首页 | 本学科首页   官方微博 | 高级检索  
文章检索
  按 检索   检索词:      
出版年份:   被引次数:   他引次数: 提示:输入*表示无穷大
  收费全文   5篇
  免费   0篇
内科学   1篇
外科学   4篇
  2019年   3篇
  2018年   1篇
  2013年   1篇
排序方式: 共有5条查询结果,搜索用时 15 毫秒
1
1.
2.

Objective

Anemia is associated with increased cardiac adverse events during the early postoperative period because of high physiologic stress and increased cardiac demand. The aim of this study was to assess the surgical outcomes and prognostic implications of anemia in patients undergoing repair of intact abdominal aortic aneurysms (AAAs).

Methods

A retrospective analysis of all patients who underwent open aortic repair (OAR) or endovascular aneurysm repair (EVAR) in the Vascular Quality Initiative database (2008-2017) was performed. Patients with preoperative polycythemia, patients with ruptured aneurysms, and patients transfused with >4 units of packed red blood cells were excluded. Hemoglobin levels were categorized into three groups: moderate-severe anemia (<10 g/dL), mild anemia (10-12 g/dL in women and 10-13 g/dL in men), and no anemia (>12 g/dL in women and >13 g/dL in men). Multivariate logistic models and coarsened exact matching were used to analyze the association between anemia and 30-day mortality and between anemia and major in-hospital complications after OAR and EVAR.

Results

A total of 34,397 patients were identified undergoing AAA repair. Of those, 28.5% had mild anemia and 4.3% had moderate-severe anemia. In both OAR (n = 6112) and EVAR (n = 28,285), patients with moderate-severe anemia had significantly higher rates of in-hospital adverse events, such as in-hospital mortality, myocardial infarction, renal and respiratory complications, and reoperation, compared with patients with mild or no anemia. They also had higher rates of 30-day mortality. After multivariate analysis and 1:1 coarsened exact matching, no association was found between anemia and 30-day mortality and other in-hospital outcomes in patients undergoing OAR. On the other hand, in EVAR, moderate-severe anemia was associated with 2.7 times the odds of 30-day mortality (odds ratio [OR], 2.65; 95% confidence interval [CI], 1.69-4.18), 2.5 times the odds of renal complications (OR, 2.47; 95% CI, 1.78-3.43; P < .05), and twice the risk of acute congestive heart failure (OR, 1.96; 95% CI, 1.18-3.25) and respiratory complications (OR, 2.01; 95% CI, 1.26-3.19). Mild anemia was also associated with increased odds of 30-day mortality and renal and respiratory complications in patients undergoing EVAR. Interestingly, preoperative blood transfusion in mildly anemic patients undergoing EVAR was associated with double the odds of in-hospital major adverse cardiac events (stroke, death, and myocardial infarction; OR, 2.1; 95% CI, 1.38-3.11; P < .001).

Conclusions

Preoperative anemia is associated with higher odds of 30-day mortality and in-hospital adverse outcomes after EVAR but not after OAR. These findings highlight the need to incorporate anemia into the preoperative risk assessment of patients undergoing EVAR. Future studies are needed to assess the efficacy of medical therapies in improving postoperative outcomes in anemic patients undergoing AAA repair.  相似文献   
3.

Objective

The benefit of statins has been well established in reducing morbidities and mortality after carotid endarterectomy. However, the potential advantage of statin use in patients undergoing carotid artery stenting (CAS) remains largely unknown. The purpose of this study was to evaluate the effect of statins on postoperative outcomes after CAS.

Methods

The Premier Healthcare Database was retrospectively analyzed to identify all patients who underwent CAS from 2009 to 2015. Univariate (χ2 test, t-test) and multivariate models (logistic regression) were used to evaluate the effect of statins on postoperative outcomes.

Results

A total of 17,800 patients underwent CAS during the study period; 12,416 (70%) patients were taking statins. The statin group had more symptomatic patients (41% vs 31%; P < .001) and had significantly higher comorbidities including hypertension, diabetes, coronary artery disease, dyslipidemia, history of congestive heart failure, history of stroke, history of myocardial infarction (MI), and peripheral artery disease (all P < .05). Postoperative mortality was 1.0% vs 1.8% in the statin and nonstatin groups, respectively (P < .001). Statin use had no effect on odds of postoperative stroke (odds ratio [OR], 1.09; 95% confidence interval [CI], 0.88-1.34; P = .44) and higher odds of MI (OR, 2.08; 95% CI, 1.26-3.45; P = .004). After adjustment for potential confounders, statins were associated with 64% reduction in the odds of death (OR, 0.36; 95% CI, 0.27-0.47; P < .001) and 18% reduction in stroke/death (OR, 0.82; 95% CI, 0.68-0.99; P = .03). In patients who had a stroke or MI, statin users had significantly lower failure to rescue (lower mortality) compared with nonstatin users (11.4% vs 30.8%; P < .001).

Conclusions

Statin use is associated with significant reduction in mortality and failure to rescue in patients who develop major complications (stroke/MI) after CAS. Therefore, statin use should be strongly encouraged in all patients undergoing CAS.  相似文献   
4.
Phosphoinositide 3-kinase gamma (PI3Kγ) has profound roles downstream of G-protein–coupled receptors in inflammation, cardiac function, and tumor progression. To gain insight into how the enzyme’s activity is shaped by association with its p101 adaptor subunit, lipid membranes, and Gβγ heterodimers, we mapped these regulatory interactions using hydrogen–deuterium exchange mass spectrometry. We identify residues in both the p110γ and p101 subunits that contribute critical interactions with Gβγ heterodimers, leading to PI3Kγ activation. Mutating Gβγ-interaction sites of either p110γ or p101 ablates G-protein–coupled receptor-mediated signaling to p110γ/p101 in cells and severely affects chemotaxis and cell transformation induced by PI3Kγ overexpression. Hydrogen–deuterium exchange mass spectrometry shows that association with the p101 regulatory subunit causes substantial protection of the RBD-C2 linker as well as the helical domain of p110γ. Lipid interaction massively exposes that same helical site, which is then stabilized by Gβγ. Membrane-elicited conformational change of the helical domain could help prepare the enzyme for Gβγ binding. Our studies and others identify the helical domain of the class I PI3Ks as a hub for diverse regulatory interactions that include the p101, p87 (also known as p84), and p85 adaptor subunits; Rab5 and Gβγ heterodimers; and the β-adrenergic receptor kinase.The phosphoinositide 3-kinase γ (PI3Kγ) has far-reaching roles in the processes of mammalian biology, including inflammation, cell migration, cardiac function, response to pathogens, wound healing, olfaction, nociception, and tumor progression. Activation of p110γ produces the lipid second messenger phosphatidylinositol (3,4,5)-trisphosphate (PIP3), which in turn recruits downstream effectors, such as protein kinase B that bears PIP3-recognizing PH domains.PI3Kγ plays a critical role in inflammation, with mice lacking the Pik3cg gene for p110γ having reduced inflammatory responses (13), increased protection from anaphylaxis (4), and protection from sepsis (5). Aberrant activation of the PI3K pathway is one of the most common events in cancer (6). Overexpression of p110γ induces cell transformation (7). Pharmacological inhibition of p110γ can prevent tumor growth and spreading by blocking myeloid-derived tumor inflammation and by suppressing breast cancer cell invasion (810). Depletion of p110γ or its regulatory subunit p101 inhibited primary tumor formation and metastasis by murine epithelial carcinoma cells (11). In pancreatic cancer, it has been proposed that p110γ is an important component of disease progression (12). PI3Kγ (together with PI3Kδ) is strictly required for development and maintenance of T-cell lymphoblastic leukemia that is driven by PTEN loss (13). Recently, it was also shown that PI3Kγ plays an essential role in formation of sarcomas induced by a viral GPCR (vGPCR) encoded by Kaposi’s sarcoma herpes virus and that p110γ-deficient mice were completely resistant to vGPCR-induced sarcomagenesis (14). PI3Kγ also has major functions in the heart, where it regulates cardiac contractility downstream of the β-adrenergic receptor (βAR) (15). In addition to its function as a lipid kinase, p110γ also plays a scaffolding/kinase-independent role in the heart (1619). These results have established PI3Kγ as a target for the treatment of inflammation and cardiac diseases.The PI3Kγ functions depend on direct, transient associations with various regulators, such as Gβγ heterodimers (Gβγ), Ras, βAR kinase, PKA, and PP2A. Central to its many roles is the activation of PI3Kγ downstream of G-protein–coupled receptors (GPCRs) via direct binding to Gβγ. Although p110γ was among the first PI3Ks cloned, the mechanisms of p110γ’s regulation by Gβγ heterodimers and by its regulatory subunits are still not clear. In contrast to other class I PI3Ks, p110γ uniquely associates with a p101 or a p87 (also called p84) regulatory subunit (2023). PI3Kγ shares with the class IA PI3K p110β the ability to be directly activated by Gβγ heterodimers (2426). The p110γ catalytic subunit on its own can be activated only to a limited extent by Gβγ heterodimers, whereas maximal activation requires association with the p101 subunit and with Ras (21, 25, 27, 28). In cells, p101 is required for membrane translocation and activation of p110γ in response to ligand-induced G-protein activation (28). However, a p110γ that is constitutively localized to the plasma membrane is still sensitive to G-protein activation (28, 29).In an effort to understand the molecular basis of PI3Kγ activation, we have investigated the structural determinants of the p110γ/p101 interaction with Gβγ heterodimers on membranes. Although there is a crystal structure of p110γ (30), no structural information or even domain organization for the p101 regulatory subunit is known, and similarly, there is no structural information about PI3Kγ interaction with membranes. Hydrogen–deuterium exchange mass spectrometry (HDX-MS) is a useful tool for analyzing interactions of proteins with membranes (31), and it has been important for understanding how PI3K complexes become activated on lipid membranes (24). The method also provides insight into protein dynamics that is difficult or impossible to obtain with other tools (3235). Using HDX-MS, we have determined the interactions and conformational changes in p110γ that accompany binding to p101, to membranes, and to Gβγ. Our studies show that the helical domain of p110γ is a critical element in the regulation of p110γ activity. We also identified mutations in p110γ and p101 that specifically affect PI3Kγ activation downstream of GPCRs and impair its cellular functions.  相似文献   
5.
BackgroundSeveral randomized clinical trials have shown that carotid artery endarterectomy (CEA) is safer than carotid artery stenting (CAS) in the elderly. However, those studies were limited by their strict inclusion criteria that might make their findings inapplicable to real-world practice. Therefore, the aim of this study was to evaluate the association of age with the efficacy of CEA and CAS in a population-based registry.MethodsThe Vascular Quality Initiative database was inquired (2005-2017). The primary outcome was 30-day and 2-year stroke and a combined outcome of stroke/death. Logistic regression models with age-by-treatment interaction term were fitted adjusting for patients' characteristics. Restricted cubic spline modelling was also implemented. Two-year events were assessed via survival analysis methods.ResultsOverall, 89,853 patients were included, 26.9% were less than 65 years of age, 39.1% were 65 to 74 years of age, and 34.1% were 75 years of age or older. The CAS-to-CEA odds of 30-day stroke became significant at age 56.5 and doubled at age 72.5 years. After CEA, the risk of stroke rose by 1.3-fold when age increased from 76 to 85 (odds ratio [OR], 1.30; 95% confidence interval [CI], 1.05-1.62). Yet after CAS, when age increased from 65 to 71 years, the OR of stroke was 1.36 (95% CI, 1.04-1.76); from 71 to 76 years, the OR was 1.47 (95% CI, 1.10-1.96), and from 76 to 85 years the OR was 1.38 (95% CI, 1.06-1.81). The superiority of CEA with increasing age extended to 2 years after the procedure. The CAS-to-CEA 2-year hazard of stroke was significant at age 53 and it doubled at 71.5 years.ConclusionsIn this multicenter registry, we confirmed the effect modification role that age plays in the safety and efficacy of carotid revascularizations. The risk-adjusted effectiveness of CAS was particularly sensitive to patient age, whereas CEA performance was relatively stable across various age strata. Of note, the observed effect was more pronounced and a decade earlier than what previously reported in the ideal setting of a randomized clinical trial.  相似文献   
1
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号