Context The chest pain history, physical examination, determination of coronary artery disease (CAD) risk factors, and the initial electrocardiogram compose the information immediately available to clinicians to help determine the probability of acute myocardial infarction (AMI) or acute coronary syndrome (ACS) in patients with chest pain. However, conflicting data exist about the usefulness of the chest pain history and which components are most useful. Objective To identify the elements of the chest pain history that may be most helpful to the clinician in identifying ACS in patients presenting with chest pain. Evidence Acquisition MEDLINE and Ovid were searched from 1970 to September 2005 by using specific key words and Medical Subject Heading terms. Reference lists of these articles and current cardiology textbooks were also consulted. Evidence Synthesis Certain chest pain characteristics decrease the likelihood of ACS or AMI, namely, pain that is stabbing, pleuritic, positional, or reproducible by palpation (likelihood ratios [LRs] 0.2-0.3). Conversely, chest pain that radiates to one shoulder or both shoulders or arms or is precipitated by exertion is associated with LRs (2.3-4.7) that increase the likelihood of ACS. The chest pain history itself has not proven to be a powerful enough predictive tool to obviate the need for at least some diagnostic testing. Combinations of elements of the chest pain history with other initially available information, such as a history of CAD, have identified certain groups that may be safe for discharge without further evaluation, but further study is needed before such a recommendation can be considered reasonable. Conclusion Although certain elements of the chest pain history are associated with increased or decreased likelihoods of a diagnosis of ACS or AMI, none of them alone or in combination identify a group of patients that can be safely discharged without further diagnostic testing.

Background: Millions of head computed tomography (CT) scans are ordered annually, but the extent of

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Apoptotic myonuclei appear during myogenesis and in diseased muscles. To investigate cell death regulation in skeletal muscle, we examined how members of the Bcl‐2 family of apoptosis regulators are expressed and function in the C2C12 muscle cell line and in primary muscle cells at different stages of development. Both anti‐apoptotic (Bcl‐W, Bcl‐XL) and pro‐apoptotic (Bad, Bak, Bax) members of the Bcl‐2 family were expressed in developing skeletal muscle in vivo. Each was also expressed in embryonic (E11–12), fetal (E15–16), and neonatal muscle stem cells, myoblasts, and myotubes in vitro. In contrast, Bcl‐2 expression was limited to a small group of mononucleate, desmin‐positive, myogenin‐negative muscle cells that were seen in fetal and neonatal, but not embryonic, muscle cell cultures. The cell surface protein Sca‐1, which is associated with muscle and blood stem cells, was found on ∼1/2 of these Bcl‐2–positive cells. Loss of Bcl‐2 did not affect expression of other family members, because neonatal muscles of wild‐type and Bcl‐2–null mice had similar amounts of Bcl‐XL, Bcl‐W, Bad, Bak, and Bax mRNAs. Loss of Bcl‐2 did have functional consequences; however, because neonatal muscles of Bcl‐2–null mice had only ∼2/3 as many fast muscle fibers as muscles in wild‐type mice. Thus, Bcl‐2 function is required for particular stages of fetal and postnatal myogenesis. © 2001 Wiley‐Liss, Inc.

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