Proteinase­3­antineutrophil cytoplasmic antibody­associated vasculitis secondary to subacute infective endocarditis: A case report.

A 58-year-old male patient was admitted to Peking University First Hospital (Beijing, China) due to recurrent hematuria, proteinuria and kidney dysfunction. The patient was positive for proteinase-3 (PR3)-antineutrophil cytoplasmic antibody (ANCA). Pathology of the kidney showed focal proliferative necrotizing glomerulonephritis with crescent formation and immune complex-mediated glomerulonephritis. The patient was diagnosed with PR3-ANCA-associated vasculitis (AAV), received intensive immunosuppressive therapy and experienced two relapses within 1 year. After admission, aortic valve vegetation was observed via echocardiography. The patient subsequently received antibiotic treatment and valve replacement, and achieved complete remission of kidney and cardiac function. The present case emphasized the importance of identifying secondary reasons for ANCA formation, especially infective endocarditis in patients with PR3-AAV.

Clinical outcomes after coronary artery bypass grafting in patients with dialysis-dependent end-stage renal disease and an analysis of the related influencing factors.

Perioperative and short/mid-term survival rates of dialysis-dependent patients with end-stage renal disease (ESRD), who undergo coronary artery bypass grafting (CABG), and the factors influencing mortality are not well evaluated In China. We retrospectively analyzed the perioperative and postoperative 1-, 3-, and 5-year survival rates of 53 dialysis-dependent ESRD patients who underwent CABG, and compared the factors related to perioperative mortality and all-cause mortality during the postoperative follow-up. Survival rates were expressed as Kaplan-Meier survival curves, and factors influencing the follow-up survival rates were analyzed using the log rank (Mantel-Cox) test. There were eight perioperative deaths, resulting in 15.1% mortality. Intraoperative intra-aortic balloon pump use (P = 0.01), advanced age (P = 0.0027), and high EuroSCORE II score (P = 0.047) were associated with increased perioperative mortality. Forty-five discharged patients were followed from 2 months to 10 years (median, 4.2 years) postoperatively. There were 19 all-cause deaths, including 10 cardiac deaths (10/19, 52.6%). Comparisons between groups indicated that the presence of peripheral artery disease (PAD) increased mortality during follow-up (P = 0.025); 1-, 3-, and 5-year survival rates were 93.3, 79.5, and 66.8%, respectively. The results of the long-rank analysis indicated that the presence of PAD was a risk factor for postoperative survival (log rank χ2 = 4.543; P = 0.033). Dialysis-dependent patients with ESRD had high perioperative mortality and unsatisfactory short- and medium-term survival after CABG. PAD was a risk factor affecting patients' postoperative survival. Multidisciplinary teamwork is needed to enhance postoperative management and reduce complications, to improve postoperative survival in these patients.

Mutational analysis on stable expression and LasB inhibition of LasB propeptide in Pseudomonas aeruginosa.

Three major proteases, elastase B (LasB), protease IV (PIV), and elastase A (LasA) expressed in Pseudomonas aeruginosa play important roles in infections and pathogeneses. These are activated by a proteolytic cascade initiated by the activation of LasB. In this study, we investigated whether LasB could be inhibited using its propeptide (LasBpp). Although LasA and PIV were inhibited by their propeptides, LasB was not inhibited by purified LasBpp because LasB degraded LasBpp. To address this problem, mutant LasBpp variants were constructed to obtain a mutant LasBpp resistant to LasB degradation. A C-terminal deletion series of LasBpp was tested in vivo, and two positive candidates, T2 and T2-1, were selected. However, both caused growth retardation and were unstably expressed in vivo. Since deleting the C-terminal end of LasBpp significantly affected its stable expression, substitution mutations were introduced at the two amino acids near the truncation site of T2-1. The resulting mutants, LasBppE172D, LasBppG173A, and LasBppE172DG173A, significantly diminished LasB activity when overexpressed in vivo and were stably expressed in MW1, a quorum sensing mutant that does not produce LasB. In vitro analysis showed that purified LasBppE172DG173A inhibited LasB activity to a small extent. Summarizing, C-terminal modification of LasBpp profoundly affected the stable expression of LasBpp, and little enhanced the ability of LasBpp to resist degradation by LasB.

Anthranilate Acts as a Signal to Modulate Biofilm Formation, Virulence, and Antibiotic Tolerance of Pseudomonas aeruginosa and Surrounding Bacteria.

Anthranilate is a diffusible molecule produced by Pseudomonas aeruginosa and accumulates as P. aeruginosa grows. Anthranilate is an important intermediate for the synthesis of tryptophan and the Pseudomonas quinolone signal (PQS), as well as metabolized by the anthranilate dioxygenase complex (antABC operon products). Here we demonstrate that anthranilate is a key factor that modulates the pathogenicity-related phenotypes of P. aeruginosa and other surrounding bacteria in the environment, such as biofilm formation, antibiotic tolerance, and virulence. We found that the anthranilate levels in P. aeruginosa cultures rapidly increased in the stationary phase and then decreased again, forming an anthranilate peak. Biofilm formation, antibiotic susceptibility, and virulence of P. aeruginosa were significantly altered before and after this anthranilate peak. In addition, these phenotypes were all modified by the mutation of antABC and exogenous addition of anthranilate. Anthranilate also increased the antibiotic susceptibility of other species of bacteria, such as Escherichia coli, Salmonella enterica, Bacillus subtilis, and Staphylococcus aureus. Before the anthranilate peak, the low intracellular anthranilate level was maintained through degradation from the antABC function, in which induction of antABC was also limited to a small extent. The premature degradation of anthranilate, due to its high levels, and antABC expression early in the growth phase, appears to be toxic to the cells. From these results, we propose that by generating an anthranilate peak as a signal, P. aeruginosa may induce some sort of physiological change in surrounding cells. IMPORTANCE Pseudomonas aeruginosa is a notorious pathogen with high antibiotic resistance, strong virulence, and ability to cause biofilm-mediated chronic infection. We found that these characteristics change profoundly before and after the time when anthranilate is produced as an "anthranilate peak". This peak acts as a signal that induces physiological changes in surrounding cells, decreasing their antibiotic tolerance and biofilm formation. This study is important in that it provides a new insight into how microbial signaling substances can induce changes in the pathogenicity-related phenotypes of cells in the environment. In addition, this study shows that anthranilate can be used as an adjuvant to antibiotics.

Alleviation of Pseudomonas aeruginosa Infection by Propeptide-Mediated Inhibition of Protease IV.

Pseudomonas aeruginosa, an opportunistic human pathogen, expresses protease IV (PIV) for infection. Since the PIV activity can be inhibited by its propeptide, we tried to alleviate the severity of P. aeruginosa infection using the purified PIV propeptide (PIVpp). The PIVpp treatment of P. aeruginosa could significantly inhibit the PIV activity and reduce the virulence of P. aeruginosa in multiple invertebrate infection models, such as nematodes, brine shrimp, and mealworms. The effectiveness of PIVpp was further confirmed using mouse skin infection and acute/chronic lung infection models. The amount of PIVpp that inhibited the PIV activity of P. aeruginosa by 65% could alleviate the severity of infection significantly in all of the skin and acute/chronic lung infections. In addition, the PIVpp treatment of P. aeruginosa facilitated the healing of the skin wound infections and repressed the growth of P. aeruginosa in the infected lung. The PIVpp itself did not cause the induction of inflammatory cytokines or have any harmful effects on host tissues and did not affect bacterial growth. Taken together, P. aeruginosa infections can be alleviated by PIVpp treatment. IMPORTANCE Pseudomonas aeruginosa is a highly antibiotic-resistant pathogen and is extremely difficult to treat. Instead of using conventional antibiotics, we attempted to alleviate P. aeruginosa infection using factors that P. aeruginosa itself produces naturally. Extracellular proteases are powerful virulence factors and important targets to control the P. aeruginosa infections. Propeptides are originally expressed as part of extracellular proteases, inhibiting their activity until they go out of the cell, preventing them from becoming toxic to the cells themselves. We confirmed, from multiple animal experiments, that treating P. aeruginosa with the purified propeptide can alleviate its infectivity. Propeptides specifically inhibit only their cognate protease without inhibiting other essential proteases of the host. The development of resistance can be avoided because the propeptide-mediated inhibition is an inherent mechanism of P. aeruginosa; hence, it will be difficult for P. aeruginosa to alter this mechanism. Since propeptides do not affect bacterial growth, there is no selective pressure to develop resistant cells.

Highly Transparent, Robust Hydrophobic, and Amphiphilic Organic-Inorganic Hybrid Coatings for Antifogging and Antibacterial Applications.

The control of surface wettability through a combination of surface roughness, chemical composition, and structural modification has attracted significant attention for antifogging and antibacterial applications. Herein, a two-step spin-coating method for amphiphilic organic-inorganic hybrid materials with incorporated transition metal ions is presented. The coating solution was prepared via photochemical thiol-ene click reaction between the mercapto functional group in trimethylolpropane tris(3-mercaptopropionate) and the vinyl functionalized silica precursor 3-(trimethoxysilyl)propyl methacrylate. In the first step of coating, a glass substrate was coated using a solution of metal nitrate hydrates and subsequently showed hydrophobic properties. As the second step, the spin-coated glass substrate was further coated with silica nanoparticles (SiO2 NPs) and polycaprolactone triol (PCT) suspension, where the contents of SiO2 NPs were fixed at 0.1 wt %, unless otherwise noted. The coated substrate exhibited hydrophilic properties. For comparison, the coating was also formulated with the SiO2 NPs/PCT suspension without SiO2 NPs and with 0.5 wt % SiO2 NPs as well as by adjusting different coating layer thicknesses. The surface morphology and chemical compositions of the obtained coating materials were analyzed by field emission scanning electron microscopy with energy-dispersive X-ray spectroscopy and X-ray photoelectron spectroscopy. The transparency and static contact angle of coated samples were measured by UV-visible spectrophotometry and drop shape analysis, respectively. It was concluded that our novel hybrid coating materials exhibited excellent antibacterial and antifogging properties with extremely high scratch resistance and transparency.

Thermoregulation of Pseudomonas aeruginosa Biofilm Formation.

We investigated the effect of temperature on the biofilm formation of Pseudomonas aeruginosa and revealed that the biofilm formation increased rapidly at temperatures lower than 25°C. P. aeruginosa formed the most robust biofilm of a conspicuous mushroom-like structure at 20°C. However, when the temperature increased to 25°C, the biofilm formation rapidly decreased. Above 25°C, as the temperature rose, the biofilm formation increased again little by little despite its less-structured form, indicating that 25°C is the low point of biofilm formation. The intracellular 3',5'-cyclic diguanylate (c-di-GMP) levels also decreased rapidly as the temperature rose from 20 to 25°C. The expression levels of pelA, algD, and pslA encoding Pel, alginate, and Psl, respectively, were also dramatically affected by temperature, with pelA being regulated in a pattern similar to that of the intracellular c-di-GMP levels, and the pattern seen for algD regulation was the most similar to the actual biofilm formation pattern. Total exopolysaccharide production was thermoregulated and followed the regulation pattern of c-di-GMP. Interestingly, the thermoregulation patterns in biofilm formation were different depending on the strain of P. aeruginosa Unlike PAO1, another strain, PA14, showed a gradual decrease in biofilm formation and c-di-GMP in the range of 20 to 37°C, and P. aeruginosa clinical isolates also showed slightly different patterns in biofilm formation in conjunction with temperature change, suggesting that different strains may sense different temperature ranges for biofilm formation. However, it is obvious that P. aeruginosa forms more biofilms at lower temperatures and that temperature is an important factor in determining the biofilm formation.IMPORTANCE Biofilm formation is an important protection mechanism used by most microorganisms and provides cells with many advantages, like high infectivity, antibiotic resistance, and strong survivability. Since most persistent bacterial infections are believed to be associated with biofilms, biofilm control is an important issue in medicine, environmental engineering, and industry. Biofilm formation is influenced by various environmental factors. Temperature is the most direct environmental cue encountered by microorganisms. Here, we investigated the effect of temperature on the biofilm formation of P. aeruginosa, a notorious pathogen, and found that temperature is an important factor determining the amount and structure of biofilms. Low temperatures greatly increase biofilm formation and give biofilms a highly conspicuous structure. Although thermoregulation of biofilm formation is mainly mediated by c-di-GMP, some c-di-GMP-independent regulations were also observed. This study shows how biofilms are formed at various temperatures and provides new insights to control biofilms using temperature.

Quorum sensing-dependent post-secretional activation of extracellular proteases in Pseudomonas aeruginosa.

Pseudomonas aeruginosa secretes multiple proteases that are implicated in its pathogenesis, and most of them are regulated by quorum sensing (QS). In this study, we found that the activities of three major extracellular proteases, protease IV (PIV), elastase A (LasA), and elastase B (LasB), are reduced considerably when expressed in a QS mutant (MW1). PIV and LasA expressed in MW1 exhibited little activity, even when purified, and their activities were inhibited by noncleavage or binding of their propeptides. LasB was activated by a QS-dependent factor, indicating that, unlike what has been proposed previously, LasB is not autoactivated. When LasB was relieved from inhibition, it activated PIV, which then sequentially processed pro-LasA to mature LasA. When activated, LasB was not inhibited by exogenous addition of its propeptide, but LasA and PIV were inhibited by their propeptides, even after prior activation. These differences may be explained by the fact that LasB can degrade its own propeptide but PIV and LasA cannot. We also found that, although PIV is the preferred LasA-activating factor, LasB can also partially activate LasA. Overall, LasB, PIV, and LasA were activated postsecretionally in a cascading manner in which the initial activation of LasB was controlled tightly by QS at the protein level in addition to the well-known transcriptional control of these proteases by QS. Interestingly, human elastase also activated LasA, indicating that the activation cascade is triggered by host factors during infection. In summary, a QS-induced proteolytic cascade activates secreted proteases from P. aeruginosa.

Antibiofilm effect of biofilm-dispersing agents on clinical isolates of Pseudomonas aeruginosa with various biofilm structures.

Pseudomonas aeruginosa, an opportunistic human pathogen, causes many biofilm-mediated chronic infections. In this study, biofilm structures of various clinical strains of P. aeruginosa isolated from hospitalized patients were examined and their influence on the biofilm-dispersing effects of chemicals was investigated. The clinical isolates formed structurally distinct biofilms that could be classified into three different groups: 1) mushroom-like, 2) thin flat, and 3) thick flat structures. A dispersion of these differently structured biofilms was induced using two biofilm-dispersing agents, anthranilate and sodium nitroprusside (SNP). Although both SNP and anthranilate could disperse all types of biofilms, the thick flat biofilms were dispersed less efficiently than the biofilms of other structures. This suggests that biofilm-dispersing agents have higher potency on the biofilms of porous structures than on densely packed biofilms.

Bacterial ornithine lipid, a surrogate membrane lipid under phosphate-limiting conditions, plays important roles in bacterial persistence and interaction with host.

Ornithine lipids (OLs) are bacteria-specific lipids that are found in the outer membrane of Gram (-) bacteria and increase as surrogates of phospholipids under phosphate-limited environmental conditions. We investigated the effects of OL increase in bacterial membranes on pathogen virulence and the host immune response. In Pseudomonas aeruginosa, we increased OL levels in membranes by overexpressing the OL-synthesizing operon (olsBA). These increases changed the bacterial surface charge and hydrophobicity, which reduced bacterial susceptibility to antibiotics and antimicrobial peptides (AMPs), interfered with the binding of macrophages to bacterial cells and enhanced bacterial biofilm formation. When grown under low phosphate conditions, P. aeruginosa became more persistent in the treatment of antibiotics and AMPs in an olsBA-dependent manner. While OLs increased persistence, they attenuated P. aeruginosa virulence; in host cells, they reduced the production of inflammatory factors (iNOS, COX-2, PGE2 and nitric oxide) and increased intracellular Ca2+ release. Exogenously added OL had similar effects on P. aeruginosa and host cells. Our results suggest that bacterial OL plays important roles in bacteria-host interaction in a way that enhances bacterial persistence and develops chronic adaptation to infection.

Antibiofilm agents: A new perspective for antimicrobial strategy.

Biofilms are complex microbial architectures that attach to surfaces and encase microorganisms in a matrix composed of self-produced hydrated extracellular polymeric substances (EPSs). In biofilms, microorganisms become much more resistant to antimicrobial treatments, harsh environmental conditions, and host immunity. Biofilm formation by microbial pathogens greatly enhances survival in hosts and causes chronic infections that result in persistent inflammation and tissue damages. Currently, it is believed over 80% of chronic infectious diseases are mediated by biofilms, and it is known that conventional antibiotic medications are inadequate at eradicating these biofilm-mediated infections. This situation demands new strategies for biofilm-associated infections, and currently, researchers focus on the development of antibiofilm agents that are specific to biofilms, but are nontoxic, because it is believed that this prevents the development of drug resistance. Here, we review the most promising antibiofilm agents undergoing intensive research and development.

Anti-biofilm effects of anthranilate on a broad range of bacteria.

Anthranilate, one of tryptophan degradation products has been reported to interfere with biofilm formation by Pseudomonas aeruginosa. Here, we investigated the effects of anthranilate on biofilm formation by various bacteria and the mechanisms responsible. Anthranilate commonly inhibited biofilm formation by P. aeruginosa, Vibrio vulnificus, Bacillus subtilis, Salmonella enterica serovar Typhimurium, and Staphylococcus aureus, and disrupted biofilms preformed by these bacteria. Because anthranilate reduced intracellular c-di-GMP and enhanced swimming and swarming motilities in P. aeruginosa, V. vulnificus, B. subtilis, and S. enterica, it is likely that anthranilate disrupts biofilms by inducing the dispersion of these bacteria. On the other hand, in S. aureus, a non-flagellate bacterium that has no c-di-GMP signaling, anthranilate probably inhibits biofilm formation by reducing slime production. These results suggest that anthranilate has multiple ways for biofilm inhibition. Furthermore, because of its good biofilm inhibitory effects and lack of cytotoxicity to human cells even at high concentration, anthranilate appears to be a promising agent for inhibiting biofilm formation by a broad range of bacteria.

Post-secretional activation of Protease IV by quorum sensing in Pseudomonas aeruginosa.

Protease IV (PIV), a key virulence factor of Pseudomonas aeruginosa is a secreted lysyl-endopeptidase whose expression is induced by quorum sensing (QS). We found that PIV expressed in QS mutant has severe reduction of activity in culture supernatant (CS), even though it is overexpressed to high level. PIV purified from the QS mutant (M-PIV) had much lower activity than the PIV purified from wild type (P-PIV). We found that the propeptide cleaved from prepro-PIV was co-purified with M-PIV, but never with P-PIV. Since the activity of M-PIV was restored by adding the CS of QS-positive and PIV-deficient strain, we hypothesized that the propeptide binds to and inhibits PIV, and is degraded to activate PIV by a QS-dependent factor. In fact, the CS of the QS-positive and PIV-deficient strain was able to degrade the propeptide. Since the responsible factor should be a QS-dependently expressed extracellular protease, we tested QS-dependent proteases of P. aeruginosa and found that LasB (elastase) can degrade the propeptide and activate M-PIV. We purified the propeptide of PIV and confirmed that the propeptide can bind to and inhibit PIV. We suggest that PIV is post-secretionally activated through the extracellular degradation of the propeptide by LasB, a QS-dependent protease.

Simultaneous surgery in patients with both cardiac and noncardiac diseases.

BACKGROUND: To investigate the possibility and feasibility of simultaneous cardiac and noncardiac surgery. METHODS: From August 2000 to March 2015, 64 patients suffering from cardiac and noncardiac diseases have been treated by simultaneous surgeries. RESULTS: Two patients died after operations in hospital; thus, the hospital mortality rate was 3.1%. One patient with coronary heart disease, acute myocardial infarction, and a recurrence of bladder cancer accepted emergency simultaneous coronary artery bypass grafting (CABG), bladder cystectomy, and ureterostomy. He died of acute cerebral infarction complicated with multiple organ failure on the 153rd day after operation. The other patient with chronic constrictive pericarditis and right lung cancer underwent pericardial stripping and right lung lower lobectomy, which resulted in multiple organ failure, and the patient died on the tenth day postoperatively. The remaining 62 patients recovered and were discharged. The total operative morbidity was 17.2%: postoperative hemorrhage (n, % [1, 1.6%]), pulmonary infection and hypoxemia (2, 3.1%), hemorrhage of upper digestive tract (1, 1.6%), incisional infection (3, 4.7%), subphrenic abscess (1, 1.6%), and postoperative acute renal failure and hemofiltration (3, 4.7%). Of the 62 patients discharged, 61 patients were followed up. Eleven patients died with 10 months to 10 years during the follow-up. The mean survival time is 116.2±12.4 months. The cumulative survival rate is 50.8%. CONCLUSION: Simultaneous surgeries in patients suffering from both cardiac and noncardiac benign or malignant diseases are safe and possible with satisfactory short-term and long-term survival.

Bacterial virulence analysis using brine shrimp as an infection model in relation to the importance of quorum sensing and proteases.

Brine shrimp are aquatic crustaceans belonging to a genus of Artemia. This organism is widely used for testing the toxicity of chemicals. In this study, brine shrimp were evaluated as an infection model organism to study bacterial virulence. Artemia nauplii were infected with various pathogenic bacteria, such as Vibrio vulnificus, Pseudomonas aeruginosa, Burkholderia vietnamiensis, Staphylococcus aureus, and Escherichia coli, and the susceptibility to these bacteria was investigated by counting the survival of the infected nauplii. While all of the tested bacteria have significant virulence to brine shrimp, killing the nauplii in a few days, V. vulnificus showed the strongest virulence. P. aeruginosa also showed a dose-dependent virulence to brine shrimp, but the virulence was weaker than that of V. vulnificus. The virulence tests using the virulence-attenuated mutants of V. vulnificus and P. aeruginosa, such as quorum sensing (QS) mutants or protease-deficient mutants showed a significant attenuation of virulence, demonstrating that the QS mechanism is important in the virulence of these bacteria to brine shrimp. B. vietnamiensis, S. aureus, and E. coli were also virulent to brine shrimp and the virulence was correlated with dosage within 24 h under our conditions. Salmonella enterica Typhimurium and Bacillus subtilis were also virulent to brine shrimp, but the virulence was weak and slowly exerted compared with that of other bacteria. Taken together, we suggest that brine shrimp are a good infection model to assay bacterial virulence, especially for V. vulnificus and P. aeruginosa, and QS is important in the bacterial virulence to brine shrimp.

Protease IV, a quorum sensing-dependent protease of Pseudomonas aeruginosa modulates insect innate immunity.

In Pseudomonas aeruginosa, quorum sensing (QS) plays an essential role in pathogenesis and the QS response controls many virulence factors. Using a mealworm, Tenebrio molitor as a host model, we found that Protease IV, a QS-regulated exoprotease of P. aeruginosa functions as a key virulence effector causing the melanization and death of T. molitor larvae. Protease IV was able to degrade zymogens of spätzle processing enzyme (SPE) and SPE-activating enzyme (SAE) without the activation of the antimicrobial peptide (AMP) production. Since SPE and SAE function to activate spätzle, a ligand of Toll receptor in the innate immune system of T. molitor, we suggest that Protease IV may interfere with the activation of the Toll signaling. Independently of the Toll pathway, the melanization response, another innate immunity was still generated, since Protease IV directly converted Tenebrio prophenoloxidase into active phenoloxidase. Protease IV also worked as an important factor in the virulence to brine shrimp and nematode. These results suggest that Protease IV provides P. aeruginosa with a sophisticated way to escape the immune attack of host by interfering with the production of AMPs.

[Peri-operative management and follow-up outcomes of cardiac surgery in dialysis-dependent patients with end stage renal disease].

OBJECTIVE: To summarize the perioperative management experience of patients with end-stage renal diseases (ESRD) undergoing cardiac surgery and the follow-up outcomes. METHODS: From September 2004 to February 2012, 18 dialysis-dependent patients with ESRD received cardiac surgery in Department of Cardiac Surgery, Peking University First Hospital. A series of methods were employed to maintain water-electrolyte and acid-base balance and coagulation function. We followed up the patients by clinic service or telephone. RESULTS: The spectra of surgical interventions included isolated coronary artery bypass graft (CABG, n=13), isolated valve replacement (VR, n=2) and concomitant CABG and VR (n=3). Of the 18 patients, 3 died within the Peri-operative period and 15 recovered and were discharged. The follow up period was 6-91 months [(27.6±27.5) months]. Within the follow up period, 2 patients died (66th month and 76th month), non-fatal complications occurred in 3 patients. Cardiac functions of the survived patients were good according to the New York Heart Association (NYHA) classification, 4 of them were within NYHA class I and 9 within NYHA class II. CONCLUSION: Dialysis-dependent patients with end-stage renal diseases are a high risk group receiving cardiac surgery, but a comprehensive Peri-operative management of water-electrolyte and acid-base balance and coagulation function could yield a better outcome.

[Risk factors for operative mortality in 1,098 patients with coronary artery bypass grafting surgery: a single center report].

OBJECTIVE: To analyze the risk factors for operative mortality in 1 098 cases of coronary artery bypass grafting (CABG) procedures. METHODS: A total of 1 098 cases of CABG including 113 cases of left ventricular ejection fraction (LVEF) lower than 35% from December 1999 through December 2009 were chosen for the retrospective study. Univariate and multivariate stepwise logistic analyses were performed based on the data of the whole group to locate the mortality risk factors. RESULTS: Age, acute coronary syndrome, emergent surgery, chronic renal failure (CRF), concomitant peripheral vascular disease, LVEF ≤ 35%, left ventricular end diastolic diameter (LVEDD), moderate to severe mitral regurgitation, aneurysm of the heart wall, aortic regurgitation, mitral repair/replacement, resection of aneurysm, concomitant aortic valve replacement, peri-operative intra-aortic balloon pump (IABP), left ventricular assist device (LVAD), and off-pump CABG were the risk factors for the univariate analysis. In the further multivariate regression analysis, off-pump CABG appeared statistically as a protective factor while age, female, emergent surgery, CRF, and the peri-operative application of IABP were the risk factors correspondingly for the whole group. CONCLUSION: Age, female, emergent surgery, CRF, and the application of IABP, were the risk factors for mortality in the entire group of patients, implicating the necessity of specific and cautious management. CABG concomitant with non-cardiac surgery, concomitant with the treatment of moderate-severe mitral regurgitation and resection of heart wall aneurysm were not the risk factors for peri-operative mortality.

[Investigations of influential factors of acute renal injury after coronary artery bypass grafting].

OBJECTIVE: To investigate the incidence, correlate factors and effect on convalescent of acute kidney injury (AKI) after coronary artery bypass grafting (CABG). METHODS: Sixty-eight consecutive patients who underwent scheduled CABG were included. AKI was diagnosed according to the diagnostic criteria from expert group of AKI. The patients were divided into AKI group with AKI and control group without AKI. Difference of clinic features was contrasted between the two groups. And multivariable logistic regression modeling was used to identify the risk factors of AKI. RESULTS: AKI occurred in 27.94% patients (19/68). There was significant difference between the two groups in gender, hypertension, hyperlipemia, number of grafts, the duration of mechanic ventilation, the time of ICU and the length of stay post operation. Hypertension(Wald 3.27, P=0.07, 95% CI 0.85-53.59), number of grafts(Wald 7.67, P=0.01, 95%CI 1.48-9.73), the duration of mechanic ventilation(Wald 4.94, P=0.03, 95%CI 1.00-1.18) were risk factors of AKI in multivariable logistic regression modeling. CONCLUSION: The incidence of AKI was high (27.94%). Female, hypertension, hyperlipemia, number of grafts, the duration of mechanic ventilation were risk factors in monovariance analysis, and AKI may increase the time of ICU and the length of stay post operation. Hypertension, number of grafts, duration of mechanic ventilation were independent risk factors of AKI in multivariable logistic regression model.

[Treatment of a case of Kawasaki's disease complicated with myocardial infarction].

Coronary artery by-pass graft (CABG) and ventricular aneurysmectomy were done for a 2.5 years old girl with Kawasaki's disease complicated by myocardial ischemia and old myocardial infarction, left ventricular aneurysm formation and heart failure. Post-operatively, the cardiac out-put of the patient increased, the heart failure syndrome disappeared, and cardiac function improved to class I(NYHA) one month later. In the 6-year follow-up, the patient kept her heart function at class I, and had normal growth and development. Coronary artery by-pass graft is an effective therapeutic strategy for childhood myocardial ischemia, and attention should be paid to some special considerations.