KIM Dae-Hee

Dae-Hee KIM

Cardiac Imaging Center, Asan Medical Center, University of Ulsan College of Medicine, Korea

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To date, advance in real time 3D echocardiography technique made it possible to measure mitral leaflet area （MLA） non-invasively under physiologic condition and had been validated against excised specimen.
Mitral leaflets are not static structure. It is distensible, and capable of active remodeling. Acute stressful physiologic tension can increasese the length of mitral leaftlet up to 15％. Leaflet length reverts to normal when tension is released. Moreover, chronic tension caused by leaflet tethering leads to permanent increases of MLA more than 30％ in patients with inferior myocardial infarction or dilated cardiomyopathy compared with normal subject. Recent investigations using in vivo imaging and molecular biology techniques have proven that anatomically normal human valve leaflets can undergo active elongation when stretched by displaced papillary muscles in the infarcted heart, yet such adaptation is often insufficient, resulting in ischemic or functional mitral regurgitation. Active leaflet adaptation can be induced by transition of endothelial to mesenchymal progenitor cell by growth factors. Among these cytokines, there is growing recognition about transforming growth factor-β （TGF-β） pathways influencing valve growth. Moreover, TGF-β is multifunctional cytokine involved in organ development, cardiac fibrosis, cardiac hypertrophy and inflammation. Given that recent studies suggest that the expression of TGF-β is upregulated in parallel with left ventricular mass in animal model or patients with pressure overloaded left ventricular hypertrophy, it is likely that hypertrophic stimuli may influence on the mitral leaflet. However, the effects of LV hypertrophic response on MLA itself and other mitral valve apparatus have not been elucidated.
With regard to aortic valve, a fundamental question is whether the aortic leaflets enlarge in response to aortic root stretch, and whether such adaptation effectively compensates for root dilatation. We therefore tested the hypothesis using new technique: aortic leaflet enlargement occurs with aortic root dilatation; but the degree of leaflet enlargement relative to the annulus becomes limited with greater root dilatation, resulting in insufficient leaflet tissue and aortic regurgitation.