| Literature DB >> 9859037 |
C Piper1, M Wiemer, H P Schultheiss, D Horstkotte.
Abstract
While morphologic alteration of parts of the mitral valve apparatus (ventricular wall, papillary muscles, chordae tendineae, valve annulus and leaflets) may result in a loss of its functional integrity (primary mitral regurgitation, MR) mitral annulus dilatation following left ventricular enlargement or change in chamber geometry and consecutive opening of the angle between papillary muscles and valve annulus cause secondary MR. Irrespective of these etiologies MR is chronically progressive and much more than the severity of MR the grade of myocardial adaptation to the chronic volume overload is of prognostic significance. Inadequate myocardial adaptation is demonstrated by an increase of the echocardiographically determined radius (r) to wall thickness (Th) ratio (r/Th > 3.0), indicating increasing left ventricular wall stress or by an insufficient increase of the left ventricular ejection fraction (< or = 5% of resting values) under exercise conditions, e.g. with radionuclide angiocardiography (RNV). Stressecho may replace RNV in the future for this indication. Actually, stress echo is not reliable to determine changes in left ventricular ejection fraction at rest versus exercise because of systematic errors and error reproduction. There are preliminary reports on biochemical markers like noradrenaline or tumor necrosis factor alpha being helpful to determine the breakdown of myocardial adaptation mechanisms. Surgical intervention is indicated in chronic MR irrespective of the hemodynamic severity, if myocardial adaptation is inadequate. If mitral reconstruction, the surgical technique of choice, remains insufficient to restore normal valve function, mitral valve replacement with preservation of the subvalvular apparatus is unavoidable. For a deceleration of the progressive volume overload in chronic MR for which a surgical intervention is not yet indicated, a long-term afterload reducing medical therapy preferably with long acting ACE-inhibitors seem to be prognostically favorable.Entities:
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Year: 1998 PMID: 9859037 DOI: 10.1007/bf03043403
Source DB: PubMed Journal: Herz ISSN: 0340-9937 Impact factor: 1.443