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Updated: Jun 17, 2026

Measuring Ascending Aortic Stiffness In Vivo in Mice Using Ultrasound
Published on: December 2, 2014
The association between left ventricular diastolic dysfunction and increased aortic stiffness can be explained by
Hüseyin Sürücü1, Ersan Tatli, Hakki Boz
1Cardiology Department, Private Avcilar Anadolu Hospital, Istanbul, Turkey. huseyinsurucu@yahoo.com.tr
Insights
Left ventricular diastolic dysfunction (LVDDF) is linked to increased aortic stiffness (IAS) in patients without coronary artery disease. This association may stem from neurohumoral factors rather than hemodynamic changes.
Area of Science:
- Cardiovascular Physiology
- Echocardiography
- Vascular Biology
Background:
- Left ventricular diastolic dysfunction (LVDDF) and increased aortic stiffness (IAS) are common cardiovascular conditions.
- Understanding the link between LVDDF and IAS is crucial for managing cardiovascular risk.
Purpose of the Study:
- To investigate the association between left ventricular diastolic dysfunction (LVDDF) and increased aortic stiffness (IAS) in patients without coronary artery disease (CAD).
- To explore potential mechanisms, including hemodynamic and neurohumoral factors, that explain this association.
Main Methods:
- Categorized patients without CAD into three groups based on left ventricular (LV) inflow patterns using tissue Doppler imaging (TDI).
- Measured aortic diameters and calculated aortic strain (AS) and aortic distensibility (AD).
- Analyzed echocardiographic parameters evaluating LV and aortic function.
Main Results:
- Aortic strain (AS) was significantly lower in patients with pseudonormalization (Group 3) and impaired LV relaxation (Group 2) compared to normal LV inflow (Group 1).
- Aortic distensibility (AD) was higher in the normal LV inflow group compared to the other two groups.
- No significant differences were found in hemodynamic parameters like stroke volume or pulse pressure among the groups.
Conclusions:
- The study confirms an association between LVDDF and IAS in patients without CAD.
- The findings suggest that neurohumoral mechanisms, rather than hemodynamic factors, may underlie the link between LVDDF and IAS.
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.
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