Sex-specific difference in the association between arterial stiffness and subclinical left ventricular dysfunction

Abstract

Abstract Background Increased arterial stiffness has been proposed as one of the key mechanisms of incident heart failure with preserved ejection fraction (HFpEF). However, the possible association between arterial stiffness and subclinical left ventricular (LV) dysfunction and possible sex-specific differences remain unclarified. LV strain is emerging as a highly sensitive tool to unmask early LV abnormalities. Purpose We investigated whether increased arterial stiffness is independently associated with subclinical LV dysfunction in a large community-based cohort without overt cardiovascular disease. Methods We examined 1,155 participants 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). Results Mean age was 62±12 years, and 56% were male. CAVI as continuous variable was associated with abnormal LVGLS (>−18.6%), independent of cardiovascular risk factors and pertinent laboratory and echocardiographic parameters (adjusted odds ratio [OR] 1.23, p=0.034), whereas there was no relationship 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; Figure). Multivariable analyses demonstrated that 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 in women (adjusted OR 1.49, p=0.041), but not in men (adjusted OR 1.15, p=0.209). Conclusion Increased arterial stiffness was independently associated with decreased LVGLS even in the absence of 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. Funding Acknowledgement Type of funding source: None