(Circulation. 2007;116:II_368.)
© 2007 American Heart Association, Inc.
Vivien Thomas Young Investigator Competition |
Abstract 1746: Alterations in Transmural Myocardial Strain: An Early Marker of Left Ventricular Dysfunction in Mitral Regurgitation?
1 Stanford Univ, Stanford, CA
2 Rsch Institute of Palo Alto Med Foundation, Palo Alto, CA
3 Stanford Univ, Stanford, CA
INTRODUCTION: In asymptomatic patients with severe mitral regurgitation (MR), identifying subclinical LV dysfunction can guide the timing of surgical repair. We hypothesized that changes in LV transmural myocardial strain represent early markers of LV dysfunction in an ovine chronic MR model of low pressure volume overload.
METHODS: Twenty sheep were randomized to control (CTRL, n=8) or experimental (EXP, n=12) groups. In EXP, a 3.5– 4.8mm hole was created in the posterior mitral leaflet to generate "pure" MR. Thirteen radiopaque markers were surgically implanted to silhouette the LV chamber, and LV myocardial strains were measured using transmural bead columns inserted into the lateral equatorial and anterobasal LV walls. One and 12 weeks thereafter, 4-D marker coordinates every 17 msec were obtained radiographically in closed-chest, anesthetized conditions. Transmural normal strains were calculated from bead displacements along circumferential (ECC), longitudinal (ELL), and radial (ERR) axes during systole and diastolic filling.
RESULTS: MR grade was higher in EXP versus CTRL at both 1 and 12 weeks (3.0±0.4 vs. 0.7±0.8; 2.7±0.9 vs. 0.5±0.5, respectively, both P<0.001). At 12 weeks, LV mass index was greater in EXP vs. CTRL (201±18 vs. 173±17 g/m2, P<0.01). LVEDVI increased in EXP (115±17 to 134±31 mL/m2, P<0.05) from 1 to 12 weeks. Between the 1 and 12 week values, the change in BNP (–4.5±4.4 vs. –3.0±3.6 pmol/L), PRSW (9±13 vs. 23±18 mm Hg), tau (–3±11 vs. –4±7 ms), and systolic strains was similar between EXP and CTRL. The changes in longitudinal diastolic filling strains between 1 and 12 weeks, however, were greater in EXP vs. CTRL, predominantly subendocardial ELL (lateral: –0.08±0.05 vs. 0.02±0.14; anterior: –0.10±0.05 vs. –0.02±0.07, respectively, both P<0.01), but also in the midwall ELL (anterior: –0.09±0.07 vs. –0.02±0.05, p<0.05).
CONCLUSIONS: Twelve weeks of "pure" MR in this ovine model caused LV remodeling. Early changes in LV function were detected by longitudinal diastolic filling strains, but not by BNP, PRSW or tau. These alterations in transmural strains may prove useful in the clinical evaluation of latent LV dysfunction in asymptomatic patients with severe MR.
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