96 research outputs found
DIAGNOSING ACUTE CORONARY SYNDROME IN THE EMERGENCY DEPARTMENT USING HIGH SENSITIVITY TROPONIN I
Timely diagnosis of acute coronary syndrome (ACS), the most lethal manifestation of ischemic heart disease, remains challenging. Due to limitations in the diagnostic accuracy and costs associated with current methods for diagnosing ACS, evaluating patients for ACS in the emergency department (ED) can last up to 24 hours. The consequences of such prolonged ED evaluation are: high personal cost to the patient, significant financial costs to the healthcare system (estimated at 4 billion annually), and additional strain on an already overstretched emergency medical care system.
Measurement of circulating levels of cardiac troponin (cTn) is central to the diagnosis of acute myocardial infarction. Recent advances in clinical chemistry have yielded significant improvements in the analytic performance of cardiac troponin assays (cTn), resulting in superior sensitivity and precision. These high sensitivity cTn (hsTn) assays are able to detect up to ten-fold lower concentrations of cTn than current generation cTn, resulting in earlier diagnosis of acute myocardial infarction (AMI), reclassification of some unstable angina patients as AMI and shortened duration of the rule out AMI period for some patients. However, they also result in an increase in the number of non-ACS patients who will have elevated hsTn values, amplifying the clinical challenge of determining which patients with elevated cTn warrant inpatient admission versus outpatient management. There are insufficient data to guide the use of hsTn for diagnosing ACS in the ED.
Chapter 1 is an introductory chapter that discusses the current paradigm of ACS evaluation in the emergency department (ED), and the promise and challenges associated with clinical use of hsTnI to diagnose ACS in the ED. Chapter 2 is a prospective cohort study that quantifies for the first time in an ED located in the United States of America (USA), the frequency and prognostic implications of new cTn elevations when a high sensitivity troponin I (hsTnI) assay is used. This chapter also characterizes factors associated with new cTn elevations and explores the effects of these new elevations on potential hospital admissions. Chapter 3 is a cross-sectional study that examines the frequency and determinants of high sensitivity troponin I (hsTnI) values in emergency department (ED) patients with a primary non-cardiac diagnosis. Chapter 4 is a cross-sectional study that determines whether hsTnI can be used as a screening test to identify suspected ACS patients who do not have significant coronary artery stenosis (candidates for early discharge). In the concluding chapter 5, I will discuss future directions of this work and propose a new paradigm for evaluating ACS in the ED using hsTnI
Dynamic Changes in HighāSensitivity Cardiac Troponin I Are Associated with Dynamic Changes in Sum Absolute QRST Integral on Surface Electrocardiogram in Acute Decompensated Heart Failure
Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/135259/1/anec12379_am.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/135259/2/anec12379.pd
Bayesian hierarchical EMAX model for doseĆ¢ response in early phase efficacy clinical trials
Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/149669/1/sim8167_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/149669/2/sim8167.pd
Developing Technical Expertise in Emergency MedicineāThe Role of Simulation in Procedural Skill Acquisition
Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/72919/1/j.1553-2712.2008.00218.x.pd
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Association of High-Sensitivity Troponin with Cardiac CT Angiography Evidence of Myocardial and Coronary Disease in a Primary Prevention Cohort of Men: Results from MACS.
BackgroundHigh-sensitivity cardiac troponin (hs-cTn) elevations are associated with incident cardiovascular disease events in primary prevention samples. However, the mechanisms underlying this association remain unclear.MethodsWe studied 458 men without known cardiovascular disease who participated in the cardiovascular disease substudy of the Multicenter AIDS Cohort Study and had cardiac CT angiography. We used multivariable linear and logistic regression models to examine the cross-sectional associations between coronary artery stenosis, coronary artery plaque, indexed left ventricular mass (LVMi), and the outcome of hs-cTnI. We also evaluated the associations between HIV serostatus or use of highly active antiretroviral therapy (HAART) and hs-cTnI.ResultsThe mean age was 54 years, 54% were white, and 61% were HIV infected. In multivariable-adjusted logistic models, comparing the highest quartile of LVMi with the lowest quartile, the odds ratio (OR) of hs-cTnI ā„75th percentile was 2.59 (95% CI, 1.20-5.75). There was no significant association between coronary stenosis severity or plaque type and hs-cTnI in linear models; however, in logistic regression models, coronary artery stenosis ā„70% (8% of sample) was marginally associated with a higher likelihood (OR, 2.75 [95% CI, 1.03, 7.27]) of having hs-cTnI ā„75th percentile. There were no associations between HIV serostatus or HAART use and hs-cTnI in either linear or logistic models.ConclusionAmong primary prevention men with or at risk for HIV, hs-cTnI concentrations were strongly associated with LVMi but were not associated with HIV infection or treatment status or with coronary plaque type or stenosis until the extremes of severity (ā„70% stenosis)
DRD2 C957T polymorphism is associated with improved 6-month verbal learning following traumatic brain injury
Traumatic brain injury (TBI) often leads to heterogeneous clinical outcomes, which may be influenced by genetic variation. A single-nucleotide polymorphism (SNP) in the dopamine D2 receptor (DRD2) may influence cognitive deficits following TBI. However, part of the association with DRD2 has been attributed to genetic variability within the adjacent ankyrin repeat and kinase domain containing 1 protein (ANKK1). Here, we utilize the Transforming Research and Clinical Knowledge in Traumatic Brain Injury Pilot (TRACK-TBI Pilot) study to investigate whether a novel DRD2 C957T polymorphism (rs6277) influences outcome on a cognitive battery at 6 months following TBI-California Verbal Learning Test (CVLT-II), Wechsler Adult Intelligence Test Processing Speed Index Composite Score (WAIS-PSI), and Trail Making Test (TMT). Results in 128 Caucasian subjects show that the rs6277 T-allele associates with better verbal learning and recall on CVLT-II Trials 1-5 (T-allele carrier 52.8 Ā± 1.3 points, C/C 47.9 Ā± 1.7 points; mean increase 4.9 points, 95% confidence interval [0.9 to 8.8]; p = 0.018), Short-Delay Free Recall (T-carrier 10.9 Ā± 0.4 points, C/C 9.7 Ā± 0.5 points; mean increase 1.2 points [0.1 to 2.5]; p = 0.046), and Long-Delay Free Recall (T-carrier 11.5 Ā± 0.4 points, C/C 10.2 Ā± 0.5 points; mean increase 1.3 points [0.1 to 2.5]; p = 0.041) after adjusting for age, education years, Glasgow Coma Scale, presence of acute intracranial pathology on head computed tomography scan, and genotype of the ANKK1 SNP rs1800497 using multivariable regression. No association was found between DRD2 C947T and non-verbal processing speed (WAIS-PSI) or mental flexibility (TMT) at 6 months. Hence, DRD2 C947T (rs6277) may be associated with better performance on select cognitive domains independent of ANKK1 following TBI
DRD2 C957T polymorphism is associated with improved 6-month verbal learning following traumatic brain injury
Traumatic brain injury (TBI) often leads to heterogeneous clinical outcomes, which may be influenced by genetic variation. A single-nucleotide polymorphism (SNP) in the dopamine D2 receptor (DRD2) may influence cognitive deficits following TBI. However, part of the association with DRD2 has been attributed to genetic variability within the adjacent ankyrin repeat and kinase domain containing 1 protein (ANKK1). Here, we utilize the Transforming Research and Clinical Knowledge in Traumatic Brain Injury Pilot (TRACK-TBI Pilot) study to investigate whether a novel DRD2 C957T polymorphism (rs6277) influences outcome on a cognitive battery at 6 months following TBI-California Verbal Learning Test (CVLT-II), Wechsler Adult Intelligence Test Processing Speed Index Composite Score (WAIS-PSI), and Trail Making Test (TMT). Results in 128 Caucasian subjects show that the rs6277 T-allele associates with better verbal learning and recall on CVLT-II Trials 1-5 (T-allele carrier 52.8 Ā± 1.3 points, C/C 47.9 Ā± 1.7 points; mean increase 4.9 points, 95% confidence interval [0.9 to 8.8]; p = 0.018), Short-Delay Free Recall (T-carrier 10.9 Ā± 0.4 points, C/C 9.7 Ā± 0.5 points; mean increase 1.2 points [0.1 to 2.5]; p = 0.046), and Long-Delay Free Recall (T-carrier 11.5 Ā± 0.4 points, C/C 10.2 Ā± 0.5 points; mean increase 1.3 points [0.1 to 2.5]; p = 0.041) after adjusting for age, education years, Glasgow Coma Scale, presence of acute intracranial pathology on head computed tomography scan, and genotype of the ANKK1 SNP rs1800497 using multivariable regression. No association was found between DRD2 C947T and non-verbal processing speed (WAIS-PSI) or mental flexibility (TMT) at 6 months. Hence, DRD2 C947T (rs6277) may be associated with better performance on select cognitive domains independent of ANKK1 following TBI
Apolipoprotein E epsilon 4 (APOE-Īµ4) genotype is associated with decreased 6-month verbal memory performance after mild traumatic brain injury
Introduction: The apolipoprotein E (APOE) Īµ4 allele associates with memory impairment in neurodegenerative diseases. Its association with memory after mild traumatic brain injury (mTBI) is unclear. Methods: mTBI patients (Glasgow Coma Scale score 13ā15, no neurosurgical intervention, extracranial Abbreviated Injury Scale score ā¤1) aged ā„18 years with APOE genotyping results were extracted from the Transforming Research and Clinical Knowledge in Traumatic Brain Injury Pilot (TRACK-TBI Pilot) study. Cohorts determined by APOE-Īµ4(+/ā) were assessed for associations with 6-month verbal memory, measured by California Verbal Learning Test, Second Edition (CVLT-II) subscales: Immediate Recall Trials 1ā5 (IRT), Short-Delay Free Recall (SDFR), Short-Delay Cued Recall (SDCR), Long-Delay F
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Prior traumatic brain injury is a risk factor for in-hospital mortality in moderate to severe traumatic brain injury: a TRACK-TBI cohort study.
OBJECTIVES: An estimated 14-23% of patients with traumatic brain injury (TBI) incur multiple lifetime TBIs. The relationship between prior TBI and outcomes in patients with moderate to severe TBI (msTBI) is not well delineated. We examined the associations between prior TBI, in-hospital mortality, and outcomes up to 12 months after injury in a prospective US msTBI cohort. METHODS: Data from hospitalized subjects with Glasgow Coma Scale score of 3-12 were extracted from the Transforming Research and Clinical Knowledge in Traumatic Brain Injury Study (enrollment period: 2014-2019). Prior TBI with amnesia or alteration of consciousness was assessed using the Ohio State University TBI Identification Method. Competing risk regressions adjusting for age, sex, psychiatric history, cranial injury and extracranial injury severity examined the associations between prior TBI and in-hospital mortality, with hospital discharged alive as the competing risk. Adjusted HRs (aHR (95% CI)) were reported. Multivariable logistic regressions assessed the associations between prior TBI, mortality, and unfavorable outcome (Glasgow Outcome Scale-Extended score 1-3 (vs. 4-8)) at 3, 6, and 12 months after injury. RESULTS: Of 405 acute msTBI subjects, 21.5% had prior TBI, which was associated with male sex (87.4% vs. 77.0%, p=0.037) and psychiatric history (34.5% vs. 20.7%, p=0.010). In-hospital mortality was 10.1% (prior TBI: 17.2%, no prior TBI: 8.2%, p=0.025). Competing risk regressions indicated that prior TBI was associated with likelihood of in-hospital mortality (aHR=2.06 (1.01-4.22)), but not with hospital discharged alive. Prior TBI was not associated with mortality or unfavorable outcomes at 3, 6, and 12 months. CONCLUSIONS: After acute msTBI, prior TBI history is independently associated with in-hospital mortality but not with mortality or unfavorable outcomes within 12 months after injury. This selective association underscores the importance of collecting standardized prior TBI history data early after acute hospitalization to inform risk stratification. Prospective validation studies are needed. LEVEL OF EVIDENCE: IV. TRIAL REGISTRATION NUMBER: NCT02119182
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