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      Eclipsed Mitral Regurgitation: A New Form of Functional Mitral Regurgitation for an Unusual Cause of Heart Failure with Normal Ejection Fraction

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          Abstract

          Background: Transient functional mitral regurgitation (MR) has never been reported as a cause of heart failure (HF) with normal ejection fraction (EF) in the absence of epicardial coronary artery stenosis. Results: Performance of echocardiography in patients with acute HF before initiation of HF medical treatment allowed identification of three patients with normal EF but transient massive functional MR during the HF episode. In all patients, massive MR occurred as a consequence of sudden extreme apical tenting of both leaflets with total lack of coaptation, despite normal EF and absence of detectable left ventricular (LV) remodeling, and despite absence of significant stenosis on coronary arteries. In all patients MR was triggered by methylergonovine injection and was reversible either spontaneously or after nitroglycerine administration, leaving patients with normal echocardiogram between HF episodes. In two patients, long-term administration of calcium channel blockers prevented recurrences of MR and HF, whereas in one, mitral valve was eventually replaced. Conclusion: Sudden reversible apical tenting of mitral leaflets with subsequent torrential MR and acute HF can occur despite normal EF, absence of pre-existing LV remodeling and absence of coronary artery stenosis. This atypical type of functional MR is an unusual mechanism of HF in patients with normal LVEF.

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          Most cited references 12

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          The pathogenesis of acute pulmonary edema associated with hypertension.

          Patients with acute pulmonary edema often have marked hypertension but, after reduction of the blood pressure, have a normal left ventricular ejection fraction (> or =0.50). However, the pulmonary edema may not have resulted from isolated diastolic dysfunction but, instead, may be due to transient systolic dysfunction, acute mitral regurgitation, or both. We studied 38 patients (14 men and 24 women; mean [+/-SD] age, 67+/-13 years) with acute pulmonary edema and systolic blood pressure greater than 160 mm Hg. We evaluated the ejection fraction and regional function by two-dimensional Doppler echocardiography, both during the acute episode and one to three days after treatment. The mean systolic blood pressure was 200+/-26 mm Hg during the initial echocardiographic examination and was reduced to 139+/-17 mm Hg (P< 0.01) at the time of the follow-up examination. Despite the marked difference in blood pressure, the ejection fraction was similar during the acute episode (0.50+/-0.15) and after treatment (0.50+/-0.13). The left ventricular regional wall-motion index (the mean value for 16 segments) was also the same during the acute episode (1.6+/-0.6) and after treatment (1.6+/-0.6). No patient had severe mitral regurgitation during the acute episode. Eighteen patients had a normal ejection fraction (at least 0.50) after treatment. In 16 of these 18 patients, the ejection fraction was at least 0.50 during the acute episode. In patients with hypertensive pulmonary edema, a normal ejection fraction after treatment suggests that the edema was due to the exacerbation of diastolic dysfunction by hypertension--not to transient systolic dysfunction or mitral regurgitation.
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            Diastolic heart failure can be diagnosed by comprehensive two-dimensional and Doppler echocardiography.

            There are many myocardial and non-myocardial conditions that cause heart failure with normal left ventricular ejection fraction (LVEF). Among them, diastolic heart failure (heart failure due to diastolic dysfunction) is the most common cause of heart failure with normal LVEF. Diastolic heart failure easily can be diagnosed by comprehensive two-dimensional and Doppler echocardiography, which can demonstrate abnormal myocardial relaxation, decreased compliance, and increased filling pressure in the setting of normal LV dimensions and preserved LVEF. Therefore, diastolic heart failure should always be considered when LVEF is normal on two-dimensional echocardiography in patients with clinical evidence of heart failure. The diagnosis can be confirmed if Doppler echocardiography and myocardial tissue imaging provide evidence for impaired myocardial relaxation (i.e., decreased longitudinal velocity of the mitral annulus during early diastole and decreased propagation velocity mitral inflow), decreased compliance (shortened mitral A-wave duration and mitral deceleration time), and increased filling pressure (shortened isovolumic relaxation time and an increased ratio between early diastolic mitral and mitral annular velocities). Early identification of diastolic dysfunction in asymptomatic patients by the use of echocardiography may provide an opportunity to manage the underlying etiology to prevent progression to diastolic heart failure.
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              The role of ischemic mitral regurgitation in the pathogenesis of acute pulmonary edema.

              Acute mitral regurgitation may cause pulmonary edema, but the pathogenetic role of chronic ischemic mitral regurgitation, a dynamic condition, has not yet been characterized. We prospectively studied 28 patients (mean [+/-SD] age, 65+/-11 years) with acute pulmonary edema and left ventricular systolic dysfunction and 46 patients without a history of acute pulmonary edema. The two groups were matched for all baseline characteristics. Patients underwent quantitative Doppler echocardiography during exercise. Exercise-induced changes in the left ventricular volume, the ejection fraction, the mitral regurgitant volume, the effective regurgitant orifice area, and the transtricuspid pressure gradient were compared in patients with and without acute pulmonary edema. The two groups had similar clinical and baseline echocardiographic characteristics. They also had similar exercise-induced changes in heart rate, systolic blood pressure, and left ventricular volumes. In the univariate analysis, patients with recent pulmonary edema had a much higher increase than did the patients without pulmonary edema in mitral regurgitant volume (26+/-14 ml vs. 5+/-14 ml, P<0.001), the effective regurgitant orifice area (16+/-10 mm2 vs. 2+/-9 mm2, P<0.001), and the transtricuspid pressure gradient (29+/-10 mm Hg vs. 13+/-11 mm Hg, P<0.001). In the multivariate analysis, exercise-induced changes in the effective regurgitant orifice area (P<0.001), in the transtricuspid pressure gradient (P=0.001), and in the left ventricular ejection fraction (P=0.02) were independently associated with a history of recent pulmonary edema. In patients with left ventricular systolic dysfunction, acute pulmonary edema is associated with the dynamic changes in ischemic mitral regurgitation and the resulting increase in pulmonary vascular pressure. Copyright 2004 Massachusetts Medical Society.
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                Author and article information

                Journal
                CRD
                Cardiology
                10.1159/issn.0008-6312
                Cardiology
                S. Karger AG
                0008-6312
                1421-9751
                2008
                April 2008
                10 October 2007
                : 110
                : 1
                : 29-34
                Affiliations
                aCardiology Department and bService Central de Biophysique et Médecine Nucléaire, Timone Hospital, Marseille, France; cDivision of Cardiovascular Diseases and Internal Medicine, Mayo Clinic and Mayo Foundation, Rochester, Minn., USA
                Article
                109403 Cardiology 2008;110:29–34
                10.1159/000109403
                17934266
                © 2007 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, References: 19, Pages: 6
                Categories
                Novel Insights from Clinical Experience

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