Abstract 12806: A Speckle-tracking Echocardiographic Multi-layer LV Global Strain Study to Evaluate Specific Compensation Mechanisms to Maintain Cardiac Function in Subjects With Hypertrophied LV Myocardium
Introduction: A novel transthoracic echocardiography (TTE) technique enables multi-layer measurement of left ventricular (LV) endocardial and epicardial layer myocardial strain.
Hypothesis: There may be compensation mechanisms to maintain cardiac function in subjects with hypertrophied LV myocardium. To evaluate mechanisms in hypertrophied LV myocardium in subjects with preserved LV ejection fraction (LVEF) using multi-layer TTE analysis.
Methods: A total of 105 subjects with preserved LVEF (41 hypertrophic cardiomyopathy subjects (31 male; 62±15 yr), 40 with severe aortic stenosis (19 male; 74±5 yr; transaortic maximum velocity 4.8±0.6m/s; aortic valve area index 0.46±0.12cm2/m2), and 24 controls (12 male; 54±18 yr)) underwent TTE (Vivid E9). Apical 4-, 2-, and 3-chamber GLS views and parasternal short axis GCS views at mitral valve level, papillary muscle, and apex were acquired. Strain measurements (absolute values) of endocarial and epicardial layers were performed.
Results: Correlation coefficients (CC) between inter ventricular septum thickness in end diastole (IVSTd) and endocardial and epicardial GLS were -0.62, and -0.60 for apical 4 chamber, -0.60, and -0.62 for 2 chamber, and -0.58, and -0.57 for 3 chamber views, and -0.64, and -0.64 for averaged, respectively. GLS values showed significant negative correlation with degree of LV hypertrophy. CC between IVSTd and GCS values of endocardial and epicardial layer were -0.17, and -0.42 for mitral valve, -0.17, and -0.38 for papillary muscle, -0.15, and -0.37 for apex levels, respectively. GCS degree of correlation with IVSTd was < GLS, especially in endocardial layer. GCS values of endocardial layer did not significantly correlate with IVSTd for all levels.
Conclusions: GLS and GCS decrease proportionally with increase in degree of LV hypertrophy. Degree of decrement of GCS was smaller than with GLS, especially in endocardial layer. This may be a compensation mechanism to maintain cardiac function.
Author Disclosures: K. Ozawa: None. N. Funabashi: None. H. Takaoka: None. Y. Kobayashi: None.
- © 2015 by American Heart Association, Inc.