Left ventricular global function index assessed by cardiovascular magnetic resonance for the prediction of cardiovascular events in ST-elevation myocardial infarction

Background

The left ventricular performance index (LVGFI) as a comprehensive marker of cardiac performance integrates LV structure with global function within one index. In a prospective cohort study of healthy individuals the LVGFI demonstrated a superior prognostic value as compared to LV ejection fraction (LVEF). In patients after ST-segment elevation myocardial infarction (STEMI), however, the role of the LVGFI is unknown. Aim of this study was to investigate the relationship between the LVGFI and infarct characteristics as well as prognosis in a large multicenter STEMI population.

Methods

In total 795 STEMI patients reperfused by primary angioplasty (<12 h after symptom onset) underwent cardiovascular magnetic resonance (CMR) at 8 centers. CMR was completed within one week after infarction using a standardized protocol including LV dimensions, mass and function for calculation of the LVGFI. The primary clinical endpoint of the study was the occurrence of major adverse cardiac events (MACE).

Results

The median LVGFI was 31.2 % (interquartile range 25.7 to 36.6). Patients with LVGFI < median had significantly larger infarcts, less myocardial salvage, a larger extent of microvascular obstruction, higher incidence of intramyocardial hemorrhage and more pronounced LV dysfunction (p < 0.001 for all). MACE and mortality rates were significantly higher in the LVGFI < median group (p < 0.001 and p = 0.003, respectively). The LVGFI had an incremental prognostic value in addition to LVEF for prediction of all-cause mortality.

Conclusions

The LVGFI strongly correlates with markers of severe myocardial and microvascular damage in patients with STEMI, offering prognostic information beyond traditional cardiac risk factors including the LVEF.

Trials registration

ClinicalTrials.gov: {"type":"clinical-trial","attrs":{"text":"NCT00712101","term_id":"NCT00712101"}}NCT00712101     

The relationship between serum levels of uric acid and prognosis of infection in critically ill patients

BACKGROUND:

Serum uric acid level is associated with some chronic diseases and prognosis of severe infection. This study aimed to investigate the relationship between serum uric acid (SUA) and prognosis of infection in critically ill patients.

METHODS:

The data from 471 patients with infection admitted from January 2003 to April 2010 were analyzed retrospectively at Huashan Hospital Affiliated to Fudan University, Shanghai, China. The data of SUA, serum creatinine, blood urea nitrogen (BUN) and other relevant examinations within 24 hours after admission were recorded and the levels of SUA in those patients were described, then Student’s t test was used to evaluate the relationship between SUA and pre-existing disorders. Different levels of SUA were graded for further analysis. The Chi-square test was used to examine the difference in the prognosis of infection.

RESULTS:

The mean initial level of SUA within 24 hours after admission was 0.232±0.131 mmol/L and the median was 0.199 mmol/L. Remarkable variations in the initial levels of SUA were observed in patients with pre-existing hypertension (t=–3.084, P=0.002), diabetes mellitus (t=–2.487, P=0.013), cerebral infarction (t=–3.061, P=0.002), renal insufficiency (t=–4.547, P<0.001), central nervous system infection (t=5.096, P<0.001) and trauma (t=2.875, P=0.004). SUA was linearly correlated with serum creatinine and BUN (F=159.470 and 165.059, respectively, P<0.001). No statistical correlation was found between the initial levels of SUA and prognosis of infection (χ2=60.892, P=0.100).

CONCLUSION:

The current study found no direct correlation between the initial levels of SUA after admission and prognosis of infection in critically ill patients.KEY WORDS: Intensive care unit, Infection, Uric acid, Blood urea nitrogen, Creatinine, Pneumonia, Central nervous system infection, Renal insufficiency, Prognosis     

Serum brain natriuretic peptide in children with Kawasaki disease

BACKGROUND:

Kawasaki disease (KD) is a common cause of acquired heart disease in children. Recent studies have focused on the biochemical markers of the myocardium, their high sensitivity and specificity and significance in the diagnosis of KD. This study aimed to determine the serum level of brain natriuretic peptide (BNP) and its relation with the heart function of children with KD and to explore its clinical value in diagnosis of KD.

METHODS:

Forty-three KD children, aged from 5 months to 8 years (mean 2.3±0.6 years), were admitted to Qingdao Children’s Hospital from February 2007 to April 2009. Among them 27 were male, and 16 female. The 43 patients served as a KD group. Patients with myocarditis, cardiomyopathy, congenital heart disease and other primary heart diseases were excluded. Thirty healthy children, aged from 3 months to 15 years (mean 2.5±0.8 years) or 17 males and 13 females served as a control group. There were no significant differences in age and gender between the two groups (P>0.05). In the KD group, ELISA was used to measure the levels of serum BNP in acute and convalescent stages; and in the control group, the levels of serum BNP were measured once randomly. Left ventricular ejection fraction (LVEF), left ventricular shorten fraction (LVSF), cardiac index (CI) and left ventricular inflow velocity through the mitral annulus (including E-velocity and A-velocity) were measured by two-dimensional echocardiography in the acute and convalescent stages in the KD group. All data were expressed as mean±SD. The methods of analysis included Student’s t test and the linear regression analysis test. P<0.05 was considered statistically significant.

RESULTS:

The level of serum BNP in the acute stage (517.26±213.40) ng/ml was significantly higher than that in the convalescent stage (91.56±47.97) ng/ml in the control group (37.55±7.56) ng/ml (P<0.01). The levels of LVEF, LVSF and CI in the acute stage were significantly lower than those in the convalescent stage (P<0.05), but the E/A level was not significantly different between the acute and convalescent stages (P>0.05). Linear regression analysis showed that the BNP level was negatively correlated with the levels of LVEF, LVSF and CI(r=-0.63, -0.52, -0.53, P<0.05), but not significantly correlated with the E/A level (r=-0.18, P>0.05).

CONCLUSION:

The levels of serum BNP are significantly increased in KD patients, and are negatively correlated with the levels of LVEF, LVSF, and CI. The detection of serum BNP level is of clinical significance in the diagnosis of KD.KEY WORDS: Natriuretic peptide, brain; Kawasaki disease; Ejection fraction; left ventricular; Shorten fraction, left ventricular; Cardiac index; E/A; Correlation; Children     

Poster 21: Does severe left ventricular dysfunction impact the result of cardiac rehabilitation?

Objective: To evaluate the effect of severe left ventricular dysfunction on the improvement of functional capacity (FC) in cardiac patients undergoing phase 2 of a cardiac rehabilitation program (CRP). Design: Retrospective cohort study. Setting: Hospital-based CRP. Participants: 199 male cardiac patients. Group 1 (n=169) had a left ventricular ejection fraction (LVEF) >30% (age, 66.2±9.8y); group 2 (n=30) had a LVEF ≤30% (age, 69.0±8.1y). Intervention: 10 weeks, thrice weekly, of phase 2 CRP, consisting of 60 minutes of supervised exercise to reach the target heart rate determined by the Karvonen method. Main Outcome Measures: We measured FC before and after completion of the CRP and the improvement expressed in percents of FC before the CRP. The FC results were compared using the Student t test. Results: FC in both patient groups improved after the CRP. In group 1 patients, FC increased from 5.6±2.3 metabolic equivalents (METS) before the CRP to 7.5±2.6 METS after the CRP (P<.01). In group 2 patients, FC increased from 4.7±2.1 METS before the CRP to 6.2±2.2 METS after the CRP (P<.01). Before the CRP, group 2 patients had significantly lower FC compared with group 1 patients (P<.05). Similarly, after the CRP, the FC of group 2 patients remained lower than FC of group 1 patients (P<.05). However, the percentage of improvement for group 1 patients (40.6%±34.3%) did not differ significantly from the percentage of improvement for group 2 patients (39.9%±34.5%). Conclusions: The CRP improved FC of all cardiac patients, including those with severe left ventricular dysfunction. Patients with severe left ventricular dysfunction have lower FC before and after the CRP. However, the FC of these patients improved to the same degree as the patients with better left ventricular function. These findings are important in designing strategies for the CRP in patients with severely impaired LVEF.     

Urokinase-type plasminogen activator receptor as a predictor of poor outcome in patients with systemic inflammatory response syndrome

BACKGROUND:

Urokinase-type plasminogen activator (uPA) and urokinase-type plasminogen activator receptor (uPAR) are known as important factors, which mediate a variety of functions in terms of vascular homeostasis, inflammation and tissue repair. However, their role in systemic inflammatory response syndrome (SIRS) has been less well studied. This study aimed to test the hypothesis that the abnormalities of fibrinolysis and degradation of extracellular matrix mediated by uPA and uPAR are directly related to the patients with SIRS. We therefore analyzed their role and clinicopathological significance in patients with SIRS.

METHODS:

A case-control study was conducted with 85 patients who were divided into two groups according to the diagnostic criteria of SIRS: SIRS group (n=50) and non-SIRS group (n=35). The SIRS group was divided into MODS group (n=26) and non-MODS group (n=24) by their severity, and survival group (n=35) and non-survival group (n=15) by their prognosis. Another 30 healthy adults served as normal controls. uPA and uPAR in plasma were detected by commercial enzyme-linked immunosorbent assay (ELISA) kits.

RESULTS:

The plasma level of uPA was lower in the SIRS group than in the non-SIRS group and controls (P<0.001 and P<0.001). It was lower in sepsis patients and the MODS group than in the non-sepsis patients and the non-MODS patients (all P<0.05). However, there was no difference in uPA level between survivors and non-survivors (P>0.05). The plasma level of uPAR increased in the SIRS group compared with the non-SIRS group and controls (P<0.001 and P<0.001). There was a significant elevation of uPAR in sepsis patients, MODS patients and non-survivors as compared with non-sepsis patients, non-MODS patients and survivors respectively (all P<0.05). Plasma uPAR levels were positively correlated with APACHE II score (r=0.575, P<0.001) and SOFA score (r=0.349, P=0.013). AUCs for the prediction of SIRS mortality were 0.67 and 0.51, respectively, for uPA and uPAR.

CONCLUSION:

uPAR could be a predictor of poor outcome in patients with SIRS.KEY WORDS: Systemic inflammatory response syndrome, Multiple organ dysfunction syndrome, Urokinase-type plasminogen activator, Urokinase-type plasminogen activator receptor     

Characteristics and prognosis in patients with false-positive ST-elevation myocardial infarction in the ED

Background

There are several causes of ST-segment elevation (STE) besides acute myocardial infarction (MI).

Objectives

We design this study to determine the prevalence, etiology, clinical manifestation, electrocardiographic characteristics, and outcome in patients with false-positive STEMI.

Methods

This is a retrospective case-control study design. At our emergency department, 297 patients who underwent emergent coronary angiography for suspected STEMI were enrolled from January 2004 to December 2010.

Results

Of the 297 patients who underwent coronary angiography, 31 patients (10.4%) did not have a clear culprit coronary lesion and were classified as false-positive STEMI. False-positive STEMI patients had a lower incidence of typical chest pain or chest tightness (58.1% vs 87.6%, P < .001). Inferior STE occurred significantly more often in the patients with true-positive STEMI (49.6% vs 25.8%, P = .012), and diffuse STE, more often in the patients with false-positive STEMI (19.4% vs 0.38%, P = .001). Total height of STE was lower in false-positive STEMI patients (7.5 ± 4.9 vs 10.9 ± 7.9 mm, P = .002) if excluding 5 patients of marked STE just after cardiopulmonary resuscitation. Concave STE and no reciprocal ST-segment depression occurred more often in false-positive STEMI patients (51.6% vs 24.1%, P = .001; 64.5% vs 19.2%, P < .001). There was no significant difference of in-hospital major adverse events in the patients with false-positive and true-positive STEMI.

Conclusions

The diagnosis of false-positive STEMI is not uncommon. Detailed clinical evaluation and electrocardiogram interpretation may avoid partly unnecessary catheterization laboratory activation.     

Uric acid,allopurinol therapy,and mortality in patients with acute heart failure—results of the Acute HEart FAilure Database registry

Study Objective

The aim of this study was to explore the prognostic role of serum uric acid (UA) measurement in the hospital and long-term mortality assessment in subjects with acute heart failure (AHF) from the Acute HEart FAilure Database registry (AHEAD). The AHEAD registry comprised 4153 patients with AHF syndromes hospitalized at the AHEAD participating centers.

Patients and Methods

The study included 1255 patients who were admitted to the AHEAD participating centers with acute decompensated chronic heart failure, de novo heart failure, or cardiogenic shock between September 2006 and October 2009 and who had information about serum UA concentration available at the time of hospital admission. The hospital and long-term mortality was followed using the centralized database of the Ministry of Health, Czech Republic.The mean age of the cohort was 73.4 years, the female population represented 43%, the median hospital stay was 8 days, and the mean hospital mortality was 7.6%.

Results

The median UA concentration of the patients with AHF was 432 μmol/L (7.26 mg/dL), the median estimated glomerular filtration rate (eGFR) was 49.0 mL/min, and N-terminal pro–brain natriuretic peptide level was 5510 pg/mL. Among other laboratory variables, UA concentration greater than 515 μmol/L (8.67 mg/dL) was associated with increased hospital mortality (P < .001), as well as eGFR less than 30 mL/min (P < .001), Na 135 mmol/L or less, and positive troponin. Uric acid concentration greater than 500 μmol/L (8.41 mg/dL) was associated with increased long-term mortality (P < .001), followed by eGFR less than 30 mL/min (P < .001), Na 135 mmol/L or less, and hemoglobin level lower than 130 g/L (P < .001). The 1-year survival rate of patients discharged from hospital (n = 1159) was 75.6%, and the 2-year rate was 66.8%. Survival of patients treated with allopurinol for hyperuricemia was significantly lower compared with untreated subjects (70.1 vs 77.2 for 1-year survival and 60.3 vs 68.5 for 2-year survival).

Conclusion

In patients with AHF, increased UA levels and documented allopurinol therapy for hyperuricemia were associated with increased hospital and long-term mortality. Allopurinol therapy is not a cause but the identifier of the subjects at risk.     

Functional changes of intestinal mucosal barrier in surgically critical patients

BACKGROUND:

The gut is capable of inducing multiple organ dysfunction syndrome (MODS). In the diagnosis and treatment of critical ill patients, doctors should pay particular attention to the protection or recovery of intestinal barrier function. However, no reliable diagnostic criteria are available clinically. This study aimed to assess the changes of intestinal mucosal barrier function in surgically critical ill patients as well as their significance.

METHODS:

Thirty-eight surgically critical ill patients were enrolled as a study group (APACHE II>8 scores), and 15 non-critical ill patients without intestinal dysfunction were selected as a control group (APACHE II<6). General information, symptoms, physical signs, and APACHE II scores of the patients were recorded. The patients in the study group were subdivided into an intestinal dysfunction group (n=26) and a non-intestinal dysfunction group (n=12). Three ml venous blood was collected from the control group on admission and the same volume of plasma was collected from the study group both on admission and in the period of recovery. The plasma concentrations of endotoxin, diamine oxidase (DAO), D-lactate, and intestinal fatty-acid binding protein (iFABP) were detected respectively. The data collected were analyzed by the SPSS 17.0 software for Windows.

RESULTS:

The levels of variables were significantly higher in the study group than in the control group (P<0.01). They were higher in the intestinal dysfunction group than in the non-intestinal dysfunction group (DAO P<0.05, endotoxin, D-lactate, iFABP P<0.01). In the non-intestinal dysfunction group compared with the control group, the level of endotoxin was not significant (P>0.05), but the levels of DAO, D-lactate and iFABP were statistically significant (P<0.05). The levels of variables in acute stage were higher than those in recovery stage (P<0.01). The death group showed higher levels of variables than the survival group (endotoxin and D-lactate P<0.01, DAO and iFABP P<0.05).

CONCLUSION:

The plasma concentrations of endotoxin, DAO, D-lactate, and intestinal fatty-acid binding protein (iFABP) could reflect a better function of the intestinal mucosa barrier in surgically critical ill patients.KEY WORDS: Intestinal mucosal barrier, Endotoxin, Diamine oxidase, D-lactate, Intestinal fatty-acid binding protein     

Determinants of markedly increased B-type natriuretic peptide in patients with ST-segment elevation myocardial infarction

Background

A modestly increased plasma B-type natriuretic peptide (BNP) level of greater than 80 pg/mL has been associated with increased mortality in patients with ST-segment elevation myocardial infarction (STEMI). However, the prognostic significance of larger increases in BNP during STEMI has not been reported.

Methods

A total of 420 patients with STEMI were identified from an administrative database, and 91 were found to have a BNP level measured within 24 hours of hospitalization. All patients underwent detailed angiographic and echocardiographic evaluation. Charts were abstracted in a blinded fashion to the BNP results.

Results

The mean ± SD age of the participants was 64 ± 13 years, and 53 (58%) of the participants were men. The median, 25th percentile, and 75th percentile of the BNP value were 366, 142, and 1011 pg/mL, respectively. The BNP level increased progressively in 1-, 2-, and 3-vessel coronary disease with medians of 253, 351, and 818 pg/mL, respectively (P = .009). Patients with grade 3/4 diastolic dysfunction had significantly increased median BNP values vs all others, 786 vs 306 pg/mL (P = .03). Eight (9%) patients died during their hospitalization. The median BNP values for 83 (91%) survivors and 8 (9%) nonsurvivors were 344 and 1420 pg/mL, respectively (P = .007). By multiple logistic regression, BNP level more than 500 pg/mL was independently associated with female sex, increased number of vessels diseased (>75% stenosis), lower ejection fraction, higher creatine kinase level, and lower body mass index.

Conclusion

In patients with STEMI, markedly increased BNP level seems to reflect the extent of coronary disease, the degree of associated systolic and diastolic dysfunction, and a higher risk of in-hospital mortality.     

Intracoronary versus intravenous bolus abciximab application in patients with ST-elevation myocardial infarction undergoing primary percutaneous coronary intervention: 6-month effects on infarct size and left ventricular function

Background

Administration of abciximab during primary percutaneous coronary intervention (PCI) reduces major adverse cardiac events (MACE) in patients with ST-elevation myocardial infarction (STEMI). Intracoronary (IC) abciximab bolus application during PCI results in high local drug concentration, improved perfusion, reduction of infarct size, and less microvascular obstruction early after infarction. Aim of this study was to investigate whether the early benefits of an IC abciximab administration in STEMI patients undergoing PCI are sustained at 6?months.

Methods

We performed 6-month follow-up of 154 STEMI patients undergoing PCI, who were randomised to either IC (n?=?77) or intravenous (IV) (n?=?77) bolus abciximab administration with subsequent 12-h intravenous infusion. The primary endpoint was infarct size at 6-month follow-up as assessed by delayed enhancement magnetic resonance imaging. Clinical end points were MACEs within 6?months after infarction.

Results

The median infarct size after 6?months was significantly reduced in the IC abciximab group (16.7 vs. 24.1%, p?=?0.002). A significant recovery of LV function was only observed in the IC abciximab group (p?<?0.001), and IC abciximab group patients had significantly less adverse remodelling as compared to standard IV abciximab treatment (p?=?0.03). These beneficial effects also translated into a strong trend towards a reduced MACE rate in the IC abciximab group at 6-month follow-up (10 vs. 21%, p?=?0.07).

Conclusions

Intracoronary abciximab application in STEMI patients undergoing PCI is superior to standard IV treatment with respect to infarct size, recovery of LV function and reverse remodelling 6?months after infarction.     

Protective effect of glutamine in critical patients with acute liver injury

BACKGROUND:

Glutamine (Gln) supplementation is known to decrease oxidative stress and inflammatory response, enhance resistance to infectious pathogens, shorten hospital stay, and decrease medical costs of patients. This study was undertaken to evaluate the relationship between the effect of early parenteral glutamine (Gln) supplement on acute liver injury (ALI) and heat shock protein 70 (HSP-70) expression in critical patients.

METHODS:

Forty-four patients who had been admitted to the emergency intensive care unit (EICU) of Nanjing First Hospital Affiliated to Nanjing Medical University were randomly divided into a control group (n=22) and a Gln group (n=22). The patients of the two groups received enteral and parenteral nutrition. In addition, parenteral Gln 0.4 g/kg per day was given for 7 days in the Gln group. Serum HSP-70 and Gln were measured at admission and at 7 days after admission. Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and total bilirubin (TBiL), serum levels of HSP-70 and Gln, mechanical ventilation (MV) time, ICU stay, peripheral blood of TNF-α, IL-6, CD3, CD4 and CD4/CD8 levels were also measured in the two groups.

RESULTS:

In the Gln group, the levels of serum HSP-70 and Gln were significantly higher after Gln treatment than those before the treatment (P<0.01). HSP-70 level was positively correlated with the Gln level in the Gln group after administration of parenteral Gln (P<0.01). The levels of serum ALT, AST, TBiL and TNF-α, IL-6 were lower in the Gln group than in the non-Gln group (P<0.01). MV time and ICU stay were significantly different between the two groups (P<0.05). The levels of CD3, CD4 and CD4/CD8 were significantly higher in the Gln group than in the control group after treatment (P<0.05).

CONCLUSION:

Parenteral Gln significantly increases the level of serum HSP70 in critically ill patients. The enhanced expression of HSP70 is correlated with improved outcomes of Gln-treated patients with acute liver injury.KEY WORDS: Glutamine, Heat shock protein, Critically ill patients, Acute liver injury     

Effects of α-methylnorepinephrine on cardiac function and myocardium at early stage of resuscitation in rabbits

BACKGROUND:

Recent studies have shown that α2-adrenergic agonists can reduce postresuscitation myocardial injury. This study was undertaken to observe changes of hemodynamics, myocardial injury markers cTnT and cardiac morphology by establishing a cardiopulmonary resuscitation model with rabbits, and to detect whether α-methyl norepinephrine (α-MNE) can reduce the myocardial injury after CPR and improve cardiac function.

METHODS:

Eighteen health rabbits, weighing 2.5-3.5 kg, both male and female, were provided by the Lanzhou Institute of Veterinary Medicine. After setting up a rabbit model of cardiopulmonary resuscitation, 18 rabbits were randomly divided into three groups. The rabbits in group A as an operation-control group were subjected to anesthesia, endotracheal intubation, and surgery without induction of ventricular fibrillation. The rabbits in group B as an epinephrine group were administered with 30 μg/kg epinephrineduring CPR. The rabbits in group C as a MNE group were administered with 100 μg/kg a-MNE during CPR. The left ventricular end-diastolic pressure (LVEDP), left ventricular pressure rise and fall rate (±dp/dt) and serum concentrations of BNP were measured. Statistical package of SPSS 10.0 was used for data analysis and significant differences between means were evaluated by ANOVA.

RESULTS:

Compared to group A, the LVEDP of other two groups increased respectively (P<0.01 all), and peak±dp/dt decreased in the other two groups (P<0.01). The increase of LVEDP was lower in group C than in group B (P<0.05), whereas peak±dp/dt was higher in group C than in group B (P<0.05) at the same stage. Compared to group A, the cTnT of the remaining two groups increased, respectively (P<0.01), and peaked at 30 minutes. cTnT was less elevated in group C than in group B (P<0.05) during the same period. In groups B and C, myocardial injury was seen under a light microscope, but the injury in group C was lighter than that in group B.

CONCLUSION:

Methylnorepinephrine can lessen myocardial dysfunction after CPR.KEY WORDS: Cardiopulmonary resuscitation;, α2-adrenergic agonist;, Post-resuscitation myocardial dysfunction     

Increased Circulating Copeptin Levels Are Associated with Vaso-Occlusive Crisis and Right Ventricular Dysfunction in Sickle Cell Anemia

ObjectiveVaso-occlusive crisis (VOC) is a common clinical manifestation of sickle cell anemia (SCA) and is associated with increased proinflammatory mediators. Copeptin is the C-terminal part of the prohormone for provasopressin and seems clinically relevant in various clinical conditions. Right ventricular (RV) dysfunction significantly appears in SCA patients due to pulmonary hypertension. This study aimed to investigate the association of copeptin levels in VOC patients and evaluate RV dysfunction.Materials and MethodsA total of 108 patients were enrolled in the study. Twenty-eight SCA patients in steady state (30.2 ± 0.9 years), 25 SCA patients in VOC (36.8 ± 11.8 years), and 55 healthy individuals (31.9 ± 9.4 years) with HbAA genotype were included. Clinical, echocardiographic, and laboratory data were recorded. ELISA was used for the determination of serum levels of copeptin.ResultsVOC patients had significantly higher copeptin level compared both with controls and SCA subjects in steady state (22.6 ± 13.0 vs. 11.3 ± 5.7 pmol/L, 22.6 ± 13.0 vs. 12.4 ± 5.8 pmol/L, p = 0.009 for both). Additionally, the copeptin level was significantly higher in SCA patients with RV dysfunction than those without RV dysfunction (23.2 ± 12.2 vs. 15.3 ± 9.5 pmol/L, p = 0.024). Multiple logistic regression analysis revealed that high-sensitivity C-reactive protein and copeptin levels were found to be associated with VOC.ConclusionThis study showed that copeptin and hs-CRP levels were increased in patients with VOC, and it was found that RV dysfunction was more common in SCA patients with VOC than in the control group. Copeptin can be considered for use as a potential biomarker in predicting VOC crisis in SCA patients and in the early detection of patients with SCA who have the potential to develop RV dysfunction.     

Prognostic significance of urokinase-type plasminogen activator and its receptor in patients with systemic inflammatory response syndrome

BACKGROUND:

This study aimed to determine the plasma levels of urokinase-type plasminogen activator (uPA), urokinase-type plasminogen activator receptor (uPAR), D-dimer, IL-6 and TNF-α and observe the relations among uPA, uPAR, D-dimer, IL-6 and TNF-α in patients with systemic inflammatory response syndrome (SIRS).

METHODS:

A prospective, clinical case-control study was conducted in patients with SIRS at age of more than 55 years old treated during 2008-2010 at Wuhan Central Hospital. Venous blood samples were collected by routine venipuncture. Eighty-five patients were divided into two groups according to diagnostic criteria of SIRS: SIRS patients from intensive care units (n=50), and non-SIRS patients from medical wards (n=35). Thirty healthy blood donors who visited the General Health Check-up Division at Wuhan Central Hospital served as controls. Excluded from the study were (1) those patients with pregnancy; (2) those with cancer; (3) those died after admission into the ICU in 7 days; (4) those received cardiopulmonary resuscitation; (5) those who had previous blood system diseases; and (6) those with SIRS before admission into the ICU. The levels of uPA, uPAR, D-D, IL-6 and TNF-α in blood were detected by commercial enzyme-linked immunosorbent assay (ELISA) kit. The data were analyzed using SPSS version 17.0 and expressed as mean ± standard. Student''s t test and the Mann-Whitney U test were used in the analysis. The relations of uPA, uPAR and D-dimer, IL-6 TNF-α levels were analyzed using Spearman''s rank-order correlation coefficient test.

RESULTS:

The plasma levels of uPA, uPAR, D-dimer,IL-6 and TNF-α in the patients with SIRS were obviously higher than those in the non-SIRS patients and controls (P<0.001). Correlation analysis showed a positive correlation between uPAR and IL-6 levels (r=0.395, P=0.004) and between uPAR and TNF-α levels (r=0.606, P<0.001), but no correlation between uPAR and D-dimer levels (r=0.069, P=0.632). No correlation was observed between uPA, D-dimer, IL-6 and TNF-α levels (P>0.05). The establishment of ROC curve was based on the levels of uPAR, D-dimer, IL-6 and TNF-α in 24 hours for the diagnosis of multiple organ dysfunction syndrome (MODS), and the ROC areas under the curve were 0.76, 0.58, 0.86 and 0.83, respectively.

CONCLUSIONS:

uPA and uPAR play a major role in patients with SIRS in the process of coagulation disorder, but the mechanism of SIRS is not the same. uPAR may play a central role in the development of SIRS to MODS.KEY WORDS: Systemic inflammatory response syndrome, Multiple organ dysfunction syndrome, D-dimer, Interleukin-6, Tumor necrosis factor-alpha, Coagulant function     

Mean HEART scores for hospitalized chest pain patients are higher in more experienced providers

Background

The HEART score has been validated as a predictor of major adverse cardiac events (MACEs) in emergency department patients complaining of chest pain. Our objective was to determine the extent of physician variation in the HEART score of admitted patients stratified by years of experience.

Serum uric acid levels and incident chronic kidney disease in patients with type 2 diabetes and preserved kidney function

OBJECTIVE

Recent studies have suggested an association between hyperuricemia and adverse renal outcomes in nondiabetic populations. Data on the relationship between hyperuricemia and the risk of incident chronic kidney disease (CKD) in type 2 diabetic patients with normal or near-normal kidney function are lacking. We determined whether baseline serum uric acid levels predict the subsequent development of CKD in patients with type 2 diabetes.

RESEARCH DESIGN AND METHODS

We followed 1,449 type 2 diabetic patients with normal kidney function and without overt proteinuria for 5 years for the occurrence of incident CKD (defined as overt proteinuria or estimated glomerular filtration rate [eGFR] <60 mL/min/1.73 m²).

RESULTS

During a 5-year follow-up period, 194 (13.4%) patients developed incident CKD. The cumulative incidence of CKD was significantly greater in patients with hyperuricemia than in those without hyperuricemia (29.5 vs. 11.4%, P < 0.001). In univariate logistic regression analysis, the presence of hyperuricemia roughly doubled the risk of developing CKD (odds ratio [OR] 2.55 [95% CI 1.71–3.85], P < 0.001). After adjusting for age, sex, BMI, smoking status, diabetes duration, systolic blood pressure, antihypertensive treatment, insulin therapy, HbA_1c, eGFR, and albuminuria, hyperuricemia was associated with an increased risk of incident CKD (adjusted OR 2.10 [1.16–3.76], P < 0.01). In continuous analyses, a 1-SD increment in the serum uric acid level was significantly associated with a 21% increased risk of CKD.

CONCLUSIONS

In type 2 diabetic individuals with preserved kidney function, hyperuricemia seems to be an independent risk factor for the development of incident CKD.The tide of type 2 diabetes is rising in the U.S. and all over the world, thereby becoming an increasingly powerful threat to global health (1). Type 2 diabetes also has become the leading cause of end-stage renal disease in the world, and the number of patients diagnosed each year with end-stage renal disease attributed to type 2 diabetes is rising (2).The pathophysiology of diabetic nephropathy is complex and still not fully elucidated (3). Several prospective studies have suggested that hyperuricemia is associated with an increased risk of incident cardiovascular events and death in both nondiabetic and type 2 diabetic individuals (4–9). Hyperuricemia also is largely prevalent in patients with chronic kidney disease (CKD) (10,11). However, hyperuricemia might have a pathogenic role in the development and progression of CKD, rather than solely reflecting decreased renal uric acid excretion. Indeed, several (12–17), but not all (18–20), prospective studies recently have shown a significant association between hyperuricemia and adverse renal outcomes in both the general population and other nondiabetic high-risk patient populations. However, epidemiologic data are limited about the relationship between hyperuricemia and adverse renal outcomes in patients with type 1 (21,22) or type 2 (23) diabetes.In a post hoc analysis of 1,342 patients with type 2 diabetes and nephropathy participating in the Reduction of End Points in Non–Insulin-Dependent Diabetes Mellitus With the Angiotensin II Antagonist Losartan (RENAAL) Trial, the investigators reported that the risk of adverse renal outcomes was decreased by 6% per 0.5 mg/dL decrement in serum uric acid levels during the first 6 months of treatment with losartan (23). These findings support the view that serum uric acid may be a modifiable risk factor for renal disease in type 2 diabetic patients (23).To our knowledge, however, no large prospective studies are available on the relationship between hyperuricemia and incident CKD in patients with type 2 diabetes and normal or near-normal kidney function. Thus, the purpose of this prospective, observational study was to determine whether baseline serum uric acid levels are associated with an increased incidence of CKD in a large cohort of type 2 diabetic patients with preserved kidney function at baseline and without a previous history of cardiovascular disease.     

Prognostic value of admission blood glucose level in patients with and without diabetes mellitus who sustain ST segment elevation myocardial infarction complicated by cardiogenic shock

Introduction

Admission blood glucose (BG) level is a predictor of mortality in patients with ST-segment elevation myocardial infarction (STEMI). However, limited data are available relating admission BG to mortality in patients with STEMI complicated by cardiogenic shock, and it is not known whether diabetic status has an independent effect on this relationship.

Methods

Between November 2005 and September 2010, 816 STEMI patients with cardiogenic shock were enrolled in a nationwide, prospective, multi-center registry; 239 (29.3%) had diabetes mellitus (DM). Patients were categorized according to BG levels at admission: <7.8, 7.8–10.9, 11.0–16.5 and ≥ 16.6 mmol/L. The primary outcome was 30-day mortality. The added values of BG to the Thrombolysis in Myocardial Infarction (TIMI) and Global Registry of Acute Coronary Events (GRACE) scores were assessed by receiver operating characteristic curves and integrated discrimination improvement analyses.

Results

Thirty-day mortality was higher in patients with higher admission BG (20.4%, 23.3%, 39.8%, and 43.1% p < 0.001). Among non-diabetic patients, 30-day mortality was predicted by TIMI scores with a c-statistic of 0.615 (95% confidence interval [CI], 0.561–0.662) and GRACE scores with a c-statistic of 0.652 (95% CI, 0.604–0.695). Incorporation of admission BG increased the c-statistic for TIMI score to 0.685 (95% CI, 0.639–0.720, p < 0.001) and GRACE score to 0.708 (95% CI 0.664–0.742, p < 0.001). Additional predictive values for BG were not observed for diabetes. Integrated discrimination improvements (TIMI vs. additional BG and GRACE vs. additional BG) were 0.041 (p < 0.001) and 0.039 (p < 0.001) in non-diabetic patients.

Conclusions

In a cohort of patients with STEMI complicated by cardiogenic shock, admission BG was an independent predictor of increased risk of mortality only among patients without DM.     

Blood hemoperfusion with resin adsorption combined continuous veno-venous hemofiltration for patients with multiple organ dysfunction syndrome

BACKGROUND:

Blood hemoperfusion with resin adsorption can clean larger molecules that exceed the molecular weight cutoff of combined continuous veno-venous hemofiltration (CVVH). Hence blood hemoperfusion with resin adsorption combined CVVH (HP+CVVH) has higher ability of mediator clearance, and can improve clinical outcomes in theory. This study aimed to investigate the effect of blood hemoperfusion with resin adsorption combined continuous veno-venous hemofiltration (HP+CVVH) on plasm cytokines like TNF-α, IL-1β, IL-6, cellular immunity and prognosis in patients with multiple organ dysfunction syndrome (MODS).

METHODS:

This was a prospective, randomized clinical trial. A total of 30 patients who had been diagnosed with MODS were enrolled in this study. Patients were randomly allocated to routine treatment+HP+CVVH group (treatment group) and routine treatment+only CVVH group (control group). In the treatment group, patients received blood hemoperfusion with resin adsorption for 2 hours, and then received CVVH for 10 hours every day. In the control group, patients received CVVH for 12 hours only every day. The patients in the two groups received blood purification therapy for three days. The plasma of patients in the treatment group was obtained at 0, 2, 12, 24, 26, 36, 48, 50, 60 hours, 5th day, 7th day and 10th day, respectively. The plasma of patients in the control group was obtained at 0, 12, 24, 36, 48, 60 hours, 5th day, 7th day and 10th day, respectively. APACHE II score, T-lymphocytes subpopulations, blood lactate acid concentration, heart rate, breathing rate, and oxygenation index were observed.

RESULTS:

Plasma cytokines like TNF-α, IL-1β, IL-6 decreased markedly after HP (P<0.01); T-lymphocytes subpopulations CD3+, CD4+, CD8+, CD4+/CD8+ increased after HP+CVVH or only CVVH. The plasma concentrations of TNF-α, IL-1β and IL-6 in the two groups were not markedly different at 12, 36, and 50 hours. But on the 5th day, the plasma concentrations of TNF-α, IL-1β and IL-6 in the treatment group were lower than those in the control group (P<0.05). On the 28th day, 5 patients died in the treatment group, and 6 patients in the control group.

CONCLUSIONS:

Both HP+CVVH and CVVH can clean plasma cytokines like TNF-α, IL-1β, and IL-6, and improve cellular immunity and clinical symptoms and signs of patients. Compared with only CVVH, the plasma concentrations of TNF-α, IL-1β and IL-6 were lower on the 5th day, and patients have an increased survival rate on the 28 day in the HP+CVVH group.KEY WORDS: Hemoperfusion with resin adsorption, Continuous veno-venous hemofiltration, Multiple organ dysfunction syndrome, Cytokines     

Increased Serum Uric Acid Levels Are Correlated with Decreased Left Atrial Appendage Peak Flow Velocity in Patients with Atrial Fibrillation

Objective

We aimed to examine the relationship between serum uric acid levels and left atrial appendage (LAA) peak flow velocity, an indicator of the mechanical functions of the LAA, and atrial fibrillation (AF).

Subjects and Methods

Transesophageal echocardiography was performed before cardioversion in 153 patients with AF. The patients were categorized into 2 groups based on their LAA blood flow velocity. Group 1 included 87 patients with a low LAA flow velocity (<35 cm/s), and group 2 comprised 66 patients with a normal LAA flow velocity (≥35 cm/s). The χ² and Student''s t tests were used to compare categorical and quantitative data between the groups. Linear regression analyses were performed to demonstrate the independent association between serum uric acid levels and LAA peak flow velocity.

Results

The LAA blood flow velocity was 24.62 ± 5.90 cm/s in group 1 and 49.28 ± 13.72 cm/s in group 2, respectively (p < 0.001). The serum uric acid levels were 6.88 ± 1.85 mg/dl in group 1 and 5.97 ± 1.51 mg/dl in group 2, and the difference was statistically significant (p = 0.001). There was a negative correlation between serum uric acid levels and LAA blood flow velocity (r = −0.216, p = 0.007). Multivariate regression analysis showed that serum uric acid levels, age and gender differences were significant predictors of the LAA peak flow velocity.

Conclusions

High serum uric acid levels were associated with a low contractile function of the LAA and could provide additional prognostic information on future thromboembolic events in patients with AF.Key Words: Atrial fibrillation, Left atrial appendage peak flow velocity, Serum uric acid level