ST-Segment Depression in Leads I and aVL: Artifactual or Pathophysiological Findings?

The 12-lead electrocardiogram (ECG) is a routinely performed test but is susceptible to misinterpretation even byexperienced physicians. We report a case of a 72-year-old lady with no prior cardiac history presented to our hospitalwith atypical chest pain. Her initial electrocardiogram shows an initial ST depression followed by positive deflectionsleads I and aVL. Non-physiological ST segment and T-wave changes are also observed in the precordial leads V2 to V6. By contrast, these abnormalities are notably absent in lead II. A repeat of the ECG taken 30 minutes later reveals the resolution of most abnormalities seen in the initial ECG on a background of high-frequency noise in the limb leads. She was referred to the cardiology department for further management. An urgent echocardiogram revealed no regional wall motion abnormalities with preserved ejection fraction, and her coronary angiogram revealed no significant coronary stenosis. This case illustrates the importance of understanding different factors that can cause ST segment abnormalities, notably artifactual changes that can mimic ST segment myocardial infarction.

Histology of Brain Trauma and Hypoxia-Ischemia

Forensic pathologists encounter hypoxic-ischemic (HI) brain damage or traumatic brain injuries (TBI) on an almost daily basis. Evaluation of the findings guides decisions regarding cause and manner of death. When there are gross findings of brain trauma, the cause of death is often obvious. However, microscopic evaluation should be used to augment the macroscopic diagnoses. Histology can be used to seek evidence for TBI in the absence of gross findings, e.g., in the context of reported or suspected TBI. Estimating the survival interval after an insult is often of medicolegal interest; this requires targeted tissue sampling and careful histologic evaluation. Retained tissue blocks serve as forensic evidence and also provide invaluable teaching and research material. In certain contexts, histology can be used to demonstrate nontraumatic causes of seemingly traumatic lesions. Macroscopic and histologic findings of brain trauma can be confounded by concomitant HI brain injury when an individual survives temporarily after TBI. Here we review the histologic approaches for evaluating TBI, hemorrhage, and HI brain injury. Amyloid precursor protein (APP) immunohistochemistry is helpful for identifying damaged axons, but patterns of damage cannot unambiguously distinguish TBI from HI. The evolution of hemorrhagic lesions will be discussed in detail; however, timing of any lesion is at best approximate. It is important to recognize artifactual changes (e.g., dark neurons) that can resemble HI damage. Despite the shortcomings, histology is a critical adjunct to the gross examination of brains.

Pearls and pitfalls in neural CGRP immunohistochemistry

This review outlines the pearls and pitfalls of calcitonin-gene related protein (CGRP) immunohistochemistry of the brain. Pearls In 1985, CGRP was first described in cerebral arteries using immunohistochemistry. Since then, cerebral CGRP (and, using novel antibodies, its receptor components) has been widely scrutinized. Here, we describe the distribution of cerebral CGRP and pay special attention to the surprising reliability of results over time. Pitfalls Pitfalls might include a fixation procedure, antibody clone and dilution, and interpretation of results. Standardization of staining protocols and true quantitative methods are lacking. The use of computerized image analysis has led us to believe that our examination is objective. However, in the steps of performing such an analysis, we make subjective choices. By pointing out these pitfalls, we aim to further improve immunohistochemical quality. Recommendations Having a clear picture of the tissue/cell morphology is a necessity. A primary morphological evaluation with, for example, hematoxylin-eosin, helps to ensure that small changes are not missed and that background and artifactual changes, which may include vacuoles, pigments, and dark neurons, are not over-interpreted as compound-related changes. The antigen-antibody reaction appears simple and clear in theory, but many steps might go wrong. Remember that methods including the antigen-antibody complex rely on handling/fixation of tissues or cells, antibody shipping/storing issues, antibody titration, temperature/duration of antibody incubation, visualization of the antibody and interpretation of the results. Optimize staining protocols to the material you are using.

Equipment-related Electrocardiographic Artifacts

Interference of the monitored or recorded electrocardiogram is common within operating room and intensive care unit environments. Artifactual signals, which corrupt the normal cardiac signal, may arise from internal or external sources. Electrical devices used in the clinical setting can induce artifacts by various different mechanisms. Newer diagnostic and therapeutic modalities may generate artifactual changes. These artifacts may be nonspecific or may resemble serious arrhythmia. Clinical signs, along with monitored waveforms from other simultaneously monitored parameters, may provide the clues to differentiate artifacts from true changes on the electrocardiogram. Simple measures, such as proper attention to basic principles of electrocardiographic measurement, can eliminate some artifacts. However, in persistent cases, expert help may be required to identify the precise source and minimize interference on the electrocardiogram. Technological advancements in processing the electrocardiographic signal may be useful to detect and eliminate artifacts. Ultimately, an improved understanding of the artifacts generated by equipment, and their identifying characteristics, is important to avoid misinterpretation, misdiagnosis, and iatrogenic complication.