[STEMI mimics : ST elevations on ECG: alternative diagnoses to acute coronary occlusion]. / "STEMI mimics" : ST-Hebungen im EKG: Alternative Diagnosen zum akuten Koronarverschluss.

BACKGROUND: The electrocardiogram (ECG) is an integral part of basic emergency medical diagnosis and preoperative evaluation. In cases of ST elevation myocardial infarction (STEMI) immediate treatment is mandatory after correlation of ischemic symptoms with the ECG pattern. However, there are also ECG patterns that can imitate STEMI, possibly resulting in the true underlying diagnosis being missed and inappropriate therapy being initiated. OBJECTIVES: This paper provides an overview of the most important diagnoses that can imitate STEMI on ECG. MATERIAL AND METHODS: A literature search was carried out to determine the most important differential diagnoses of ST elevation on ECG. These STEMI mimics are discussed in detail and their relevance for emergency medicine is explained. RESULTS: This article provides an overview of differential diagnoses that should be known in emergency medicine when assessing an ECG with ST elevations. CONCLUSION: Good knowledge of the ECG patterns presented here can support decision-making in emergency medicine.

[High-risk ECGs in acute chest pain : Signs of acute ischemia beyond STEMI]. / Hochrisiko-EKG bei akutem Thoraxschmerz : Akute Ischämiezeichen abseits des STEMI.

BACKGROUND: Obtaining an electrocardiogram (ECG) is the gold standard for initial diagnostics of atraumatic chest pain. To provide optimal patient care, the treating physician has to be proficient in recognizing early signs of myocardial ischemia. Information from the clinical assessment and typical ECG signs have to be recognized promptly in order to diagnose myocardial ischemia early. METHODS: A selective literature search in international databases (PubMed, Cochrane Library, Google Scholar) was conducted; current, topic-specific websites and literature were also included and evaluated. RESULTS: Several subtle ECG abnormalities exist besides the typical ST-elevation myocardial infarction (STEMI) and well-known STEMI equivalents and may point to possible myocardial ischemia. DISCUSSION: To fully evaluate the ECG in patients with atraumatic chest pain, typical signs of ischemia like STEMI as well as subtle ECG signs should be recognized to allow early cardiac intervention.

Angiotensin II Receptor 1 Blockage Limits Brain Damage and Improves Functional Outcome After Brain Injury in Aged Animals Despite Age-Dependent Reduction in AT1 Expression.

Traumatic brain injury (TBI) is a frequent pathology associated with poor neurological outcome in the aged population. We recently observed accelerated cerebral inflammation in aged mice in response to TBI. Candesartan is a potent specific inhibitor of angiotensin II receptor type 1 (AT1) which limits cerebral inflammation and brain damage in juvenile animals after experimental TBI. In the present study, we show significantly lower posttraumatic AT1 mRNA levels in aged (21 months) compared to young (2 months) mice. Despite low cerebral At1 expression, pharmacologic blockade by treatment with candesartan [daily, beginning 30 min after experimental TBI by controlled cortical impact (CCI)] was highly effective in both young and aged animals and reduced histological brain damage by -20% after 5 days. In young mice, neurological improvement was enhanced by AT1 inhibition 5 days after CCI. In older animals, candesartan treatment reduced functional impairment already on day 3 after TBI and post-traumatic body weight (BW) loss was attenuated. Candesartan reduced microglia activation (-40%) in young and aged animals, and neutrophil infiltration (-40% to 50%) in aged mice, whereas T-cell infiltration was not changed in either age group. In young animals, markers of anti-inflammatory microglia M2a polarization [arginase 1 (Arg1), chitinase3-like 3 (Ym1)] were increased by candesartan at days 1 and 5 after insult. In older mice 5 days after insult, expression of Arg1 was significantly higher independently of the treatment, whereas Ym1 gene expression was further enhanced by AT1 inhibition. Despite age-dependent posttraumatic differences in At1 expression levels, inhibition of AT1 was highly effective in a posttreatment paradigm. Targeting inflammation with candesartan is, therefore, a promising therapeutic strategy to limit secondary brain damage independent of the age.

Influence of age on brain edema formation, secondary brain damage and inflammatory response after brain trauma in mice.

After traumatic brain injury (TBI) elderly patients suffer from higher mortality rate and worse functional outcome compared to young patients. However, experimental TBI research is primarily performed in young animals. Aim of the present study was to clarify whether age affects functional outcome, neuroinflammation and secondary brain damage after brain trauma in mice. Young (2 months) and old (21 months) male C57Bl6N mice were anesthetized and subjected to a controlled cortical impact injury (CCI) on the right parietal cortex. Animals of both ages were randomly assigned to 15 min, 24 h, and 72 h survival. At the end of the observation periods, contusion volume, brain water content, neurologic function, cerebral and systemic inflammation (CD3+ T cell migration, inflammatory cytokine expression in brain and lung, blood differential cell count) were determined. Old animals showed worse neurological function 72 h after CCI and a high mortality rate (19.2%) compared to young (0%). This did not correlate with histopathological damage, as contusion volumes were equal in both age groups. Although a more pronounced brain edema formation was detected in old mice 24 hours after TBI, lack of correlation between brain water content and neurological deficit indicated that brain edema formation is not solely responsible for age-dependent differences in neurological outcome. Brains of old naïve mice were about 8% smaller compared to young naïve brains, suggesting age-related brain atrophy with possible decline in plasticity. Onset of cerebral inflammation started earlier and primarily ipsilateral to damage in old mice, whereas in young mice inflammation was delayed and present in both hemispheres with a characteristic T cell migration pattern. Pulmonary interleukin 1ß expression was up-regulated after cerebral injury only in young, not aged mice. The results therefore indicate that old animals are prone to functional deficits and strong ipsilateral cerebral inflammation without major differences in morphological brain damage compared to young.