Showing papers by "Elliott M. Antman published in 1995"

Evaluation of a rapid bedside assay for detection of serum cardiac troponin T.

Abstract: Objective. —To evaluate a rapid, qualitative, bedside immunoassay for cardiac-specific troponin T (cTnT) using a handheld device containing monoclonal antibodies. Design. —Comparison of rapid cTnT assay with clinical standard for diagnosis of myocardial infarction (Ml). Setting. —Tertiary care university medical center. Patients. —A cohort of 100 patients admitted for evaluation of chest pain who had sufficient blood samples at presentation for measurement of creatine kinase, creatine kinase MB fraction, and rapid cTnT as well as adequate clinical data to establish the diagnosis of Ml. Intervention. —None; treating physicians were blinded to rapid cTnT results. Main Outcome Measures. —Sensitivity and specificity of rapid cTnT assay for Ml; likelihood ratios of positive and negative rapid cTnT assay results; relative risk (RR) for serious cardiac events with positive rapid cTnT assay result on admission. Results. —Sensitivity of the rapid cTnT assay increased from 33% within 2 hours from the onset of chest pain to 86% after 8 hours ( P Conclusions. —The rapid cTnT assay is a simple, efficient test that for the first time provides clinicians with a useful laboratory tool for point-of-care evaluation of patients with chest pain. ( JAMA . 1995;273:1279-1282)

Magnesium in Acute MI Timing Is Critical

Abstract: It is an axiom of coronary care medicine that infarct size is a pivotal determinant of the prognosis of patients with acute myocardial infarction (AMI). When one is able to limit the size of an AMI, one is rewarded with a reduction in the number of potentially life-threatening complications such as pulmonary edema, cardiogenic shock, ventricular septal defects, papillary muscle rupture, and ventricular tachyarrhythmias.1 Salvage of even a rim of epicardial tissue as the wave front of necrosis spreads from the endocardium might prevent infarct expansion, ventricular remodeling, and congestive heart failure.2 3 Reperfusion that is sufficiently early (within 15 to 20 minutes) after AMI may prevent ischemic zones of myocardium from progressing to infarction. However, with the possible exceptions of an AMI that develops during cardiac catheterization, of patients who receive prehospital thrombolysis, or of the rare patient who occludes a coronary artery in the Emergency Department or coronary care unit and receives extraordinarily prompt and successful thrombolysis, reperfusion in cases of human AMI results in a mixture of necrotic and salvaged myocytes. The amount of myocardium that is irreversibly damaged (area of necrosis divided by area at risk) is directly related to the duration of occlusion. Interventions that delay cell death (eg, β-blockers) may help to protect ischemic myocytes and leave a greater quantity of viable cells that can subsequently be rescued by reperfusion. More than a decade ago, Braunwald and Kloner2 emphasized that reperfusion therapy, while beneficial in terms of myocardial salvage, may come at a cost because of a process referred to as reperfusion injury. Four aspects of reperfusion injury have been recognized4 : (1) lethal reperfusion injury (reperfusion-induced death of cells that were still viable at the moment of restoration of blood flow), (2) vascular reperfusion injury (no-reflow phenomenon and loss …

Cardiac troponin T and point-of-care testing for myocardial infarction.

Abstract: To the Editor. —Despite their obvious enthusiasm for point-of-care testing for cardiac troponin T (cTnT), Dr Antman and colleagues 1 have not provided convincing evidence that this technology is either applicable or appropriate in the clinical setting. Many of the arguments used to justify using a test with a false-positive rate of 35% and a sensitivity ranging rom only 33% to a maximum of 86% are paper tigers. The time needed to perform creatine kinase (CK), CK-MB, and troponin assays on modern random-access chemistry and immunochemistry analyzers is as little as 17 minutes in the clinical laboratory, not 2 hours as the authors cited. Moreover, recent studies 2,3 comparing immunoassays for cardiac troponin (troponin T or I) with CK-MB show similar sensitivity of cardiac troponin to CK-MB for detection of acute mycocardial infarction. According to these studies, in the laboratory setting there was also an increased specificity for myocardial damage