|稗田 道成（ひえだ みちなり）||データ更新日：2022.04.05|
助教 ／ 医学研究院
|1.||Hieda M, Sarma S, Hearon CM Jr, MacNamara JP, Dias KA, Samels M, Palmer D, Livingston S, Morris M, Levine BD. , One-Year Committed Exercise Training Reverses Abnormal Left Ventricular Myocardial Stiffness in Patients With Stage B Heart Failure With Preserved Ejection Fraction, Circulation, 10.1161/CIRCULATIONAHA.121.054117, 144, 12, 934-946, 2021.09, [URL].|
|2.||Hieda M, Esposito G, Bossone E, Novel Clinical and Pathophysiologic Concepts in Cardiovascular Emergencies., Heart Fail Clin., 10.1016/j.hfc.2020.04.001, 16, 3, XI-XII, 2020.07.|
|3.||Hieda M, Noninvasive Positive Pressure Ventilation for Acute Decompensated Heart Failure., Heart Fail Clin., 10.1016/j.hfc.2020.02.005, 16, 3, 271-282, 2020.07.|
|4.||Hieda M, Goto Y, Cardiac Mechanoenergetics in Patients with Acute Myocardial Infarction: From Pressure-Volume Loop Diagram Related to Cardiac Oxygen Consumption., Heart Fail Clin., 10.1016/j.hfc.2020.02.002, 16, 3, 255-269, 2020.07.|
|5.||Hieda M, Esposito G, Bossone E, The Latest Clinical Understandings and Theory of the Cardiovascular Systems for Cardiovascular Emergencies and Their Management., Heart Fail Clin, 10.1016/j.hfc.2020.01.001, 16, 2, Ⅸ-Ⅹ, 2020.04.|
|6.||Hieda M, Satyam S, Hearon Jr. C, Dias K, Martinez J, Samels M, Everding B, Palmer D, Livingston S, Morris M, Howden E, Levine BD, Increased Myocardial Stiffness in Patients With High-Risk Left Ventricular Hypertrophy: The Hallmark of Stage-B Heart Failure With Preserved Ejection., Circulation, 10.1161/CIRCULATIONAHA.119.040332, 141, 2, 115-123, 2019.12.|
|7.||Hieda M, Yoo JK, Badrov BM, Parker SR, Anderson HE, Wiblin LJ, Kawalsky J, North SC, Suris A, and Fu Q, Reduced Left Ventricular Diastolic Function in Women with Post-Traumatic Stress Disorder., American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 10.1152/ajpregu.00002.2019, 317, 1, 108-112, 2019.07.|
|8.||Hieda M, Howden E, Sarma S, Cornwell W, Lawley J, Tarumi T, Palmer D, Samels M, Everding B, Livingston S, Fu Q, Zhang R, and Levine BD, The Impact of 2-Years of High Intensity Exercise Training on a Model of Integrated Cardiovascular Regulation., Journal of Physiology, 10.1113/JP276676, 597, 2, 419-429, 2019.01, KEY POINTS: Heart rate variability, a common and easily measured index of cardiovascular dynamics, is the output variable of complicated cardiovascular and respiratory control systems. Both neural and non-neural control mechanisms may contribute to changes in heart rate variability. We previously developed an innovative method using transfer function analysis to assess the effect of prolonged exercise training on integrated cardiovascular regulation. In the present study, we modified and applied this to investigate the effect of 2 years of high-intensity training on circulatory components to tease out the primary effects of training. Our method incorporated the dynamic Starling mechanism, dynamic arterial elastance and arterial-cardiac baroreflex function. The dynamic Starling mechanism gain and arterial-cardiac baroreflex gain were significantly increased in the exercise group. These parameters remained unchanged in the controls. Conversely, neither group experienced a change in dynamic arterial elastance. The integrated cardiovascular regulation gain in the exercise group was 1.34-fold larger than that in the control group after the intervention. In these previously sedentary, otherwise healthy, middle-aged adults, 2 years of high-intensity exercise training improved integrated cardiovascular regulation by enhancing the dynamic Starling mechanism and arterial-cardiac baroreflex sensitivity. ABSTRACT: Assessing the effects of exercise training on cardiovascular variability is challenging because of the complexity of multiple mechanisms. In a prospective, parallel-group, randomized controlled study, we examined the effect of 2 years of high-intensity exercise training on integrated cardiovascular function, which incorporates the dynamic Starling mechanism, dynamic arterial elastance and arterial-cardiac baroreflex function. Sixty-one healthy participants (48% male, aged 53 years, range 52-54 years) were randomized to either 2 years of exercise training (exercise group: n = 34) or control/yoga group (controls: n = 27). Before and after 2 years, subjects underwent a 6 min recording of beat-by-beat pulmonary artery diastolic pressure (PAD), stroke volume index (SV index), systolic blood pressure (sBP) and RR interval measurements with controlled respiration at 0.2 Hz. The dynamic Starling mechanism, dynamic arterial elastance and arterial-cardiac baroreflex function were calculated by transfer function gain between PAD and SV index; SV index and sBP; and sBP and RR interval, respectively. Fifty-three participants (controls: n = 25; exercise group: n = 28) completed the intervention. After 2 years, the dynamic Starling mechanism gain (Group × Time interaction: P = 0.008) and the arterial-cardiac baroreflex gain (P = 0.005) were significantly increased in the exercise group but remained unchanged in the controls. There was no change in dynamic arterial elastance in either of the two groups. The integrated cardiovascular function gain in the exercise group increased 1.34-fold, whereas there was no change in the controls (P = 0.02). In these previously sedentary, otherwise healthy middle-aged adults, a 2 year programme of high-intensity exercise training improved integrated cardiovascular regulation by enhancing the dynamic Starling mechanism and arterial-cardiac baroreflex sensitivity, without changing dynamic arterial elastance..|
|9.||Hieda M, Howden E, Shibata S, Fujimoto N, Bhella PS, Hastings JL, Tarumi T, Satyam S, Fu Q, Zhang R, Levine BD, Impact of Lifelong Exercise Training Dose on Ventricular-Arterial Coupling., Circulation, 10.1161/CIRCULATIONAHA.118.035116, 138, 23, 2638-2647, 2018.12, BACKGROUND: The dynamic Starling mechanism, as assessed by beat-by-beat changes in stroke volume and left ventricular end-diastolic pressure, reflects ventricular-arterial coupling. It deteriorates with age, and is preserved in highly trained masters athletes. Currently, it remains unclear how much exercise over a lifetime is necessary to preserve efficient ventricular-arterial coupling. The purpose of this study was to assess the dose-dependent relationship between lifelong exercise training and the dynamic Starling mechanism in healthy seniors. METHODS: One hundred two seniors were recruited and stratified into 4 groups based on 25 years of exercise training history: sedentary subjects (n=27, <2 sessions/week), casual exercisers (n=25, 2-3 sessions/week), committed exercisers (n=25, 4-5 sessions/week), and competitive Masters Athletes (n=25, 6-7 sessions/week). The dynamic Starling mechanism was estimated by transfer function gain between beat-by-beat changes in diastolic pulmonary artery pressure, a surrogate for left ventricular end-diastolic pressure, and stroke volume index. RESULTS: The transfer function gain of pulmonary artery pressure-stroke volume index was markedly enhanced in committed and competitive exercisers compared with more sedentary seniors and correlated with higher peak oxygen uptake (Vo2) and lower left ventricular stiffness. The power spectral density of pulmonary artery pressure was greater in sedentary adults than in committed and competitive exercisers, whereas the power spectral density of stroke volume index was greater in competitive exercisers than in the other groups. CONCLUSIONS: There is a graded, dose-dependent improvement in ventricular-arterial coupling with increasing amounts of lifelong regular exercise in healthy older individuals. Our data suggest that the optimal dose of lifelong endurance exercise to preserve ventricular-arterial coupling with age appears to be at least 4 to 5 sessions per week..|
|10.||Hieda M, Yoo JK, Sun D, Okada Y, Parker R, Roberts-Reeves M, Adams-Huet B, Nelson D, Levine DB, and Fu Q, Time Course of Changes in Maternal Left Ventricular Function during Subsequent Pregnancy in Women with a History of Gestational Hypertensive Disorders., American Journal of Physiology-Regulatory, Integrativeand and Comparative Physiology, 10.1152/ajpregu.00040.2018, 315, 4, 587-594, 2018.10.|
|11.||Hieda M, Parker J, Rajabi T, Fujimoto N, Bhella PS, Prasad A, Hastings JL, Sarma S, Levine BD, Left Ventricular Volume-Time Relation in Patients With Heart Failure With Preserved Ejection Fraction., Am J Cardiol, 10.1016/j.amjcard.2017.11.033, 121, 5, 609-614, 2018.03.|
|12.||Hieda M; Howden E; Shibata S; Tarumi T; Lawley J; Hearon C Jr.; Palmer D; Fu Q; Zhang R; Sarma S; Benjamin D. Levine, Pre-load Corrected Dynamic Starling Mechanism in Patients with Heart Failure with Preserved Ejection Fraction., Journal of Applied Physiology, 10.1152/japplphysiol.00718.2017, 124, 1, 76-82, 2018.01, The beat-to-beat dynamic Starling mechanism (DSM), the dynamic modulation of stroke volume (SV) because of breath-by-breath changes in left-ventricular end-diastolic pressure (LVEDP), reflects ventricular-arterial coupling. The purpose of this study was to test whether the LVEDP-SV relationship remained impaired in heart failure with preserved ejection fraction (HFpEF) patients after normalization of LVEDP. Right heart catheterization and model-flow analysis of the arterial pressure waveform were performed while preload was manipulated using lower-body negative pressure to alter LVEDP. The DSM was compared at similar levels of LVEDP between HFpEF patients ( n = 10) and age-matched healthy controls ( n = 12) (HFpEF vs. CONTROLS: 10.9 ± 3.8 vs. 11.2 ± 1.3 mmHg, P = 1.00). Transfer function analysis between diastolic pulmonary artery pressure (PAD) representing dynamic changes in LVEDP vs. SV index was applied to obtain gain and coherence of the DSM. The DSM gain was significantly lower in HFpEF patients than in the controls, even at a similar level of LVEDP (0.46 ± 0.19 vs. 0.99 ± 0.39 ml·m-2·mmHg-1, P = 0.0018). Moreover, the power spectral density of PAD, the input variability, was greater in the HFpEF group than the controls (0.75 ± 0.38 vs. 0.28 ± 0.26 mmHg2, P = 0.01). Conversely, the power spectral density of SV index, the output variability, was not different between the groups ( P = 0.97). There was no difference in the coherence, which confirms the reliability of the linear transfer function between the two groups (0.71 ± 0.13 vs. 0.77 ± 0.19, P = 0.87). The DSM gain in HFpEF patients is impaired compared with age-matched controls even at a similar level of LVEDP, which may reflect intrinsic LV diastolic dysfunction and incompetence of ventricular-arterial coupling. NEW & NOTEWORTHY The beat-to-beat dynamic Starling mechanism (DSM), the dynamic modulation of stroke volume because of breath-by-breath changes in left-ventricular end-diastolic pressure (LVEDP), reflects ventricular-arterial coupling. Although the DSM gain is impaired in heart failure with preserved ejection fraction (HFpEF) patients, it is not clear whether this is because of higher LVEDP or left-ventricular diastolic dysfunction. The DSM gain in HFpEF patients is severely impaired, even at a similar level of LVEDP, which may reflect intrinsic left-ventricular diastolic dysfunction..|
|13.||Hieda M, Seguchi O, Mutara Y, Sunami H, Sato T, Yanase M, Hiroki H, Fujita T, Nakatani T, Acute response test to adaptive servo-ventilation, a possible modality to assessing the reversibility of pulmonary vascular resistance., J Artif Organs, 10.1007/s10047-015-0833-1, 18, 3, 280-283, 2015.09.|
|14.||Hieda M, Sata M, Nakatani T, The Importance of the Management of Infectious Complications for Patients with Left Ventricular Assist Device., Healthcare, 10.3390/healthcare3030750, 3, 3, 750-756, 2015.08.|
|15.||Hieda M, Sata M, Seguchi O, Yanase M, Murata Y, Sato T, Sunami H, Nakajima S, Watanabe T, Hori Y, Wada K, Hata H, Fujita T, Kobayashi J, Nakatani T, Importance of Early Appropriate Intervention including Antibiotics and Wound care for Device-related Infection in Patients with Left Ventricular Assist Device., Transplant Proc, 10.1016/j.transproceed.2013.11.106, 46, 3, 907-910, 2014.04.|
|16.||稗田道成, 熊坂礼音, 小西治美, 藤原玲子, 中尾一泰, 福井重文, 大原貴裕, 簗瀬 正伸, 荒川鉄雄, 中西道郎, 後藤葉一, 急性心筋梗塞後患者の抑うつ状態と四肢骨格筋力・運動耐容能の関係, 心臓リハビリテーション, 21, suppl, 327-327.|
主要総説, 論評, 解説, 書評, 報告書等
2019.03～2020.04, Heart Failure clinics, 国際, 編集委員.
2019.01～2023.01, Asian Journal of Sports Medicine, 国際, 編集委員.
University of Texas Southwestern Medical Center, UnitedStatesofAmerica, 2016.04～2020.03.
AHA post-doctoral fellowship grant, American Heart Association, 2018.07.
2021年度～2023年度, 挑戦的研究（開拓）, 分担, 認知症リスク同定を目的とした”動脈スティフネス-脳機能連関”の解明.
2021年度～2025年度, 若手研究, 代表, 高齢者サルコペニア患者における高強度インターバル運動の運動耐容能改善効果について.
2016年度～2018年度, AHA Strategically Focused Research Network grant, 分担, 1) Prevention of Cardiovascular Stiffening with Aging and Left Ventricular Hypertrophy (LVH study) 2) Improvement of Diastolic Function by Modulating Metabolic Health in Obese Individuals (MTG study) 3) Aging, Fitness, and Failure: Mechanisms of Diastolic Dysfunction. (Joseph Hill: 14SFRN20510023-01) (Benjamin D. Levine: 14SFRN20600009-01, -02).
2018年度～2020年度, Medtronic External Research Program, 代表, Synchronizing cardiac cycle phase with foot strike to optimize LV performance in patients with advanced heart failure and cardiac resynchronization therapy (CRT) (ERP-2018-11361).
2018年度～2020年度, AHA post-doctoral fellowship grant, 代表, “Maximizing Functional Capacity of LVAD Patients: Pump-speed Optimization using Exercise to Avoid Left-Right Mismatch” (18POST33960092).
2021年度～2023年度, 臨床研究奨励基金, 代表, 経カテーテル的大動脈弁置換術（TAVI）時代における高齢者の重症大動脈弁狭窄症患者の自然歴についての研究.