Background: The aim of this study is to determine the risk factors of delirium after cardiac surgery. Methods: A systematic literature search of MEDLINE, EMBASE, the Cochrane Library, and Science Citation Index limited to 2008 to 2011 and review of studies was conducted. Eligible studies were of randomized controlled trials or cohort studies, using delirium assessment tool, reporting at least one risk factor associated with delirium, and available to full text. Results: The search identified 106 potentially relevant publications; only 25 met selection criteria. Our systematic review revealed 33 risk factors: 17 predisposing and 16 precipitating factors for delirium after elective cardiac surgery. The most established predisposing risk factors were age, depression, and history of stroke, cognitive impairment, diabetes mellitus, and atrial fibrillation. The most established precipitating risk factors were duration of surgery, prolonged intubation, surgery type, red blood cell transfusion, elevation of inflammatory markers and plasma cortisol level, and postoperative complications. Moreover, sedation with dexmedetomidine may significantly predict the absence of postoperative delirium. Conclusions: Postoperative delirium is related to several risk factors following cardiac surgery. Sedation with dexmedetomidine and fast‐track weaning protocols may decrease the incidence of delirium in cardiac surgical patients. (J Card Surg 2012;27:481‐492)

Introduction: The aim of this study was to explore the use of dexmedetomidine as a safe and efficacious sedative agent in post-cardiac surgery patients. Methods: A systematic literature search of MEDLINE, EMBASE, the Cochrane Library and Science Citation Index until January 2012 and review of studies was conducted. Eligible studies were of randomized controlled trials or cohort studies, comparing dexmedetomidine with a placebo or an alternative sedative agent in elective cardiac surgery, using dexmedetomidine for postoperative sedation and available in full text. Two reviewers independently performed study selection, quality assessment, and data extraction. Results: The search identified 530 potentially relevant publications; 11 met selection criteria in this meta-analysis. Our results revealed that dexmedetomidine was associated with a shorter length of mechanical ventilation (mean difference -2.70 [-5.05, -0.35]), a lower risk of delirium (risk ratio 0.36 [0.21, 0.64]), ventricular tachycardia (risk ratio 0.27 [0.08, 0.97]) and hyperglycemia (risk ratio 0.78 [0.61, 0.99]), but may increase the risk of bradycardia (risk ratio 2.08 [1.16, 3.74]). But there was no significant difference in ICU stay, hospital stay, and morphine equivalents between the included studies. Dexmedetomidine may not increase the risk of hypotension, atrial fibrillation, postoperative nausea and vomiting, reintubation within 5 days, cardiovascular complications, postoperative infection or hospital mortality. Conclusions: Dexmedetomidine was associated with shorter length of mechanical ventilation and lower risk of delirium following cardiac surgery. Although the risk of bradycardia was significantly higher compared with traditional sedatives, it may not increase length of hospital stay and hospital mortality. Moreover, dexmedetomidine may decrease the risk of ventricular tachycardia and hyperglycemia. Thus, dexmedetomidine could be a safe and efficacious sedative agent in cardiac surgical patients.

Background. Although the neutrophil percentage‐to‐albumin ratio (NPAR) has proven to be a robust systemic inflammation‐based predictor of mortality in a wide range of diseases, the prognostic value of the NPAR in critically ill patients with cardiogenic shock (CS) remains unknown. This study aimed at investigating the association between the admission NPAR and clinical outcomes in CS patients using real‐world data. Methods. Critically ill patients diagnosed with CS in the Medical Information Mart for Intensive Care‐III (MIMIC‐III) database were included in our study. The study endpoints included all‐cause in‐hospital, 30‐day, and 365‐day mortality in CS patients. First, the NPAR was analyzed as a continuous variable using restricted cubic spline Cox regression models. Second, X‐tile analysis was used to calculate the optimal cut‐off values for the NPAR and divide the cohort into three NPAR groups. Moreover, multivariable Cox regression analyses were used to assess the association of the NPAR groups with mortality. Results. A total of 891 patients hospitalized with CS were enrolled in this study. A nonlinear relationship between the NPAR and in‐hospital and 30‐day mortality was observed (all P values for nonlinear trend<0.001). According to the optimal cut‐off values by X‐tile, NPARs were divided into three groups: group I (NPAR < 25.3), group II (25.3 ≤ NPAR < 34.8), and group III (34.8 ≤ NPAR). Multivariable Cox analysis showed that higher NPAR was independently associated with increased risk of in‐hospital mortality (group III vs. group I: hazard ratio [HR] 2.60, 95% confidence interval [CI] 1.72‐3.92, P < 0.001), 30‐day mortality (group III vs. group I: HR 2.42, 95% CI 1.65‐3.54, P < 0.001), and 365‐day mortality (group III vs. group I: HR 6.80, 95% CI 4.10‐11.26, P < 0.001) in patients with CS. Conclusions. Admission NPAR was independently associated with in‐hospital, 30‐day, and 365‐day mortality in critically ill patients with CS.

Background/Aims: Caffeic acid (CA) is known to possess multiple biological activities including anti-cancer activities. However, the molecular mechanisms underlying these activities in non-small-cell lung cancer (NSCLC) cells are not fully understood. We attempted to clarify whether CA could enhance paclitaxel (PTX)-induced cytotoxicity in H1299 cells. Methods: First, we tested the cytotoxic effects in both H1299 cells and normal human Bease-2b cells by cell proliferation experiments. Next, we use Annexin V/propidium iodide apoptosis analysis and flow cytometric analysis to investigate apoptosis and cell cycle arrest under the treatments mentioned above. To further pinpoint changes in apoptosis, we tested the caspase-associated apoptotic pathway, which involves the activities of caspase-3 and caspase-9. Moreover, apoptosis-related proteins and MAPK pathway proteins were examined by western blot. An H1299 xenograft nude mice model was used to further evaluate the tumor-suppressing effects of CA and PTX in vivo. Results: Combination treatment with low-dose CA and PTX decreased the proliferation of NSCLC H1299 cells but not normal Beas-2b cells. Flow cytometry showed that H1299 cells were arrested in the sub-G1 phase and apoptosis was significantly increased in H1299 cells after CA treatment. Caspase-3 and caspase-9 activities were both increased after CA treatment. Furthermore, CA increased the PTX-induced activation of Bax, Bid, and downstream cleaved PARP, and phosphorylation of extracellular signal regulated kinase1/2 and c-Jun NH2-terminal protein kinase1/2. An in vivo tumor-suppression assay demonstrated that CA and PTX combined treatment exerted a more effective suppressive effect on tumor growth in H1299 xenografts without causing significant adverse effects. Conclusions: Our results indicated that CA inhibited NSCLC H1299 cell growth by inducing apoptosis and CA and PTX combined produced a synergistic anti-cancer effect in H1299 cells.

BACKGROUND:Myxomas are the most common primary heart tumors and are closely associated with embolic events. Cardiac myxomas typically arise from the interatrial septum at the border of the fossa ovalis in the left atrium. Any other location is consid...

Background/Aims: This study aimed to evaluate whether galectin-3 (Gal-3) contributes actively to atrial fibrosis both in patients and experimental atrial fibrillation (AF) models. Methods: Mouse HL-1 cardiomyocytes were subjected to rapid electrical stimulation (RES) to explore Gal-3 expression and secretion levels by western blotting (WB) and enzyme linked immunosorbent assay (ELISA). Neonatal rat cardiac fibroblasts were treated with conditioned culture medium and recombinant human Gal-3 to evaluate the activation of the transforming growth factor (TGF)-β1/α-smooth muscle actin (SMA)/collagen I (Col I) profibrotic pathway (WB) and fibroblast proliferation with a Cell Counting Kit-8 (CCK-8). Furthermore, in the rapid atrial pacing (RAP) rabbit AF model, atrial Gal-3 expression and its effects on the profibrotic pathway were evaluated (WB and Masson’s trichrome staining). Moreover, 44 consecutive patients who underwent single mitral valve repair/replacement were included, consisting of 28 patients with persistent AF (PeAF) and 16 with sinus rhythm (SR). Coronary sinus blood was also sampled to test circulating Gal-3 levels (ELISA), and atrial myocardium Gal-3 and its downstream TGF-β1/α-SMA pathway were also measured by WB and immunohistochemical staining. Results: Gal-3 expression in HL-1 cells and its secretion level in culture medium were greatly increased after 24 h RES. Treatment of neonatal rat cardiac fibroblasts with conditioned media collected from the RES group or recombinant human Gal-3 protein (10 and 30 µg/mL) for 72 h induced the activation of the TGF-β1/α-SMA/Col I profibrotic pathway. RAP increased Gal-3 levels and activated the TGF-β1/α-SMA/Col I pathway in rabbit left atria, while the Gal-3 inhibitor N-acetyllactosamine, injected at 4.5 mg/kg every 3 days, mitigated these adverse changes. Furthermore, Gal-3 levels in coronary sinus blood samples and myocardial Gal-3 expression levels were higher in the PeAF patients than in the SR patients, and higher level profibrotic pathway activation was also confirmed. Conclusions: Activation of Gal-3 expression in the atria can subsequently activate the TGF-β1/α-SMA/Col I pathway in cardiac fibroblasts, which may enhance atrial fibrosis.