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      Time Course of Endothelin-1 Plasma Level in Patients with Acute Coronary Syndromes

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          Abstract

          An elevated plasma level of endothelin-1 was reported in several cardiovascular conditions including unstable angina pectoris and myocardial infarction. The present study was designed to evaluate the time course of the endothelin-1 release in unstable angina pectoris and to assess its relationship to the development of myocardial infarction and coronary vessel occlusion. The cohort studied included 32 patients with the clinical diagnosis of unstable angina pectoris who had been admitted to the coronary care unit and subsequently underwent coronary angiography (group A). Fourteen patients with chronic stable angina pectoris referred to routine diagnostic coronary angiography served as the control group (group B). A significant difference in the endothelin-1 plasma level was found between both groups, the values being 10.2 ± 5.3 and 6.0 ± 3.1 pg/ml (p < 0.01), respectively. There were, however, no significant differences between the following subdivisions of group A: patients with and without subsequent myocardial infarction; those with angiographically documented occlusion of at least one major branch of the coronary artery and no occlusion; and finally, those with persisting symptoms of angina pectoris and with favorable response to treatment. Neither was there any difference found among the subgroups differing in the time interval between the onset of chest pain and blood sampling. The time course of endothelin plasma concentrations showed elevated values lasting for more than 96 h after the index episode of prolonged chest pain. No correlation with the subsequent clinical course could be inferred. Thus, plasma endothelin level was elevated in patients with unstable angina pectoris and myocardial infarction and the increase persisted for several days after the onset of symptoms.

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          Most cited references 5

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          Expression of endothelin-1 in the lungs of patients with pulmonary hypertension.

          Pulmonary hypertension is characterized by an increase in vascular tone or an abnormal proliferation of muscle cells in the walls of small pulmonary arteries. Endothelin-1 is a potent endothelium-derived vasoconstrictor peptide with important mitogenic properties. It has therefore been suggested that endothelin-1 may contribute to increases in pulmonary arterial tone or smooth-muscle proliferation in patients with pulmonary hypertension. We studied the sites and magnitude of endothelin-1 production in the lungs of patients with various causes of pulmonary hypertension. We studied the distribution of endothelin-1-like immunoreactivity (by immunocytochemical analysis) and endothelin-1 messenger RNA (by in situ hybridization) in lung specimens from 15 control subjects, 11 patients with plexogenic pulmonary arteriopathy (grades 4 through 6), and 17 patients with secondary pulmonary hypertension and pulmonary arteriopathy of grades 1 through 3. In the controls, endothelin-1-like immunoreactivity was rarely seen in vascular endothelial cells. In the patients with pulmonary hypertension, endothelin-1-like immunoreactivity was abundant, predominantly in endothelial cells of pulmonary arteries with medial thickening and intimal fibrosis. Likewise, endothelin-1 messenger RNA was increased in the patients with pulmonary hypertension and was expressed primarily at sites of endothelin-1-like immunoreactivity. There was a strong correlation between the intensity of endothelin-1-like immunoreactivity and pulmonary vascular resistance in the patients with plexogenic pulmonary arteriopathy, but not in those with secondary pulmonary hypertension. Pulmonary hypertension is associated with the increased expression of endothelin-1 in vascular endothelial cells, suggesting that the local production of endothelin-1 may contribute to the vascular abnormalities associated with this disorder.
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            Endothelin-1 in primary pulmonary hypertension and the Eisenmenger syndrome.

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              Relation of elevated plasma endothelin in congenital heart disease to increased pulmonary blood flow.

              Endothelin-1 (ET), a potent vasoconstrictor peptide, has been found to be elevated in children with pulmonary hypertension associated with congenital heart defects. To evaluate the effect of pulmonary blood flow on ET concentrations, 5 ml blood samples were obtained peripherally at cardiac catheterization from 35 patients, ages 0.13 to 17 years (median 2). Plasma was extracted and ET measured by radioimmunoassay. Patients were classified into 2 groups based on the presence (group A) or absence (group B) of increased pulmonary blood flow defined as a Qp/Qs > or = 1.5. When the 13 patients (37%) in group A were compared with the 22 patients (63%) in group B there were no significant differences in age, cardiac index, or pulmonary and systemic resistances. ET concentrations were significantly higher in group A patients (median 3.25, range 0 to 16.5 vs median 0, range 0 to 6.35 pg/ml; p < or = 0.05). Pulmonary blood flow and pulmonary artery pressure were also higher in group A patients (p < or = 0.01). When patients within group A were subdivided into those with and without pulmonary hypertension, no difference was present in their ET concentrations (mean/SD: 4.4/4.3 vs 4.0/6.4 pg/ml, p = NS). Thus, ET is elevated in patients with congenital heart disease associated with left-to-right shunts and it appears that this increase is related to increased pulmonary blood flow independent of pulmonary artery pressure.
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                Author and article information

                Journal
                CRD
                Cardiology
                10.1159/issn.0008-6312
                Cardiology
                S. Karger AG
                0008-6312
                1421-9751
                1999
                August 1999
                06 August 1999
                : 91
                : 2
                : 114-118
                Affiliations
                Department of Medicine II, Charles University, Prague, Czech Republic
                Article
                6890 Cardiology 1999;91:114–118
                10.1159/000006890
                10449883
                © 1999 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.

                Page count
                Figures: 2, Tables: 3, References: 43, Pages: 5
                Categories
                Coronary Care

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