Abstract 18074: Chronotropic Incompetence in Heart Failure With Preserved Ejection Fraction: Is It actually a Matter of Chronotropic Reluctance?
Background: Chronotropic incompetence (CI) occurs in roughly 30 percent of HFpEF patients and is linked to impaired aerobic capacity. We investigated the integrity of central command and cardiac β–receptor sensitivity, two predominant mechanisms responsible for exertional increases in HR in HFpEF and control subjects.
Methods: Seven age-matched controls (3M,4F) and 5 carefully screened HFpEF patients (1M,4F) underwent cardiopulmonary exercise testing, static handgrip exercise to assess central command over HR, and graded isoproterenol infusion (ISO) to quantify cardiac β–receptor mediated HR responses. Seven young control subjects also underwent ISO to define age related changes in β–receptor function. To limit neural influence on HR during ISO, dexmedetomidine (α-2 agonist) and glycopyrrolate (muscarinic antagonist) were used to “denervate” the sinus node. ISO dose was increased in increments until HR increased by 30 bpm. Plasma ISO levels were measured by liquid chromatography with electrochemical detection at each increment and plotted against HR. AV nodal blocking agents were held 5 half-lives prior to test days.
Results: Peak VO2 (12.2 ± 1.2 vs 22.1 ± 5.0 ml/kg/min; p=0.002) and HR (122 ± 23 vs 154 ± 16 bpm; p=0.017) were lower in HFpEF than in age-matched controls. There were no differences in peak HR response during static handgrip between groups. HFpEF and older controls had lower cardiac β–receptor sensitivity compared to young controls consistent with age related declines in receptor function. (Figure) However there were no differences in the curves relating the HR to plama ISO between HFpEF and senior controls.
Conclusion: Despite lower peak exercise HR, increases in HR due to central command and to β-receptor stimulation were intact in HFpEF subjects. Our findings suggest that apparent chronotropic incompetence might reflect premature cessation of exercise rather than deficient central command or ß-adrenoceptor responsiveness.
Author Disclosures: S. Sarma: None. D. Stoller: None. J. Hendrix: None. S. Livingston: None. M. Morris: None. M.D. Palmer: None. D.S. Goldstein: None. C. Holmes: None. B.D. Levine: None.
- © 2016 by American Heart Association, Inc.