Key result
Slow heart rate recovery after exercise was independently associated with increased exercise-induced carotid arterial stiffness (standardized β -0.26, p=0.002) in normotensive patients without overt atherosclerosis.
Why the study?
To evaluate whether blunted autonomic activity measured by heart rate recovery is associated with increased exercise-induced arterial stiffness in normotensive patients without overt atherosclerosis.
Is slow heart rate recovery associated with increased arterial stiffness in normotensive patients without overt atherosclerosis?
Cross-Sectional (n=154)
No
Is slow heart rate recovery associated with increased arterial stiffness in normotensive patients without overt atherosclerosis?
Effect estimate: Standardized β -0.26
p-value: p=0.002
Slow heart rate recovery is independently associated with increased exercise-induced carotid arterial stiffness in normotensive patients without overt atherosclerosis, suggesting a link between sympathovagal imbalance and vascular endothelial dysfunction.
May link autonomic recovery to early stiffness; hypothesis-generating and should not change practice without longitudinal data.
BACKGROUND: This study evaluated whether blunted autonomic activity as measured by heart rate recovery (HRR) was associated with increased arterial stiffness, especially increased exercise-induced arterial stiffness, in normotensive patients without overt atherosclerosis. METHODS: One hundred fifty-four normotensive patients without overt atherosclerosis who had undergone a treadmill exercise test were consecutively enrolled. HRR was measured at one minute after exercise. Brachial-ankle pulse wave velocity (baPWV) at rest was measured, and carotid arterial stiffness indices at rest (CSI at rest) and after exercise (CSI after exercise) were assessed. RESULTS: Patients with slow HRR were older and tended to be male, and they had diabetes, higher resting and peak systolic blood pressures, higher resting heart rate, lower peak heart rate, lower metabolic equivalents, increased baPWV, and increased CSIs at rest and after exercise. HRR was inversely associated with baPWV and CSI after exercise when established cardiovascular risk factors were adjusted as confounding factors, and HRR was associated with CSI after exercise when resting systolic blood pressure and metabolic equivalent of tasks on cardiovascular risk factors were added as confounding factors. CONCLUSIONS: Sympathovagal imbalance demonstrated by slow HRR was associated with increased arterial stiffness and, above all, was closely associated with exercise-induced arterial stiffness in normotensive patients without overt atherosclerosis. This phenomenon might have been observed because blunt carotid arterial vasomotion following exercise results from autonomic dysfunction as well as vascular endothelial dysfunction.
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Yang et al. (2019) conducted a cross-sectional in Normotensive without overt atherosclerosis (n=154). Slow heart rate recovery vs. Normal/fast heart rate recovery was evaluated on Carotid arterial stiffness index (CSI) after exercise (Standardized β -0.26, p=0.002). Slow heart rate recovery after exercise was independently associated with increased exercise-induced carotid arterial stiffness (standardized β -0.26, p=0.002) in normotensive patients without overt atherosclerosis.
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