Document Detail


Increases in mitral leaflet radii of curvature with chronic ischemic mitral regurgitation.
MedLine Citation:
PMID:  15473478     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND AND AIM OF THE STUDY: Leaflet curvature is a primary determinant of leaflet stress, but no quantitative in-vivo leaflet curvature data exist. Chronic ischemic mitral regurgitation (CIMR) is associated with remodeling of the valvular-ventricular complex. It was hypothesized that leaflet radii of curvature (ROC) would change with such remodeling. METHODS: Twelve sheep had placement of radiopaque markers on the anterior (APM) and posterior (PPM) papillary muscles, mitral annulus, and anterior (AL) and posterior leaflet (PL) midlines. After 8 +/- 2 days, videofluoroscopy provided baseline 3-D marker data prior to creating inferior myocardial infarction (MI) by snare occlusion of the obtuse marginal coronary arteries. After 7 +/- 1 weeks, the animals were re-studied; 3-D marker coordinates were used to determine end-systolic leaflet ROC, leaflet length, annular septal-lateral diameter, and the distance of each papillary muscle to the mid-septal annulus and each commissure. RESULTS: Before and after CIMR, the AL had compound curvature, and CIMR increased ROC of both curves (proximal ROC 1.27 +/- 0.59 to 1.38 +/- 0.60 cm (p <0.05); distal ROC 1.41 +/- 0.61 to 2.60 +/- 1.52 cm (p < 0.05)). The PL ROC also increased with CIMR (from 2.01 +/- 1.40 to 3.46 +/- 3.93) (p <0.05). Multiple regression analysis determined that annular septal-lateral diameter (proximal AL and distal AL), distance from the APM to anterior commissure (distal AL), and PPM to mid-septal annulus (PL) were independent predictors of leaflet ROC. CONCLUSION: CIMR increased ROC of both the AL and PL. Leaflet extension may be a compensatory mechanism to minimize the regurgitant orifice, but the attendant increase in ROC will tend to augment leaflet stress. Annular and subvalvular geometry both affect leaflet curvature, and should be considered during mitral repair. These novel quantitative in-vivo data are now available for modification of finite element models, and for comparison to finite element model output.
Authors:
Frederick A Tibayan; Filiberto Rodriguez; Frank Langer; Mary K Zasio; Lynn Bailey; David Liang; George T Daughters; Matts Karlsson; Neil B Ingels; D Craig Miller
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The Journal of heart valve disease     Volume:  13     ISSN:  0966-8519     ISO Abbreviation:  J. Heart Valve Dis.     Publication Date:  2004 Sep 
Date Detail:
Created Date:  2004-10-11     Completed Date:  2004-11-09     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  9312096     Medline TA:  J Heart Valve Dis     Country:  England    
Other Details:
Languages:  eng     Pagination:  772-8     Citation Subset:  IM    
Affiliation:
Department of Cardiovascular and Thoracic Surgery, Stanford University School of Medicine, Stanford, California 94305-5247, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Body Weights and Measures
Chronic Disease
Fluoroscopy / methods
Humans
Mitral Valve / physiopathology*,  radiography*
Mitral Valve Insufficiency / etiology,  physiopathology*,  radiography*
Models, Animal
Myocardial Infarction / complications*
Sheep
Ventricular Remodeling / physiology
Video Recording
Grant Support
ID/Acronym/Agency:
HL-29589/HL/NHLBI NIH HHS; HL-67025/HL/NHLBI NIH HHS; HL-67563/HL/NHLBI NIH HHS; HL67025-01S1/HL/NHLBI NIH HHS

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