Associations of Alterations in Pulsatile Arterial Load With Left Ventricular Longitudinal Strain

Zi Ye1, Thais Coutinho1, Patricia A Pellikka1

  • 1Division of Cardiovascular Diseases and the Gonda Vascular Center, Mayo Clinic, Rochester, Minnesota, USA.

Insights

Increased arterial stiffness, measured by characteristic aortic impedance (Zc), is linked to reduced left ventricular (LV) systolic function (global longitudinal strain). This finding highlights Zc as a key indicator of cardiac health in adults.

Area of Science:

  • Cardiology
  • Vascular Physiology
  • Echocardiography

Background:

  • Increased arterial stiffness elevates the heart's pulsatile load.
  • Arterial stiffness is a risk factor for cardiovascular disease.

Purpose of the Study:

  • To investigate the association between pulsatile load components and left ventricular (LV) systolic function, specifically global longitudinal strain (GLS).
  • To assess these associations in a community-based cohort with a family history of hypertension.

Main Methods:

  • 520 adults with normal LV ejection fraction underwent arterial tonometry and echocardiography with speckle tracking.
  • Measures of pulsatile load (characteristic aortic impedance (Zc), total arterial compliance (TAC), augmentation index (AI)) and GLS were quantified.
  • Sex-specific z-scores were used to assess associations of log-Zc, log-TAC, and AI with GLS.

Main Results:

  • Univariable analysis showed higher Zc correlated with worse GLS, while higher TAC and AI correlated with better GLS.
  • In multivariable models, only Zc remained significantly associated with GLS (β = 0.28, P < 0.001) after adjusting for age, sex, heart rate, LVEF, and mean arterial load.
  • This association persisted after further adjustment for cardiovascular risk factors and history of cardiovascular events.

Conclusions:

  • Higher characteristic aortic impedance (Zc), reflecting proximal aortic stiffness, is independently associated with impaired LV longitudinal function.
  • Zc is a significant predictor of GLS, independent of other cardiovascular risk factors.
Abstract

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