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      Myocardial Stress in Patients with Acute Cerebrovascular Events

      case-report

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          Abstract

          Signs of myocardial involvement are common in patients with acute cerebrovascular events. ST segment deviations, abnormal left ventricular function, increased N-terminal pro-brain natriuretic peptide (NT-proBNP), prolonged QT interval, and/or raised troponins are observed in up to one third of the patients. The huge majority of these findings are fully reversible. The changes may mimic myocardial infarction, but are not necessarily identical to coronary thrombosis. Based on the literature these signs may represent an acute catecholamine release provoked by the cerebrovascular catastrophe itself and not coronary thrombosis. However, all patients with signs of cardiac involvement during acute cerebrovascular events should receive a cardiological follow-up in order to exclude concomitant ischemic heart disease.

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          Cardiac-specific troponin I levels to predict the risk of mortality in patients with acute coronary syndromes.

          E Braunwald, M Schactman, M J Tanasijevic … (1996)
          In patients with acute coronary syndromes, it is desirable to identify a sensitive serum marker that is closely related to the degree of myocardial damage, provides prognostic information, and can be measured rapidly. We studied the prognostic value of cardiac troponin I levels in patients with unstable angina or non-Q-wave myocardial infarction. In a multicenter study, blood specimens from 1404 symptomatic patients were analyzed for cardiac troponin I, a serum marker not detected in the blood of healthy persons. The relation between mortality at 42 days and the level of cardiac troponin I in the specimen obtained on enrollment was determined both before and after adjustment for baseline characteristics. The mortality rate at 42 days was significantly higher in the 573 patients with cardiac troponin I levels of at least 0.4 ng per milliliter (21 deaths, or 3.7 percent) than in the 831 patients with cardiac troponin I levels below 0.4 ng per milliliter (8 deaths, or 1.0 percent; P or = 65 years). In patients with acute coronary syndromes, cardiac troponin I levels provide useful prognostic information and permit the early identification of patients with an increased risk of death.
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            Catecholamines, infection, and death in acute ischemic stroke.

            Manuel Gómez-Carrillo, Sergio Amaro, Ferran Torres … (2007)
            Experimental studies have recently suggested that acute ischemia may facilitate the appearance of fatal infections as part of a brain-induced immunodepression syndrome. However, the mechanisms and neurological consequences of infections complicating acute ischemic stroke have received much less attention at the bedside. The incidence of infection and death after non-septic stroke was compared in this prospective study with longitudinal changes of cytokines, leukocytes, normetanephrine (NMN) and metanephrine (MN) in 75 consecutive patients. In multivariate analysis, infection, n = 13 (17%), was associated with the upper quartile of MN (OR 3.51, 95% CI 1.30-9.51), neurological impairment (NIHSS) on admission (OR 3.99, 95% CI 1.34-11.8), monocyte count (OR 1.78, 95% CI 1.13-2.79), and increased interleukin (IL)-10 (OR 1.54, 95% CI 1.00-2.38). Mortality at 3 months, n = 16 (21%), was associated with increased levels of NMN on admission (OR 2.34 95% CI 1.15-4.76), NIHSS score (OR 2.57, 95% CI 1.29-5.11), and higher IL-6 levels (OR 1.29, 95% 1.00-1.67). These findings suggest that acute ischemic stroke is associated with an early activation of the sympathetic adrenomedullar pathway that lowers the threshold of infection and increases the risk of death. Moreover, these findings are independent of the blood borne effects of pro- and anti-inflammatory cytokines, and circulating leukocytes.
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              Left ventricular wall motion abnormalities in patients with subarachnoid hemorrhage: neurogenic stunned myocardium.

              Tatsuji Kono, Hiroshi Morita, Toshihiko Kuroiwa … (1994)
              The purpose of this study was to determine whether a relation exists between electrocardiographic (ECG) abnormalities and left ventricular wall motion in patients with subarachnoid hemorrhage. Although ECG changes simulating acute myocardial infarction are frequently seen in patients with subarachnoid hemorrhage, their relation to left ventricular wall motion has not been established. Twelve patients with subarachnoid hemorrhage were classified according to the presence of ST segment elevation in at least two consecutive leads on admission: seven patients with ST segment elevation (group I) and five patients without ST segment elevation (group II). No patients had a previous history of heart disease. Left ventricular regional wall motion was evaluated by the centerline method. The mean (+/- SEM) duration from onset of subarachnoid hemorrhage to left ventriculography was 9 +/- 3 h in group I and 10 +/- 1 h in group II. Coronary angiography was performed to rule out wall motion abnormalities due to coronary artery disease while the ST segment was still elevated. Two-dimensional echocardiography was used to evaluate wall motion thereafter. All patients in group I showed ST segment elevation in ECG leads V4 to V6. Wall motion of the left ventricular apex was significantly reduced in group I compared with group II (-2.48 +/- 0.41 vs. -0.45 +/- 0.72, p < 0.02). No patients showed organic stenosis or vasospasm, or both, of epicardial coronary arteries. Wall motion abnormalities decreased echocardiographically in all patients, but one patient in group I died in hospital at 2 or 3 weeks after the onset of subarachnoid hemorrhage, when the T wave was inverted in leads V4 to V6. These findings suggest that patients with subarachnoid hemorrhage and ST segment elevation may demonstrate transient corresponding regional wall motion abnormalities. The mechanism of neurogenic stunned myocardium was not clearly elucidated in the present study.
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                Author and article information

                Journal
                Journal ID (publisher-id): CRD
                Journal ID (nlm-ta): Cardiology
                Journal ID (doi): 10.1159/issn.0008-6312
                Title: Cardiology
                Publisher: S. Karger AG
                ISSN (Print): 0008-6312
                ISSN (Electronic): 1421-9751
                Publication date Subscription-year: 2008
                Publication date (Print): April 2008
                Publication date (Electronic): 31 October 2007
                Volume: 110
                Issue: 2
                Pages: 123-128
                Affiliations
                aGlobal Development, Novo Nordisk, Bagsværd, and bDepartment of Cardiology Y, Bispebjerg Hospital, Copenhagen, Denmark
                Article
                Publisher ID: 110491 Other ID: Cardiology 2008;110:123–128
                DOI: 10.1159/000110491
                PubMed ID: 17975312
                SO-VID: 63bdb98c-ea5e-4ab3-bfa0-7e6119bfd901
                Copyright © © 2007 S. Karger AG, Basel
                License:

                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
                Date received : 05 January 2007
                Date accepted : 17 April 2007
                Page count
                Tables: 3, References: 51, Pages: 6
                Categories
                Subject: Review

                ScienceOpen disciplines: General medicine,Neurology,Cardiovascular Medicine,Internal medicine,Nephrology
                Keywords: ECG,Myocardial infarction,Troponin,Intracerebral hemorrhage,Stroke,N-Terminal pro-brain natriuretic peptide
                Data availability:
                ScienceOpen disciplines: General medicine, Neurology, Cardiovascular Medicine, Internal medicine, Nephrology
                Keywords: ECG, Myocardial infarction, Troponin, Intracerebral hemorrhage, Stroke, N-Terminal pro-brain natriuretic peptide

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