Sympathetic transduction to blood pressure at rest is maintained in heart failure with preserved ejection fraction

Introduction: The transduction of sympathetic vasoconstrictor drive to blood pressure (BP) at rest is blunted in patients with hypertension and heart failure with reduced ejection fraction. Whether this is the case in patients with heart failure with preserved ejection fraction (HFpEF), who have a high prevalence of hypertension, remains unknown. Furthermore, it is unclear whether the two established methods used to quantify sympathetic transduction at rest provide complementary information in patient populations. Therefore, the aim of this study was to comprehensively evaluate sympathetic transduction at rest in patients with HFpEF. We hypothesized that sympathetic transduction is blunted in patients with HFpEF compared to age-matched controls. Furthermore, we hypothesized that blunted sympathetic transduction in patients with HFpEF would be observed using both signal averaging and linear regression slope analyses techniques. Methods: BP, heart rate and muscle sympathetic nerve activity (MSNA, microneurography) were measured in 25 patients with HFpEF (70±8 (SD) years, 17 females) and 41 age-matched controls (70±6 years, 25 female; hypertension prevalence 66%) during 7-10 minutes of supine rest. In a subgroup, sympathetic transduction to diastolic BP in 13 HFpEF and 15 controls was evaluated using two analytical techniques: 1) signal averaging the beat-to-beat changes in diastolic BP following bursts of MSNA, with the peak change representing sympathetic transduction; and 2) the slope of the linear relationship between diastolic BP and MSNA burst area summed across a two cardiac cycle window at a fixed lag of 6-8 cardiac cycles preceding each diastolic BP. Results: Patients with HFpEF had similar resting BP (systolic 130±26 vs. 126±16 mmHg, P=0.89; diastolic 71±15 vs. 72±10 mmHg, P=0.64), greater heart rate (70±10 vs. 62±7 bpm, P<0.001) and a trend for greater MSNA burst frequency (39±15 vs. 32±12 bursts/min, P=0.06) but similar levels of MSNA burst incidence (55±20 vs. 51±20 bursts/100heartbeats, P=0.42) when compared with controls. In the subgroup, sympathetic transduction was comparable between HFpEF and controls when evaluated using both the signal averaging (Δ0.8±0.6 vs. Δ1±0.7 mmHg, P=0.45) and the linear regression slope (0.07±0.07 vs. 0.07±0.08 mmHg/%.s, P=0.33) methods. There was a moderate positive linear relationship between methods (r2=0.39, P<0.001). Conclusion: Contrary to our hypothesis, these preliminary findings suggest that sympathetic transduction to BP at rest is preserved in patients with HFpEF compared with age-matched hypertensive controls. Furthermore, the signal averaging and linear regression slope analyses approaches provide complementary information on resting sympathetic transduction in patients with HFpEF and age-matched controls. Whether sympathetic transduction to BP in response to physiological stressors is also altered in HFpEF remains to be determined. Supported by the National Institute of Health (P01HL137630 and R01HL091078) This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.