Yael Yaniv1, Ismayil Ahmet2, Jie Liu3, Alexey E Lyashkov4, Toni-Rose Guiriba2, Yosuke Okamoto2, Bruce D Ziman2, Edward G Lakatta5. 1. Laboratory of Cardiovascular Science, Biomedical Research Center, Intramural Research Program, National Institute on Aging, National Institutes of Health, Baltimore, Maryland; Biomedical Engineering Faculty, Technion-IIT, Haifa, Israel. Electronic address: yaely@bm.technion.ac.il. 2. Laboratory of Cardiovascular Science, Biomedical Research Center, Intramural Research Program, National Institute on Aging, National Institutes of Health, Baltimore, Maryland. 3. Laboratory of Cardiovascular Science, Biomedical Research Center, Intramural Research Program, National Institute on Aging, National Institutes of Health, Baltimore, Maryland; Cardiovascular Physiology Laboratory, School of Medical Sciences, University of Sydney, Sydney, New South Wales, Australia. 4. Department of Molecular and Comparative Pathobiology, Johns Hopkins University School of Medicine, Baltimore, Maryland. 5. Laboratory of Cardiovascular Science, Biomedical Research Center, Intramural Research Program, National Institute on Aging, National Institutes of Health, Baltimore, Maryland. Electronic address: lakattae@grc.nia.nih.gov.
Abstract
BACKGROUND: A reduction of complexity of heart beating interval variability that is associated with an increased morbidity and mortality in cardiovascular disease states is thought to derive from the balance of sympathetic and parasympathetic neural impulses to the heart. However, rhythmic clocklike behavior intrinsic to pacemaker cells in the sinoatrial node (SAN) drives their beating, even in the absence of autonomic neural input. OBJECTIVE: To test how this rhythmic clocklike behavior intrinsic to pacemaker cells interacts with autonomic impulses to the heart beating interval variability in vivo. METHODS: We analyzed beating interval variability in time and frequency domains and by fractal and entropy analyses: (1) in vivo, when the brain input to the SAN is intact; (2) during autonomic denervation in vivo; (3) in isolated SAN tissue (ie, in which the autonomic neural input is completely absent); (4) in single pacemaker cells isolated from the SAN; and (5) after autonomic receptor stimulation of these cells. RESULTS: Spontaneous beating intervals of pacemaker cells residing in the isolated SAN tissue exhibit fractal-like behavior and have lower approximate entropy compared with those in the intact heart. Isolation of pacemaker cells from SAN tissue, however, leads to a loss in the beating interval order and fractal-like behavior. β-Adrenergic receptor stimulation of isolated pacemaker cells increases intrinsic clock synchronization, decreases their action potential period, and increases system complexity. CONCLUSIONS: Both the average beating interval in vivo and beating interval complexity are conferred by the combined effects of clock periodicity intrinsic to pacemaker cells and their response to autonomic neural input. Published by Elsevier Inc.
BACKGROUND: A reduction of complexity of heart beating interval variability that is associated with an increased morbidity and mortality in cardiovascular disease states is thought to derive from the balance of sympathetic and parasympathetic neural impulses to the heart. However, rhythmic clocklike behavior intrinsic to pacemaker cells in the sinoatrial node (SAN) drives their beating, even in the absence of autonomic neural input. OBJECTIVE: To test how this rhythmic clocklike behavior intrinsic to pacemaker cells interacts with autonomic impulses to the heart beating interval variability in vivo. METHODS: We analyzed beating interval variability in time and frequency domains and by fractal and entropy analyses: (1) in vivo, when the brain input to the SAN is intact; (2) during autonomic denervation in vivo; (3) in isolated SAN tissue (ie, in which the autonomic neural input is completely absent); (4) in single pacemaker cells isolated from the SAN; and (5) after autonomic receptor stimulation of these cells. RESULTS: Spontaneous beating intervals of pacemaker cells residing in the isolated SAN tissue exhibit fractal-like behavior and have lower approximate entropy compared with those in the intact heart. Isolation of pacemaker cells from SAN tissue, however, leads to a loss in the beating interval order and fractal-like behavior. β-Adrenergic receptor stimulation of isolated pacemaker cells increases intrinsic clock synchronization, decreases their action potential period, and increases system complexity. CONCLUSIONS: Both the average beating interval in vivo and beating interval complexity are conferred by the combined effects of clock periodicity intrinsic to pacemaker cells and their response to autonomic neural input. Published by Elsevier Inc.
Authors: A L Goldberger; L A Amaral; L Glass; J M Hausdorff; P C Ivanov; R G Mark; J E Mietus; G B Moody; C K Peng; H E Stanley Journal: Circulation Date: 2000-06-13 Impact factor: 29.690
Authors: Ary L Goldberger; Luis A N Amaral; Jeffrey M Hausdorff; Plamen Ch Ivanov; C-K Peng; H Eugene Stanley Journal: Proc Natl Acad Sci U S A Date: 2002-02-19 Impact factor: 11.205
Authors: Yael Yaniv; Alexey E Lyashkov; Syevda Sirenko; Yosuke Okamoto; Toni-Rose Guiriba; Bruce D Ziman; Christopher H Morrell; Edward G Lakatta Journal: J Mol Cell Cardiol Date: 2014-09-22 Impact factor: 5.000
Authors: Jack M Moen; Christopher H Morrell; Michael G Matt; Ismayil Ahmet; Syevda Tagirova; Moran Davoodi; Michael Petr; Shaquille Charles; Rafael de Cabo; Yael Yaniv; Edward G Lakatta Journal: Geroscience Date: 2022-06-27 Impact factor: 7.713
Authors: Syevda G Sirenko; Victor A Maltsev; Yael Yaniv; Rostislav Bychkov; Daniel Yaeger; Tatiana Vinogradova; Harold A Spurgeon; Edward G Lakatta Journal: Am J Physiol Heart Circ Physiol Date: 2016-05-20 Impact factor: 4.733
Authors: Yael Yaniv; Ambhighainath Ganesan; Dongmei Yang; Bruce D Ziman; Alexey E Lyashkov; Andre Levchenko; Jin Zhang; Edward G Lakatta Journal: J Mol Cell Cardiol Date: 2015-08-01 Impact factor: 5.000