Background and aim of the study: Endocardial indices of left ventricular (LV) systolic function overestimate myocardial performance in hypertrophic left ventricles. Midwall fractional shortening (mFS) is a more reliable index of systolic performance. Aortic stenosis (AS) is a common cause of LV hypertrophy (LVH), but midwall mechanics in this condition have not been analyzed. Also, a tendency towards hyperdynamic LV chamber function has been reported in women with AS in comparison with men, but whether there exist gender-related discrepancies in midwall performance is not known.
Methods: The study group included 147 patients with AS and normal chamber systolic function. LV diameters and thicknesses, LV mass, relative wall thickness (RWT), endocardial fractional shortening, stroke volume, ejection fraction (EF), mFS and stress-corrected mFS were determined.
Results: Patients with AS showed depressed mFS (16.2 ± 2.5% versus 18.8 ± 2.4%, p <0.0001) and stress-corrected mFS (84.3 ± 13.8% versus 100.0 ± 12.6%, p <0.0001) when compared to controls. The subset with moderate AS had lower mFS (15.9 ± 2.0%)

than those with mild AS (16.9 ± 2.4%), and further depression was present in subjects with severe AS (13.8 ± 2.2%, p <0.0001). A similar trend was observed for stress-corrected mFS (mild AS, 88.5 ± 13.3%; moderate AS, 82.0 ± 11.5%; severe AS, 71.2 ± 12.0%, p <0.0001). Multivariate analysis identified RWT as the best predictor of mFS and stress-corrected mFS. Logistic regression showed that depressed stress-corrected mFS was independently associated with the presence of symptoms. Endocardial fractional shortening and EF were increased in women compared to men, but there were no gender-related differences in mFS (16.2 ± 2.5% versus 16.1 ± 2.4%, p = 0.84) and stress-corrected mFS (84.0 ± 14.1% versus 84.5 ± 13.5%, p = 0.82).
Conclusion: Aortic stenosis is associated with depression in LV midwall mechanics. Systolic midwall performance reduces as the severity of valve disease increases, and this relationship is mediated by parallel changes in LV geometry.


The Journal of Heart Valve Disease 2006;15:639-650