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Study Objective: Point-of-care testing reduces time to cardiac marker results in patients evaluated for acute coronary syndromes, yet evidence this translates to a decreased length of stay is lacking. We hypothesized that point-of-care testing decreases length of stay in patients being evaluated for acute coronary syndromes in the emergency department (ED)., Methods: Patients being evaluated for possible acute coronary syndromes at 4 EDs in the United States were randomized to having point-of-care markers as well as central laboratory markers, or central laboratory markers only (laboratory arm). Point-of-care markers were obtained using early serial testing at presentation and at 90, 180, and 360 minutes as required by the treating physician. Evaluation, treatment, and disposition decisions were at the treating physician's discretion. Length of stay was from presentation to the time of departure from the ED, either to an inpatient setting or to home., Results: There were 1,000 patients in each study arm. There were 520 patients discharged home from the ED. Median (interquartile range) time to discharge home was 4.6 hours (3.5 to 6.1 hours) in laboratory patients and 4.5 hours (3.5 to 6.1 hours) in point-of-care patients. Median (interquartile range) time to transfer to an inpatient setting for admitted patients was 5.5 hours (4.2 to 7.5 hours) in laboratory patients, and 5.4 hours (4.1 to 7.3 hours) in point-of-care patients. At one site, time to transfer to the floor was reduced in the point-of-care arm compared with the laboratory arm (difference in medians 0.45 hours; 95% confidence interval [CI] -0.14 to 1.04 hours). At one site, time to ED departure for discharged patients was higher in the point-of-care arm than the laboratory arm (difference in medians 1.25 hours; 95% CI 0.13 to 2.36 hours)., Conclusion: The effect of point-of-care testing on length of stay in the ED varies between settings. At one site, point-of-care testing decreased time to admission, whereas at another, point-of-care testing increased time to discharge. Potential effects of point-of-care testing on patient throughput should be considered in the full context of ED operations.

Study Objective: We compared the accuracy of multidetector computed tomography (CT) coronary angiography with stress nuclear imaging for the detection of an acute coronary syndrome or 30-day major adverse cardiac events in low-risk chest pain patients., Methods: This was a prospective study of the diagnostic accuracy of myocardial perfusion imaging and multidetector CT in low-risk chest pain patients. The target condition was an acute coronary syndrome (confirmed >70% coronary stenosis on coronary artery catheterization) or major adverse cardiac events within 30 days. Patients were low risk by Reilly/Goldman criteria and had negative serial ECGs and cardiac markers. All had both rest/stress sestamibi nuclear imaging and multidetector CT. Patients with abnormal stress nuclear imaging results (reversible perfusion defects) or multidetector CT results (stenosis >50% or calcium score >400) were considered for cardiac catheterization, and those with discordant results had a greater than 30-day reevaluation (including ECG) by a cardiologist. All were followed up for evidence of major adverse cardiac events within 30 days by review of hospital records and structured telephone interview. Primary outcomes were the accuracy of multidetector CT and myocardial perfusion imaging for the detection of an acute coronary syndrome and 30-day major adverse cardiac events., Results: Of the 92 patients, 7 (8%) were excluded because of uninterpretable multidetector CT scans. Of the remaining 85 study patients (49+/-11 years, 53% men), 7 (8%) were found to have the target condition, with all having significant coronary stenosis (88%+/-9%) and none having myocardial infarction or major adverse cardiac events during 30 days. Stress nuclear imaging results were negative in 72 (85%) patients, and multidetector CT results were negative in 73 (86%) patients. The sensitivity of stress nuclear imaging was 71% (95% confidence interval [CI] 36% to 92%), and multidetector CT was 86% (95% CI 49% to 97%), and the specificity was 90% (95% CI 81% to 95%) and 92% (95% CI 84% to 96%), respectively. The negative predictive value of stress nuclear imaging and multidetector CT was 97% (95% CI 90% to 99%) and 99% (95% CI 93% to 100%), respectively, and the positive predictive value was 38% (95% CI 18% to 64%) and 50% (95% CI 25% to 75%), respectively., Conclusion: The accuracy of multidetector CT is at least as good as that of stress nuclear imaging for the detection and exclusion of an acute coronary syndrome in low-risk chest pain patients.

Brain damage accompanying cardiac arrest and resuscitation is frequent and devastating. Neurons in the hippocampus CA1 and CA4 zones and cortical layers III and V are selectively vulnerable to death after injury by ischemia and reperfusion. Ultrastructural evidence indicates that most of the structural damage is associated with reperfusion, during which the vulnerable neurons develop disaggregation of polyribosomes, peroxidative damage to unsaturated fatty acids in the plasma membrane, and prominent alterations in the structure of the Golgi apparatus that is responsible for membrane assembly. Reperfusion is also associated with vulnerable neurons with prominent production of messenger RNAs for stress proteins and for the proteins of the activator protein-1 complex, but these vulnerable neurons fail to efficiently translate these messages into the proteins. The inhibition of protein synthesis during reperfusion involves alteration of translation initiation factors, specifically serine phosphorylation of the alpha-subunit of eukaryotic initiation factor-2 (elF-2 alpha). Growth factors--in particular, insulin--have the potential to reverse phosphorylation of elF-2 alpha, promote effective translation of the mRNA transcripts generated in response to ischemia and reperfusion, enhance neuronal defenses against radicals, and stimulate lipid synthesis and membrane repair. There is now substantial evidence that the insulin-class growth factors have neuron-sparing effects against damage by radicals and ischemia and reperfusion. This new knowledge may provide a fundamental basis for a rational approach to "cerebral resuscitation" that will allow substantial amelioration of the often dismal neurologic outcome now associated with resuscitation from cardiac arrest.

Lipid peroxidation is thought to be a major contributing factor in neurological injury following cardiac arrest. Because iron availability is a prerequisite for lipid peroxidation, this experiment was designed to examine the natural time course of iron release, lipid peroxidation, and cerebral polyunsaturated fatty acid content following a 15-minute cardiac arrest in dogs. Large mongrel dogs were anesthetized with ketamine and halothane and divided into three groups of five each. In two groups, cardiac arrest was induced with KCl. After 15 minutes of cardiac arrest, the dogs were resuscitated by five minutes of internal cardiac massage, epinephrine, bicarbonate, and internal defibrillation. All ten dogs were resuscitated and supported by a standard intensive care protocol until tissue harvest. A 3-g portion of parietal cerebral cortex was obtained from the nonischemic dogs (n = 5), or at two hours (n = 5), or eight hours (n = 5) after resuscitation. Total tissue iron was measured by an atomic emission spectrometer; low molecular weight species (LMWS) iron by the o-phenanthroline test on an ultrafiltered sample; and lipid peroxidation by both the thiobarbituric acid test (TBARS) and determination of the tissue content of lipid double bonds, calculated by first fractionating the lipids by gas-liquid chromatography and then measuring the double bonds in each fraction by spectrometry and summing the results. Univariate ANOVA demonstrated all variables except total tissue iron to have significance at P less than .02. At two hours of reperfusion, LMWS iron and TBARS were significantly elevated above nonischemic control levels.(ABSTRACT TRUNCATED AT 250 WORDS)