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Updated: Dec 17, 2025

Measuring Ascending Aortic Stiffness In Vivo in Mice Using Ultrasound
Published on: December 2, 2014
Sex-specific difference in the association between arterial stiffness and subclinical left ventricular dysfunction
Yuriko Yoshida1, Koki Nakanishi1, Masao Daimon1,2
1Department of Cardiovascular Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan.
Aims:
Increased arterial stiffness is one of the key mechanisms of heart failure with preserved ejection fraction (HFpEF). However, the possible association between arterial stiffness and subclinical left ventricular (LV) dysfunction and its sex-specific difference remains unclarified. LV strain is emerging as a highly sensitive tool to unmask early LV abnormalities.
Methods And Results:
We examined 1155 participants free of overt cardiovascular disease who underwent extensive cardiovascular examination. Speckle-tracking echocardiography was employed to assess LV global longitudinal strain (LVGLS) and circumferential strain (GCS), and arterial stiffness was assessed by cardio-ankle vascular index (CAVI). Mean age was 62 ± 12 years, and 56% were men. CAVI as continuous variable was associated with abnormal LVGLS (>-18.6%) independent of cardiovascular risk factors and echocardiographic parameters [adjusted odds ratio (OR) 1.23, P = 0.027] but not with LVGCS. In sex-stratified analysis, more pronounced association between quartiles of CAVI and abnormal LVGLS was observed in women than in men (unadjusted OR = 6.43 in women and 2.46 in men for upper quartile vs. lower quartile; both P < 0.01). CAVI was significantly associated with abnormal LVGLS independent of cardiovascular risk factors in both sexes. However, after further adjustment for LV mass index and diastolic parameters, the independent association persisted only in women (adjusted OR 1.67, P = 0.007), but not in men (adjusted OR 1.14, P = 0.227).
Conclusion:
Increased arterial stiffness was independently associated with decreased LVGLS even without overt cardiovascular disease; a sex-specific pattern exists in the alteration of vascular-ventricular coupling, which might partially explain the greater susceptibility to HFpEF in women.
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