6
views
0
recommends
+1 Recommend
1 collections
    0
    shares

      Call for Papers: Sex and Gender in Neurodegenerative Diseases

      Submit here before September 30, 2024

      About Neurodegenerative Diseases: 3.0 Impact Factor I 4.3 CiteScore I 0.695 Scimago Journal & Country Rank (SJR)

      • Record: found
      • Abstract: found
      • Article: found

      The Significance of Troponin Elevation for the Clinical Course and Outcome of First-Ever Ischaemic Stroke

      research-article

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Background: An increase in the troponin I (TnI) level is a marker of myocardial damage in acute coronary syndromes (ACS) and other conditions. According to the latest reports, an increase in the concentration of TnI in the acute phase of stroke relates to 1-34% of patients. The aim of this study was to evaluate the prevalence of elevated TnI concentration in patients with acute first-ever stroke and to examine its significance for the prediction of post-stroke disability degree and death within 30 days of stroke. An additional aim of the study was to compare the anatomic location of stroke in patients with normal and elevated TnI concentrations on the 1st day of stroke. Methods: Patients (M/F: 609/459; mean age 72 ± 11) with stroke numbering 1,068 were included in the prospective study. Their neurological deficit (National Institutes of Health Stroke Scale), TnI concentration (normal range ≤0.014 ng/ml), creatine kinase and ECG were examined on the 1st day of stroke. A follow-up and ECG were performed one day later in patients with abnormal TnI. The anatomical location of stroke (the right and left hemispheres and the brain stem) was compared in patients with normal and elevated TnI concentrations on the first day of stroke. The patients' functioning status was assessed using the by modified Rankin Scale (mRS) on the 30th day, and mortality was assessed within 30 days. The analysis was performed using a single and multi-factorial method of non-linear estimation for logistic regression in order to identify the independent factors for post-stroke disability at 4-6 points on the mRS on the 30th day following the onset and for death within 30 days of stroke in relation to the entire study group. The relative risk of a 4-6 point scoring on the mRS and of death among patients with abnormal TnI concentrations was also assessed. Results: Abnormal TnI concentration during stroke was observed in 9.73% of patients. The functioning status (mRS) of patients with elevated TnI was significantly worse 30 days post stroke as compared to patients with normal TnI concentration. Stroke was significantly more frequent in the right-hemisphere in patients with elevated TnI and no ischaemic changes in the ECG. For patients with ACS Tn+ during stroke, the mortality within 30 days after stroke was significantly more frequent than for patients without ACS Tn+. The abnormal TnI level neurological status on the 1st day of stroke and age were independent mortality factors within 30 days following stroke. Elevated TnI concentration, hypertension and neurological status on the 1st day of stroke were independent factors for post-stroke disability. Conclusions: Elevated TnI concentration occurs in 1/10 of patients with acute ischaemic stroke. It is connected with an unfavourable course of stroke leading to a significant disability and less independence in their everyday functioning. The right hemisphere is the most common site of stroke accompanied by elevated concentration of troponin in patients with no ischaemic changes in the electrocardiogram. Troponin-positive acute coronary syndrome in the period of acute stroke increases mortality within one month. Among patients with an abnormal troponin concentration in the acute phase of stroke, poor outcome is attributed to stroke severity on admission.

          Related collections

          Most cited references23

          • Record: found
          • Abstract: not found
          • Book: not found

          World Development Report 1993

          (1993)
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Intracellular compartmentation of cardiac troponin T and its release kinetics in patients with reperfused and nonreperfused myocardial infarction.

            In a previous study on the diagnostic efficiency of troponin T measurements in patients with suspected acute myocardial infarction (AMI), the authors found a high variability of troponin T serum concentration changes on day 1 in patients with AMI who underwent thrombolytic treatment. Therefore, the aims of the present study were to investigate the intracellular compartmentation of troponin T and to analyze the effects of AMI reperfusion on the appearance kinetics of cardiac troponin T in serum. Cardiac troponin T was measured with a newly developed bideterminant sandwich assay using cardiospecific, affinity-purified polyclonal antibodies and peroxidase-labeled monoclonal antibody. An unbound cytosolic troponin T pool was found in ultracentrifuged homogenates of myocardial tissue of different species ranging from 0.013 to 0.036 mg/g wet weight. The soluble troponin T molecule had electrophoretic properties identical to troponin T compartmented in the myofibrils. The clinical study group comprised 57 patients with AMI undergoing thrombolytic treatment. Blood flow to the infarct zone and point of time of reperfusion were tested by immediate and late angiography. The appearance of troponin T in serum on day 1 after the onset of AMI depended strongly on reperfusion and on duration of ischemia before reperfusion. Thus, in patients with early reperfused AMI, a marked peak in troponin T serum concentrations was found at 14 hours after the onset of pain. This early troponin T peak was absent in patients with AMI reperfusion occurring greater than 5.5 hours after the onset of pain and in patients with nonreperfused AMI. By contrast, the kinetics of troponin T release after the first day after AMI were unaffected by reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Lateralization in autonomic dysfunction in ischemic stroke involving the insular cortex.

              Autonomic nervous system dysfunction is a common complication of ischemic stroke. Clinical and experimental data indicate hemispheric lateralization in the control of autonomic activity. The insular cortex has also been shown to play a crucial role in the central autonomic network. The aim of this study was to assess cardio-autonomic dysfunction in patients with ischemic insular versus non-insular cortex infarction, and to demonstrate a possible lateralization in autonomic activity mediated by the insular cortex. Sympathetic function was prospectively assessed by determining plasma norepinephrine and epinephrine in 15 patients with left-hemisphere (LH; four insular infarction), and 14 with right-hemisphere (RH) middle cerebral artery (MCA) stroke (five insular infarction). Systolic and diastolic blood pressure and heart rate were recorded during the first 5 days after stroke. Sympathetic activity was significantly higher in insular than in non-insular infarction (p < 0.05) with concomitantly elevated cardiovascular parameters in insular stroke patients. The pathological activation of the sympathetic nervous system was most excessive in RH-stroke involving the insular cortex (p < 0.05). Our data indicate a hemispheric lateralization in autonomic activity which is mediated by the right-sided insular cortex. Patients with RH stroke involving the insular cortex are most susceptible to develop cardio-autonomic dysfunction.
                Bookmark

                Author and article information

                Journal
                CED
                Cerebrovasc Dis
                10.1159/issn.1015-9770
                Cerebrovascular Diseases
                S. Karger AG
                1015-9770
                1421-9786
                2014
                November 2014
                29 October 2014
                : 38
                : 3
                : 212-218
                Affiliations
                Departments of aNeurology, bGeneral Surgery and Angiology, and cNo. 2 of Cardiology, Medical University of Silesia Hospital No. 7, Professor Leszek Giec Upper Silesian Medical Centre, Katowice, Poland
                Author notes
                *Anetta Lasek-Bal, MD, PhD, Department of Neurology, Medical University of Silesia Hospital No. 7, Professor Leszek Giec Upper Silesian Medical Centre, ul. Ziołowa 45/47, PL-40-735 Katowice (Poland), E-Mail alasek@gcm.pl
                Article
                365839 Cerebrovasc Dis 2014;38:212-218
                10.1159/000365839
                25358959
                9ba12ee5-f9e4-4e1a-880a-37d8d5e1678c
                © 2014 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                History
                : 09 April 2014
                : 08 July 2014
                Page count
                Tables: 4, Pages: 7
                Categories
                Original Paper

                Geriatric medicine,Neurology,Cardiovascular Medicine,Neurosciences,Clinical Psychology & Psychiatry,Public health
                Troponin I,Acute stroke,Acute coronary syndrome

                Comments

                Comment on this article