proteins associated with the size and expansion rate of the abdominal aortic aneurysm wall as identified by proteomic analysis.

OBJECTIVES: Identification of biomarkers for the natural history of abdominal aortic aneurysms (AAA) holds the key to non-surgical intervention and improved selection for AAA repair. We aimed to associate the basic proteomic composition of AAA wall tissue with the expansion rate and size in patients with AAA. METHODS: A proteomic approach was used, consisting of two-dimensional polyacrylamide gel electrophoresis (2D-PAGE) and mass spectrometry (MS) to identify differentially expressed proteins in AAA tissue. Relevant protein spots were identified by liquid chromatography-tandem mass spectrometry (LC-MS/MS). RESULTS: Spearman's correlation analysis revealed 16 protein spots were strongly correlated with AAA expansion rate (ρ>±0.75). Nine protein spots were identified. Six protein spots showed correlation with AAA size (ρ>±0.5). Three protein spots were identified: vitronectin with traces of calreticulin, albumin and a spot containing two proteins: collagen α-3(VI) chain and vitamin D binding protein. Interestingly, in our previous study vitronectin was shown to be down-regulated in a ruptured AAA group compared with non-ruptured AAA. Western blot analysis in the present study confirmed a correlation of vitronectin bands with AAA size in aortic aneurysm tissue. CONCLUSION: A proteomic approach seems valuable, and identified several candidates not previously associated with AAA. Larger studies are required to confirm the potential and clinical role of the identified proteins.

Predictors of post-operative mortality following treatment for non-ruptured abdominal aortic aneurysm.

The aim of this prospective study of patients undergoing repair of non-ruptured abdominal aortic aneurysm between 1999 and 2003 was to evaluate and compare risk factors for mortality after surgery, to determine a complex of informative factors for lethal outcome, and to define patient risk groups. Logistic regression analysis revealed a complex of informative factors, including female gender, previous myocardial infarction, age greater than 75 years, and clinical course of abdominal aortic aneurysm as important indicators for lethal outcome. A risk score model identified low-, moderate- and high-risk groups with mortality rates of 2.9%, 8.0% and 44.4%, respectively.

[Ruptured abdominal aortic aneurysm]. / Pilvo aortos aneurizmos plysimas.

Rupture of the abdominal aortic aneurysm is a high lethal risk pathology, which requires precise diagnosis and urgent and efficient surgical treatment. Despite improved diagnostic capabilities (echoscopy, in specialized departments--angiography, computed tomography, magnetic nucleus resonance), mortality related to this pathology remains high in intensive care units. In the present article data concerning prevalence and clinical outcomes of the rupture of the abdominal aortic aneurysm for 1999-2001 is presented in detail. During this period 22 patients have undergone surgery due to abdominal aortic aneurysm rupture. Described are most prevalent complications, mortality rates and causes, analyzed are treatment strategy and tactics.