학술논문
Attenuated Sympathetic Blood Pressure Transduction in Patients With Treated Heart Failure With Reduced Ejection Fraction.
Document Type
Academic Journal
Author
Nardone M; Department of Human Health and Nutritional Sciences, University of Guelph, Ontario, Canada (M.N., P.J.M.).; Notarius CF; University Health Network and Mount Sinai Hospital Division of Cardiology, Department of Medicine, University of Toronto, Ontario, Canada (C.F.N., M.B.B., J.S.F.).; Toronto General Research Institute, Toronto General Hospital, Ontario, Canada (C.F.N., M.B.B., P.J.M., J.S.F.).; Badrov MB; University Health Network and Mount Sinai Hospital Division of Cardiology, Department of Medicine, University of Toronto, Ontario, Canada (C.F.N., M.B.B., J.S.F.).; Toronto General Research Institute, Toronto General Hospital, Ontario, Canada (C.F.N., M.B.B., P.J.M., J.S.F.).; Millar PJ; Department of Human Health and Nutritional Sciences, University of Guelph, Ontario, Canada (M.N., P.J.M.).; Toronto General Research Institute, Toronto General Hospital, Ontario, Canada (C.F.N., M.B.B., P.J.M., J.S.F.).; Floras JS; University Health Network and Mount Sinai Hospital Division of Cardiology, Department of Medicine, University of Toronto, Ontario, Canada (C.F.N., M.B.B., J.S.F.).; Toronto General Research Institute, Toronto General Hospital, Ontario, Canada (C.F.N., M.B.B., P.J.M., J.S.F.).
Source
Publisher: Lippincott, Williams & Wilkins Country of Publication: United States NLM ID: 7906255 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1524-4563 (Electronic) Linking ISSN: 0194911X NLM ISO Abbreviation: Hypertension Subsets: MEDLINE
Subject
Language
English
Abstract
Background: Heart failure with reduced ejection fraction (HFrEF) is associated with reduced cardiac β-adrenergic signal transduction in response to chronic elevations in neurally released and circulating norepinephrine. Whether elevations in muscle sympathetic nerve activity (MSNA) are accompanied by attenuated α-adrenoceptor-mediated vasoconstriction remains unclear. Therefore, the objective of the current work was to compare transduction of sympathetic firing into blood pressure (BP) in treated patients with HFrEF and healthy controls.
Methods: Twenty-three treated patients with HFrEF (4 females, left ventricular ejection fraction: 28±2%) and 22 healthy controls (6 females) underwent a 7-minute resting measurement of continuous beat-to-beat BP (finger photoplethysmography), heart rate (electrocardiography), and MSNA (microneurography). Sympathetic-BP transduction was quantified using both signal averaging, whereby the BP response to each MSNA burst was serially tracked over 15 cardiac cycles and averaged to derive the peak change in BP, and cross-spectral analysis of low-frequency (0.04-0.15 Hz) MSNA and BP oscillations.
Results: Compared with controls, patients with HFrEF had less sympathetic-BP transduction (0.7±0.3 versus 0.2±0.3 mm Hg; P <0.01), and lower low-frequency oscillations in MSNA (120±56 versus 64±32 arbitrary units2 ; P <0.01) and BP (3.1±1.6 versus 2.0±1.7 mm Hg 2 ; P <0.01). In subgroup analysis, resting sympathetic-BP transduction was lower in patients with HFrEF with normal resting MSNA compared to healthy controls (0.7±0.3 versus 0.4±0.3 mm Hg; P =0.01) and further attenuated (0.1±0.1 mm Hg; P =0.03) in patients with HFrEF with elevated resting MSNA.
Conclusions: Treated HFrEF is associated with lower sympathetic-BP transduction, even when MSNA is not elevated, and diminishes further with disease progression. These adaptations may serve to limit the adverse consequences of oscillatory surges in sympathetic vasoconstrictor discharge on stroke volume.
Methods: Twenty-three treated patients with HFrEF (4 females, left ventricular ejection fraction: 28±2%) and 22 healthy controls (6 females) underwent a 7-minute resting measurement of continuous beat-to-beat BP (finger photoplethysmography), heart rate (electrocardiography), and MSNA (microneurography). Sympathetic-BP transduction was quantified using both signal averaging, whereby the BP response to each MSNA burst was serially tracked over 15 cardiac cycles and averaged to derive the peak change in BP, and cross-spectral analysis of low-frequency (0.04-0.15 Hz) MSNA and BP oscillations.
Results: Compared with controls, patients with HFrEF had less sympathetic-BP transduction (0.7±0.3 versus 0.2±0.3 mm Hg; P <0.01), and lower low-frequency oscillations in MSNA (120±56 versus 64±32 arbitrary units
Conclusions: Treated HFrEF is associated with lower sympathetic-BP transduction, even when MSNA is not elevated, and diminishes further with disease progression. These adaptations may serve to limit the adverse consequences of oscillatory surges in sympathetic vasoconstrictor discharge on stroke volume.