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(Hypertension. 2007;50:503.)
© 2007 American Heart Association, Inc.

Original Articles

Acute and Chronic Ventricular-Arterial Coupling in Systole and Diastole

Insights From an Elderly Hypertensive Model

Brian P. Shapiro; Carolyn S.P. Lam; Jeetendra B. Patel; Selma F. Mohammed; Martina Kruger; Donna M. Meyer; Wolfgang A. Linke; Margaret M. Redfield

From the Division of Cardiovascular Diseases (B.P.S., C.S.P.L., S.F.M., D.M.M., M.M.R.), Mayo Clinic and Foundation, Rochester, Minn; the Division of Cardiology (J.B.P.), University of Utah, Salt Lake City; and the Physiology and Biophysics Unit (M.K., W.A.L.), University of Muenster, Germany.

Correspondence to Margaret M. Redfield, MD, Mayo Clinic and Foundation, 200 First Street SW, Rochester, MN 55905. E-mail redfield.margaret{at}mayo.edu

Aging and hypertension lead to arterial remodeling and tandem increases in arterial (Ea) and ventricular (LV) systolic stiffness (ventricular-arterial [VA] coupling). Age and hypertension also predispose to heart failure with normal ejection fraction (HFnlEF), where symptoms during hypertensive urgencies or exercise are common. We hypothesized that: (1) chronic VA coupling also occurs in diastole, (2) acute changes in Ea are coupled with shifts in the diastolic and systolic pressure-volume relationships (PVR), and (3) diastolic VA coupling reflects changes in LV diastolic stiffness rather than external forces or relaxation. Old chronically hypertensive (OHT, n=8) and young normal (YNL, n=7) dogs underwent assessment of PVR (caval occlusion) and of aortic pressure, dimension, and flow, at baseline and during changes in afterload and preload. Concomitant changes in the slope/position of PVR were accounted for by calculating systolic (ESV₂₀₀) and diastolic (EDV₂₀) volumes at common pressures (capacitance). OHT displayed marked vascular remodeling. Indices reflecting the pulsatile component of Ea (aortic stiffness and systemic arterial compliance) were more impaired in OHT at any distending pressure. In both groups, acute increases in Ea were associated with decreases in ESV₂₀₀ and EDV₂₀. However, at any load, OHT had lower ESV₂₀₀ and EDV₂₀, associated with LV remodeling and myocardial endothelin activation. Acute changes in EDV₂₀ were not mediated by changes in relaxation or external forces. These observations provide insight into the mechanisms whereby arterial remodeling and acute and chronic VA coupling in both systole and diastole may predispose to and interact with increases in load to cause HFnlEF.

Key Words: hypertension, experimental • hypertension, elderly • ventricular function, left • diastole • heart failure • vasculature • endothelin

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