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      ST Segment Elevation and Depressions in Supraventricular Tachycardia without Coronary Artery Disease

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      Case Reports in Cardiology

      Hindawi

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          Abstract

          ST segment changes are well documented in literature during supraventricular tachycardias. We present a case of a 21-year-old male who presents with chest pain, shortness of breath, and dizziness with an ECG showing atrioventricular reentrant tachycardia and diffuse ST segment depressions. Patient spontaneously converted to sinus rhythm, but he was still complaining of crushing chest pain. ECG taken after conversion showed sinus rhythm at a rate of 65 and showed obvious persistence of ST depressions in majority of leads. Emergent left heart catheterization showed normal coronaries. Such ST depression is suggestive of global ischemia in small intracardiac vessels that cannot be evaluated by left heart catheterization.

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          Most cited references 13

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          Narrative review: alternative causes for elevated cardiac troponin levels when acute coronary syndromes are excluded.

          Current guidelines for the diagnosis of non-ST-segment elevation myocardial infarction are largely based on an elevated troponin level. While this rapid and sensitive blood test is certainly valuable in the appropriate setting, its widespread use in a variety of clinical scenarios may lead to the detection of troponin elevation in the absence of thrombotic acute coronary syndromes. Many diseases, such as sepsis, hypovolemia, atrial fibrillation, congestive heart failure, pulmonary embolism, myocarditis, myocardial contusion, and renal failure, can be associated with an increase in troponin level. These elevations may arise from various causes other than thrombotic coronary artery occlusion. Given the lack of any supportive data at present, patients with nonthrombotic troponin elevation should not be treated with antithrombotic and antiplatelet agents. Rather, the underlying cause of the troponin elevation should be targeted. However, troponin elevation in the absence of thrombotic acute coronary syndromes still retains prognostic value. Thus, cardiac troponin elevations are common in numerous disease states and do not necessarily indicate the presence of a thrombotic acute coronary syndrome. While troponin is a sensitive biomarker to "rule out" non-ST-segment elevation myocardial infarction, it is less useful to "rule in" this event because it may lack specificity for acute coronary syndromes.
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            Causes of elevated troponin I with a normal coronary angiogram.

            The new definition of myocardial infarction (MI) emphasizes the pre-eminent role of troponin for diagnosis. Troponin rise indicates myocardial injury, but is not synonymous with infarction or ischaemia. To review the precipitating event for troponin elevation in patients with angiographically normal coronary arteries, in a district general hospital. Consecutive patients with elevated troponin I (TnI) who underwent angiography for suspected coronary disease were included in the present study if they had normal or mild disease (<50% diameter loss without complex features or thrombus). Precipitating event for TnI elevation was assigned on the totality of clinical evidence. Twenty-one patients qualified, with an average age of 50 years (range 33-73). Sixty-two per cent of participants were female. Troponin release was attributed to tachycardia in six patients, only two of whom had haemodynamic compromise. Physical exertion was the precipitating factor in two patients; pericarditis in two patients; and severe congestive heart failure in one patient. Ten of 21 patients had no identifiable cause for a rise in TnI concentration. Five of 21 patients had left-ventricular wall motion abnormalities. There were no deaths or MI at 41 +/- 24 weeks follow up. Troponin is a sensitive marker of myocardial injury and may rise following apparently minor insults. A rise in TnI concentration may have a cause other than acute coronary syndrome and may occur without significant angiographic coronary artery disease.
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              Cardiac troponin T alterations in myocardium and serum of rats after stressful, prolonged intense exercise.

              The goal of this study was to determine whether the stress of forced exercise would result in injury to the myocardium. Male rats with 8% of body weight attached to the tail were forced to swim 3.5 h (3.5S), forced to swim 5 h (5S), or pretrained for 8 days and then forced to swim 5 h (T5S). Rats were killed immediately after they swam (0 h PS) and at 3 h (3 h PS), 24 h (24 h PS), and 48 h after they swam (48 h PS). Tissue homogenates of the left ventricle were analyzed by Western blot analysis for cardiac troponin T (cTnT). Serum cTnT was quantified by immunoassay. Results indicated that, in the 3.5S, 5S, and T5S groups, serum cTnT was significantly (P < 0.01) increased at 0 and 3 h PS. The 5S group demonstrated a greater increase in serum cTnT than the 3.5S group (P < 0.01) and the T5S group (P < 0.01) at 0 h PS. Western blot analysis indicated significant decreases (P < 0. 01) in myocardial cTnT in the 5S group only at 0 h PS (P < 0.01) and 3 h PS (P < 0.05). Histological evidence of localized myocyte damage demonstrated by interstitial inflammatory infiltrates consisting of neutrophils, lymphocytes, and histiocytes, as well as vesicular nuclei-enlarged chromatin patterns, was observed in left ventricle specimens from the 5S group at 24 and 48 h PS. Our findings demonstrate that stressful, forced exercise induces alterations in myocardial cTnT and that training before exercise attenuates the exercise-induced heart damage.
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                Author and article information

                Contributors
                Journal
                Case Rep Cardiol
                Case Rep Cardiol
                CRIC
                Case Reports in Cardiology
                Hindawi
                2090-6404
                2090-6412
                2018
                13 December 2018
                : 2018
                Affiliations
                University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA
                Author notes

                Academic Editor: Alfredo E. Rodriguez

                Article
                10.1155/2018/2716312
                6311840
                Copyright © 2018 Fuad Habash et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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                Case Report

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