50 research outputs found

    Serum Cortisol Level as a Predictor of In-Hospital Mortality in Patients Undergoing Primary Percutaneous Intervention for ST Segment Elevation Myocardial Infarction

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    Introduction: Various laboratory markers have been proposed to assess prognosis in myocardial infarction. Serum cortisol is one such laboratory marker. There are only few studies done in the recent past which prove that cortisol is a prognostic marker in STEMI.Methods: We studied a total of 168 patients who presented with STEMI and underwent primary percutaneous intervention (PPCI) within 12 hours of symptom onset between April 2016 and November 2016.Results: The average age of study population was 61 ± 0.12 years. Males were predominant (n = 132, 78.57%). 155 patients survived, whereas 13 patients died in the hospital. Mean syntax score was 16.65 ±5. 33 among patients who died, whereas it was 13.11 ± 5.62 among survivors (P = 0.03). Mean cortisol was significantly higher among the patients who died (46.13 ± 14.61 mcg/dl) than the survivors (31.16 ± 13.16 mcg/dl) (P = 0.003). The ROC AUC for in-hospital mortality was 0.77 (95% confidence interval [CI], 0.645–0.897). An optimal cut-point identified from the ROC curve was a random serum cortisol concentration of 33.66 mcg/dl, with corresponding sensitivity and specificity of 69.2 % and 64 %, respectively. At a cut-point of 29.55 mcg/dl, sensitivity and specificity were 84.6 and 50 %, respectively.Conclusion: This study showed that serum cortisol level is a strong predictor of mortality in patients undergoing PPCI for STEMI. Levels more than 33.66 mcg/dl can predict mortality with a sensitivity of almost 70 percent and specificity of 64 percent

    Quantification of structural changes in the corpus callosumin children with profound hypoxic-ischaemic brain injury

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    Background Birth-related acute profound hypoxic–ischaemic brain injury has specific patterns of damage including the paracentral lobules. Objective To test the hypothesis that there is anatomically coherent regional volume loss of the corpus callosum as a result of this hemispheric abnormality. Materials and methods Study subjects included 13 children with proven acute profound hypoxic–ischaemic brain injury and 13 children with developmental delay but no brain abnormalities. A computerised system divided the corpus callosum into 100 segments, measuring each width. Principal component analysis grouped the widths into contiguous anatomical regions. We conducted analysis of variance of corpus callosum widths as well as support vector machine stratification into patient groups. Results There was statistically significant narrowing of the mid–posterior body and genu of the corpus callosum in children with hypoxic–ischaemic brain injury. Support vector machine analysis yielded over 95% accuracy in patient group stratification using the corpus callosum centile widths. Conclusion Focal volume loss is seen in the corpus callosum of children with hypoxic–ischaemic brain injury secondary to loss of commissural fibres arising in the paracentral lobules. Support vector machine stratification into the hypoxic–ischaemic brain injury group or the control group on the basis of corpus callosum width is highly accurate and points towards rapid clinical translation of this technique as a potential biomarker of hypoxic–ischaemic brain injur

    In vivo study of experimental pneumococcal meningitis using magnetic resonance imaging

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    <p>Abstract</p> <p>Background</p> <p>Magnetic Resonance Imaging (MRI) methods were evaluated as a tool for the study of experimental meningitis. The identification and characterisation of pathophysiological parameters that vary during the course of the disease could be used as markers for future studies of new treatment strategies.</p> <p>Methods</p> <p>Rats infected intracisternally with <it>S. pneumoniae </it>(n = 29) or saline (n = 13) were randomized for imaging at 6, 12, 24, 30, 36, 42 or 48 hours after infection. T1W, T2W, quantitative diffusion, and post contrast T1W images were acquired at 4.7 T. Dynamic MRI (dMRI) was used to evaluate blood-brain-barrier (BBB) permeability and to obtain a measure of cerebral and muscle perfusion. Clinical- and motor scores, bacterial counts in CSF and blood, and WBC counts in CSF were measured.</p> <p>Results</p> <p>MR images and dMRI revealed the development of a highly significant increase in BBB permeability (P < 0.002) and ventricle size (P < 0.0001) among infected rats. Clinical disease severity was closely related to ventricle expansion (P = 0.024).</p> <p>Changes in brain water distribution, assessed by ADC, and categorization of brain 'perfusion' by cortex ΔSI<sub>(bolus) </sub>were subject to increased inter-rat variation as the disease progressed, but without overall differences compared to uninfected rats (P > 0.05). Areas of well-'perfused' muscle decreased with the progression of infection indicative of septicaemia (P = 0.05).</p> <p>Conclusion</p> <p>The evolution of bacterial meningitis was successfully followed <it>in-vivo </it>with MRI. Increasing BBB-breakdown and ventricle size was observed in rats with meningitis whereas changes in brain water distribution were heterogeneous. MRI will be a valuable technique for future studies aiming at evaluating or optimizing adjunctive treatments</p

    Metabolic changes in concussed American football players during the acute and chronic post-injury phases

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    <p>Abstract</p> <p>Background</p> <p>Despite negative neuroimaging findings many athletes display neurophysiological alterations and post-concussion symptoms that may be attributable to neurometabolic alterations.</p> <p>Methods</p> <p>The present study investigated the effects of sports concussion on brain metabolism using <sup>1</sup>H-MR Spectroscopy by comparing a group of 10 non-concussed athletes with a group of 10 concussed athletes of the same age (mean: 22.5 years) and education (mean: 16 years) within both the acute and chronic post-injury phases. All athletes were scanned 1-6 days post-concussion and again 6-months later in a 3T Siemens MRI.</p> <p>Results</p> <p>Concussed athletes demonstrated neurometabolic impairment in prefrontal and motor (M1) cortices in the acute phase where NAA:Cr levels remained depressed relative to controls. There was some recovery observed in the chronic phase where Glu:Cr levels returned to those of control athletes; however, there was a pathological increase of m-I:Cr levels in M1 that was only present in the chronic phase.</p> <p>Conclusions</p> <p>These results confirm cortical neurometabolic changes in the acute post-concussion phase as well as recovery and continued metabolic abnormalities in the chronic phase. The results indicate that complex pathophysiological processes differ depending on the post-injury phase and the neurometabolite in question.</p
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