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The Association between Left Ventricular Diastolic Dysfunction and Increased Aortic Stiffness Can Be Explained by Possible Neurohumoral Mechanisms
Author(s) -
Sürücü Hüseyin,
Tatli Ersan,
Boz Hakki,
Meriç Mehmet
Publication year - 2010
Publication title -
echocardiography
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.404
H-Index - 62
eISSN - 1540-8175
pISSN - 0742-2822
DOI - 10.1111/j.1540-8175.2009.01017.x
Subject(s) - cardiology , medicine , diastole , blood pressure
Objective: In our study, we tried to find an answer to the question “How could the association between left ventricular diastolic dysfunction (LVDDF) and increased aortic stiffness (IAS) be explained?” Methods: Cases without coronary artery disease (CAD) were divided into three groups according to their left ventricular (LV) inflow patterns and their LV basal‐lateral annulus pulsed‐wave tissue Doppler imaging (pw‐TDI). Group 1 (n = 38) represented the normal LV inflow pattern while Group 2 (n = 54) represented impaired LV relaxation and Group 3 (n = 18) represented pseudonormalization. Aortic diameters were measured by using M‐mode at a level that is 3 cm above the aortic valve. Aortic strain (AS) and aortic distensibility (AD) were calculated by using aortic diameters and pulse pressure. Results: In Group 3, AS was lower compared to Groups 1 and 2 (respectively P < 0.001, P = 0.040). AS was also lower in Group 2 compared to Group 1 (P = 0.012). AD was higher in Group 1 compared to Groups 2 and 3 (respectively P = 0.01, P < 0.001). Early diastolic velocity of aortic pw‐TDI was higher in normal LV inflow compared to Groups 2 and 3 (respectively P = 0.022, P = 0.050). Unfortunately, none of echocardiographic parameters that evaluate LV and aortic functions together (stroke volume, pulse pressure/stroke volume, pulse pressure/stroke volume index) were different among the groups. Conclusion: The results of our study clearly showed the association between LVDDF and IAS in cases without CAD. Additionally, it was concluded that this togetherness could be explained not by hemodynamic factors but by possible neurohumeral mechanisms. (Echocardiography 2010;27:275‐281)