Increased proximal arterial stiffness and cardiac response with moderate exercise in patients with heart failure and preserved ejection fraction
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Published on: October 19, 2016
Lamia Tartière-Kesri1, Jean-Michel Tartière, Damien Logeart
1Hôpital Léon Bérard, Réadaptation Cardiaque, Hyères, France. lamia_kesri@yahoo.fr.
Objectives:
This study sought to demonstrate that arterial stiffness is probably underestimated in patients with heart failure with preserved ejection fraction (HFpEF) at rest and may be revealed with moderate exercise.
Background:
HFpEF is associated with ventriculoarterial stiffening.
Methods:
We compared 23 patients with stable chronic HFpEF, left ventricular ejection fraction >45%, and impaired relaxation with 15 controls without cardiac disease. Patients were compared at rest and during a 30-W exercise. The following variables were measured or calculated by Doppler echocardiography and tonometry: left ventricular volumes and end-systolic elastance (Ees), peripheral resistance, arterial elastance (Ea), arterial compliance, aortic pulse wave velocity, and carotid Peterson modulus (Ep).
Results:
Patients with HFpEF were comparable to controls in age, sex ratio, blood pressure, and heart rate. Ventriculoarterial coupling, assessed by Ees/Ea and Ees/Ep ratios, was moderately impaired at rest in patients compared with controls (both p < 0.01). HFpEF was associated during exercise with a major increase in Ep (+155 ± 193% vs. -5 ± 28%), pulse wave velocity (+20 ± 30% vs. -7 ± 24%), and Ea (+12 ± 15% vs. -5 ± 10%), and a lower decrease in peripheral resistance (-17 ± 12% vs. -26 ± 12%) (p < 0.05 for all). In addition, HFpEF patients showed a lower increase in stroke volume (+10 ± 16% vs. +21 ± 12%) despite a greater increase in Ees (+20 ± 18% vs. +3 ± 12%) (p < 0.05 for all). Also during exercise, adaptation of proximal ventriculoarterial coupling was impaired in HFpEF patients (Ees/Ep: -26 ± 47% vs. +20 ± 47% for controls) (p < 0.01), with no difference in Ees/Ea.
Conclusions:
In HFpEF patients, moderate exercise leads to a steep increase in proximal afterload that is underestimated at rest and is associated with unfavorable ventriculoarterial coupling and exercise intolerance.
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