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Acute and chronic ventricular-arterial coupling in systole and diastole: insights from an elderly hypertensive model

Brian P Shapiro1, Carolyn S P Lam, Jeetendra B Patel

  • 1Division of Cardiovascular Diseases, Mayo Clinic and Foundation, Rochester, MN 55905, USA.

Hypertension (Dallas, Tex. : 1979)
|July 11, 2007
PubMed

Insights

Aging and hypertension cause ventricular-arterial (VA) coupling in both systole and diastole. This coupling, particularly in older hypertensive dogs, is linked to heart failure with normal ejection fraction (HFnlEF).

Area of Science:

  • Cardiovascular Physiology
  • Vascular Biology
  • Heart Failure Pathophysiology

Background:

  • Aging and hypertension induce arterial remodeling, increasing arterial (Ea) and left ventricular (LV) systolic stiffness, leading to ventricular-arterial (VA) coupling.
  • These conditions predispose individuals to heart failure with normal ejection fraction (HFnlEF), characterized by symptoms during hypertensive urgencies or exercise.
  • The study investigates the potential for chronic diastolic VA coupling and its relationship with systolic coupling and HFnlEF.

Purpose of the Study:

  • To test if chronic ventricular-arterial (VA) coupling occurs in diastole.
  • To determine if acute changes in arterial elastance (Ea) correlate with shifts in diastolic and systolic pressure-volume relationships (PVR).
  • To ascertain if diastolic VA coupling is a result of changes in LV diastolic stiffness, rather than external forces or impaired relaxation.

Main Methods:

  • Assessment of PVR using caval occlusion in old chronically hypertensive (OHT) and young normal (YNL) dogs.
  • Measurement of aortic pressure, dimension, and flow at baseline and during altered afterload and preload.
  • Calculation of systolic (ESV(200)) and diastolic (EDV(20)) volumes at common pressures to account for PVR changes.

Main Results:

  • OHT dogs exhibited significant vascular remodeling with impaired indices of pulsatile Ea (aortic stiffness, systemic arterial compliance).
  • In both groups, increased Ea was associated with decreased ESV(200) and EDV(20); however, OHT dogs had lower values at any given load.
  • Acute changes in EDV(20) were independent of relaxation or external forces, suggesting a link to intrinsic LV diastolic properties.

Conclusions:

  • Chronic VA coupling exists in diastole and is associated with LV remodeling and myocardial endothelin activation in OHT dogs.
  • Acute increases in arterial elastance (Ea) influence both systolic and diastolic PVR.
  • Diastolic VA coupling reflects intrinsic changes in LV diastolic stiffness, contributing to the development of HFnlEF.

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