Predictive factors for cerebrocardiac syndrome in patients with severe traumatic brain injury: a retrospective cohort study.

Background and objective: Cerebrocardiac syndrome (CCS) is a severe complication of severe traumatic brain injury (sTBI) that carries high mortality and disability rates. Early identification of CCS poses a significant clinical challenge. The main objective of this study was to investigate potential risk factors associated with the development of secondary CCS in patients with sTBI. It was hypothesized that elevated right heart Tei index (TI), lower Glasgow Coma Scale (GCS) scores, and elevated cardiac troponin-I (cTnI) levels would independently contribute to the occurrence of CCS in sTBI patients. Methods: A retrospective cohort study was conducted to identify risk factors for CCS secondary to sTBI. One hundred and fifty-five patients were enrolled with sTBI admitted to the hospital between January 2016 and December 2020 and divided them into a CCS group (n = 75) and a non-CCS group (n = 80) based on the presence of CCS. This study involved the analysis and comparison of clinical data from two patient groups, encompassing demographic characteristics, peripheral oxygen saturation (SPO2), neuron-specific enolase (NSE), cardiac troponin-I (cTnI), N-terminal pro-brain natriuretic peptide (NT-proBNP), optic nerve sheath diameter (ONSD), cardiac ultrasound, acute physiology and chronic health evaluation (APACHE II) scores, and GCS scores and so on. Multivariate logistic regression was employed to identify independent risk factors for CCS, and receiver operating characteristic (ROC) curves were used to assess their predictive value for CCS secondary to sTBI. Results: The study revealed that 48.4% of sTBI patients developed secondary CCS. In the multivariate analysis model 1 that does not include NT-proBNP and cTnI, ONSD (OR = 2.582, 95% CI: 1.054-6.327, P = 0.038), right heart Tei index (OR = 2.81, 95% CI: 1.288-6.129, P = 0.009), and GCS (OR = 0.212, 95% CI: 0.086-0.521, P = 0.001) were independent risk factors for secondary CCS in sTBI patients. In multivariate analysis model 2 that includes NT-proBNP and cTnI, cTnI (OR = 27.711, 95%CI: 3.086-248.795, P = 0.003), right heart Tei index (OR = 2.736, 95% CI: 1.056-7.091, P = 0.038), and GCS (OR = 0.147, 95% CI: 0.045-0.481, P = 0.002) were independent risk factors for secondary CCS in sTBI patients. The area under the ROC curve for ONSD, Tei index, GCS, and cTnI were 0.596, 0.613, 0.635, and 0.881, respectively. ONSD exhibited a positive predictive value (PPV) of 0.704 and a negative predictive value (NPV) of 0.634. The Tei index demonstrated a PPV of 0.624 and an NPV of 0.726, while GCS had a PPV of 0.644 and an NPV of 0.815. On the other hand, cTnI exhibited a significantly higher PPV of 0.936 and an NPV of 0.817. These findings indicate that the Tei index, GCS score, and cTnI possess certain predictive value for secondary CCS in patients with sTBI. Conclusions: The study provides valuable insights into the identification of independent risk factors for CCS secondary to sTBI. The findings highlight the significance of right heart Tei index, GCS score, and cTnI as potential predictive factors for CCS in sTBI patients. Further larger-scale studies are warranted to corroborate these findings and to provide robust evidence for the development of early intervention strategies aimed at reducing the incidence of CCS in this patient population.

Allogeneic bone marrow transplantation compared to peripheral blood stem cell transplantation for the treatment of hematologic malignancies: a meta-analysis based on time-to-event data from randomized controlled trials.

Controversy remains regarding the transplant outcomes of human leukocyte antigen-identical related bone marrow transplantation (BMT) and peripheral blood stem cell transplantation (PBSCT) for the treatment of patients with hematological malignancies. To provide an estimate of the effect of BMT and PBSCT on clinical outcomes in patients with hematological malignancies, we conducted a meta-analysis based on time-to-event data from 17 randomized controlled trials. PubMed, EMBASE, and Cochrane Central Register of Controlled Trials (CENTRAL), from 1972 through July 2010, and conference proceedings through July 2009 and reference lists, without any language restriction, of randomized trials that compared the transplant outcomes after BMT and PBSCT in patients with hematological malignancies were searched for details. Two independent reviewers extracted the data. The outcomes examined were engraftment, graft-versus-host disease (GVHD), relapse, transplant-related mortality (TRM), leukemia-free-survival (LFS), and overall survival (OS). Compared to PBSCT, BMT had lower neutrophil (HR, 2.08; 95% CI, 1.80 to 2.42; p < 0.00001) and platelet (HR, 2.77; 95% CI, 1.78 to 4.30; p < 0.00001) engraftment. BMT was associated with a significant decrease in the development of grades II-IV (HR, 0.75; 95% CI, 0.63 to 0.90; p = 0.002) and III-IV (HR, 0.63; 95% CI, 0.47 to 0.84; p = 0.001) acute GVHD as well as overall (HR, 0.70; 95% CI, 0.59 to 0.83; p < 0.0001) and extensive (HR, 0.60; 95% CI, 0.39 to 0.91; p = 0.002) chronic GVHD. BMT was associated with a higher incidence of relapse (HR, 1.91; 95% CI, 1.34 to 2.74; p = 0.0004). Comparable TRM (1.08; 95% CI, 0.56 to 2.10; p = 0.81), LFS (HR, 1.04; 95% CI, 0.83 to 1.30; p = 0.73), and OS (HR, 1.06; 95% CI, 0.81 to 1.39; p = 0.65) were demonstrated for both treatments. An inverse linear relationship was observed between the acute GVHD difference (PBSCT minus BMT) and the outcome of OS (p = 0.016). Our meta-analysis suggest that BMT leads to slower hematological recovery, increasing rates of relapse, and a lower risk of GVHD, but no significant difference in LFS and OS. A lower incidence of acute GVHD is associated with a superior OS.

Comparison of glucose-insulin-potassium and insulin-glucose as adjunctive therapy in acute myocardial infarction: a contemporary meta-analysis of randomised controlled trials.

BACKGROUND: There is conflicting evidence regarding two different insulin regimens for acute myocardial infarction (AMI), one focusing on delivering insulin ('insulin focus', glucose-insulin-potassium (GIK)) and one focusing on tight glycaemic control ('glycaemia focus', insulin-glucose). A longstanding controversy has focused on which strategy provides the greatest reduction in mortality. The aim of this study was to perform a meta-analysis of randomised controlled trials (RCTs) comparing GIK or insulin-glucose therapy versus standard therapy for AMI in the reperfusion era. METHODS: A MEDLINE/EMBASE/CENTRAL search was conducted of RCTs evaluating GIK or insulin-glucose as adjunctive therapy for AMI. The primary endpoint was all-cause mortality. The data were analysed with a random effect model. RESULTS: A total of 11 studies (including 23 864 patients) were identified, eight evaluating insulin focus with GIK and three evaluating glycaemia focus with insulin-glucose. Overall, insulin focus with GIK was not associated with a statistically significant effect on mortality (RR 1.07, 95% CI 0.89 to 1.29, p=0.487). Before the use of reperfusion, GIK also had no clear impact on mortality (RR 0.92, 95% CI 0.70 to 1.20, p=0.522). Pooled data from the three studies evaluating glycaemia focus showed that insulin-glucose did not reduce mortality in the absence of glycaemia control in patients with AMI with diabetes (RR 1.07, 95% CI 0.85 to 1.36, p=0.547). CONCLUSIONS: Current evidence suggests that GIK with insulin does not reduce mortality in patients with AMI. However, studies of glycaemia are inconclusive and it remains possible that glycaemic control is beneficial.

Meta-analysis: Noninvasive ventilation in acute cardiogenic pulmonary edema.

BACKGROUND: Noninvasive ventilation (NIV) is commonly used to treat patients with acute cardiogenic pulmonary edema (ACPE), but the findings of a recent large clinical trial suggest that NIV may be less effective for ACPE than previously thought. PURPOSE: To provide an estimate of the effect of NIV on clinical outcomes in patients with ACPE that incorporates recent trial evidence and explore ways to interpret that evidence in the context of preceding evidence that favors NIV. DATA SOURCES: PubMed and EMBASE from 1966 to December 2009, Cochrane Central Register of Controlled Trials and conference proceedings through December 2009, and reference lists, without language restriction. STUDY SELECTION: Randomized trials that compared continuous positive airway pressure and bilevel ventilation with standard therapy or each other. DATA EXTRACTION: Two independent reviewers extracted data. Outcomes examined were mortality, intubation rate, and incidence of new myocardial infarction (MI). DATA SYNTHESIS: Compared with standard therapy, continuous positive airway pressure reduced mortality (relative risk [RR], 0.64 [95% CI, 0.44 to 0.92]) and need for intubation (RR, 0.44 [CI, 0.32 to 0.60]) but not incidence of new MI (RR, 1.07 [CI, 0.84 to 1.37]). The effect was more prominent in trials in which myocardial ischemia or infarction caused ACPE in higher proportions of patients (RR, 0.92 [CI, 0.76 to 1.10] when 10% of patients had ischemia or MI vs. 0.43 [CI, 0.17 to 1.07] when 50% had ischemia or MI). Bilevel ventilation reduced the need for intubation (RR, 0.54 [CI, 0.33 to 0.86]) but did not reduce mortality or new MI. No differences were detected between continuous positive airway pressure and bilevel ventilation on any clinical outcomes for which they were directly compared. LIMITATIONS: The quality of the evidence base was limited. Definitions, cause, and severity of ACPE differed among the trials, as did patient characteristics and clinical settings. CONCLUSION: Although a recent large trial contradicts results from previous studies, the evidence in aggregate still supports the use of NIV for patients with ACPE. Continuous positive airway pressure reduces mortality more in patients with ACPE secondary to acute myocardial ischemia or infarction. PRIMARY FUNDING SOURCE: None.

A meta-analysis of the effects of atrial overdrive pacing on sleep apnea syndrome.

BACKGROUND: Atrial overdrive pacing is a novel method that has been used to treat patients with sleep apnea syndrome (SAS) in many trials. However, the effects of atrial overdrive pacing on SAS are unclear. METHODS: Studies were retrieved from the PubMed and EMBASE databases (1966 to January 2008), the Central Cochrane Controlled Trials Register (January 2008), and reference lists. Randomized controlled trials were selected that compared atrial overdrive pacing with nonpacing in SAS. Information on study design, patient characteristics, the apnea hypopnea index (AHI), and minimum arterial oxygen saturation (SaO2) was extracted. RESULTS: Eight trials that included a total of 129 patients were identified. The analysis showed that atrial overdrive pacing, as compared to nonpacing, reduced the AHI and increased the minimum SaO2 significantly in the subgroup of patients who presented predominantly with central sleep apnea syndrome (CSAS) (for AHI, mean difference [MD]=-17.08, 95% confidence interval [CI]: -23.25 to -10.91; for minimum SaO2, MD=4.00, 95% CI: 2.48 to 5.52, respectively). The AHI (MD=-2.94, 95% CI: -5.33 to -0.54) was also significantly reduced in the subgroup of patients who showed predominant obstructive sleep apnea syndrome (OSAS), but the result of the analysis of AHI in OSAS-predominant trials was not robust to the exclusion of some trials. There was weak evidence of an increase in minimum SaO2 in the subgroup in which OSAS was predominant (MD=0.13, 95% CI: -1.18 to 1.45). CONCLUSIONS: Atrial overdrive pacing appears to be effective in patients with CSAS. The role of atrial overdrive pacing in OSAS remains unclear.

Adipocytokines: a bridge connecting obesity and insulin resistance.

Overweight or obesity has become a critical health problem in the world. The association of obesity with type 2 diabetes mellitus (T2D) has been recognized for decades, and the major basis for this link is the ability of obesity to engender insulin resistance (IR). Adipose tissue is not only an energy depot but also an active endocrine organ. Furthermore, fat distribution in the body is important for the progress of IR. Many studies show that visceral fat is more important in relation to IR than subcutaneous fat. Circulating free fatty acids (FFAs) derived from adipocytes are elevated in many IR states and have been suggested to be a main underlying mechanism of IR in obesity-associated T2D. However, compelling evidence demonstrates that adipocytokines including several adipocyte-derived cytokines or hormones are also involved in obesity-induced IR. Therefore, we hypothesise that adipocytokines may be a bridge connecting obesity and IR, and abnormal fat depot distribution or visceral fat/subcutaneous fat ratio (V/S ratio) in obesity also could be a primer for IR. When visceral fat accumulates and V/S ratio deteriorates , just like a primer,in visceral obesity it should begin to display unhealthy effect begin to take place in the body. In addition to it, as one of physiological regulation mechanisms of the body, most of the adipocytokines from the visceral fat reduce the visceral fat volume or normalize the V/S ratio. Actually, on the contrary, with serum a change in the serum adipocytokine level and an imbalance of them in the body for a long term, it will become a pathological condition and various kinds of effects may contribute to the development of IR. If confirmed, this hypothesis may lead to the formulation of new pathogenesis and new therapeutic approaches to IR. For example, an effective slimming pill will be assessed in future on the basis of the decrease of V/S and serum adipocytokines level rather than of body weight.