研究者業績

井澤 英夫

イザワ ヒデオ  (Hideo Izawa)

基本情報

所属
藤田医科大学 医学部 医学科 教授
学位
医学博士(名古屋大学)

J-GLOBAL ID
200901029584552340
researchmap会員ID
6000001679

学歴

 2

論文

 171
  • 西村 豪人, 石井 潤一, 石原 裕也, 中村 和広, 北川 文彦, 坂口 英林, 河合 秀樹, 村松 崇, 原田 将英, 山田 晶, 谷澤 貞子, 成瀬 寛之, 皿井 正義, 簗瀬 正伸, 渡邉 英一, 尾崎 行男, 井澤 英夫
    日本循環器学会学術集会抄録集 88回 PJ031-5 2024年3月  
  • Eirin Sakaguchi, Hiroyuki Naruse, Yuya Ishihara, Hidekazu Hattori, Akira Yamada, Hideki Kawai, Takashi Muramatsu, Yoshiki Tsuboi, Ryosuke Fujii, Koji Suzuki, Junnichi Ishii, Kuniaki Saito, Masayoshi Sarai, Masanobu Yanase, Yukio Ozaki, Hideo Izawa
    Scientific reports 14(1) 75-75 2024年1月2日  
    The renal angina index (RAI) is a validated scoring tool for predicting acute kidney injury (AKI). We investigated the efficacy of the RAI in 2436 heterogeneous patients (mean age, 70 years) treated in cardiac intensive care units (CICUs). The RAI was calculated from creatinine and patient condition scores. AKI was diagnosed by the Kidney Disease: Improving Global Outcome criteria. The primary and secondary endpoints were the development of severe AKI and all-cause mortality, respectively. Four hundred thirty-three patients developed AKI, 87 of them severe. In multivariate analyses, the RAI was a significant independent predictor of severe AKI. During the 12-month follow-up period, 210 patients suffered all-cause death. Elevated RAI was independently associated with all-cause mortality, as was NT-proBNP (p < 0.001). The RAI is a potent predictor not only of severe AKI but also of adverse outcomes and substantially improved the 12-month risk stratification of patients hospitalized in CICUs.
  • Shinji Jinno, Akira Yamada, Kunihiko Sugimoto, Jonathan Chan, Chihiro Nakashima, Yusuke Funato, Naoki Hoshino, Meiko Hoshino, Kayoko Takada, Yoshihiro Sato, Hideki Kawai, Masayoshi Sarai, Hiroyasu Ito, Hideo Izawa
    Echocardiography (Mount Kisco, N.Y.) 40(11) 1251-1258 2023年11月  
    INTRODUCTION: Coronary computed tomography angiography (CCTA) is known to have a high negative predictive value (NPV) in identifying coronary artery disease (CAD). This study aimed to examine whether resting echocardiographic parameters could exclude significant CAD on CCTA. METHODS: We recruited 142 patients who had undergone both CCTA and echocardiography within a 3-month window. Based on the CCTA findings, patients were divided into two groups: Group A (non-significant CAD, defined as all coronary segments having <50% stenosis) and Group B (significant CAD). Resting echocardiographic parameters were compared between the two groups to identify predictors of non-significant CAD on CCTA. RESULTS: A total 92 patients (mean age, 68 ± 13 years; males, 62%) were eligible for this study; 50 in Group A and 42 in Group B. Among the various echo parameters, left atrial volume index (LAVI) and left ventricular (LV) global longitudinal strain (GLS) were significantly lower in Group A (23.5 ± 7.6 vs. 33.6 ± 7.4 mL/m2 , p < .001; -20.2 ± 1.8% vs. -16.8 ± 2.0%, p < .001, respectively). Analysis of the receiver operating characteristic curve revealed that the cutoff value to exclude significant CAD on CCTA was 29.0 mL/m2 for LAVI (NPV 80.8%) and -18.1% for GLS (NPV 80.7%). The NPV increased to 95.0% when these parameters were combined (LAVI < 29.0 mL/m2 and GLS < -18.1%). CONCLUSION: The combination of resting LAVI and GLS was clinically useful in excluding significant CAD via CCTA.
  • Yuji Kono, Masahiko Mukaino, Yushi Ozawa, Koji Mizutani, Yuki Senju, Takayuki Ogasawara, Masumi Yamaguchi, Takashi Muramatsu, Hideo Izawa, Yohei Otaka
    Heart and vessels 2023年10月16日  査読有り
    The purposes of the present study were: (1) to investigate the relationship between hospital-associated functional decline (HAFD) and non-lying time and (2) to clarify the optimal cut-off value for non-lying time associated with HAFD in older patients undergoing transcatheter aortic valve implantation (TAVI). From January 2021 to December 2022, patients admitted to a university hospital who underwent trans-femoral TAVI were consecutively recruited. We measured short physical performance battery (SPPB) pre and post-TAVI, and non-lying time from post-operative days 3-5. HAFD was defined as at least 1 point decrease in SPPB during pre and post-TAVI. Among 75 patients (47 female, mean age of 84.5 years) enrolled, 14 patients were classified as having HAFD. Non-lying time was significantly shorter in the HAFD group than in the non-HAFD group (371 min vs. 539 min, P < 0.001). Receiver-operating characteristic analysis determined an optimal cut-off value of 477 min for differentiating the patients more likely to experience HAFD (sensitivity, 75%; specificity, 92%; area under the curve, 0.798). The non-lying time could be one of the associated factors of HAFD in older patients with TAVI. Non-lying time of about 480 min (8 h) during hospitalization may be an initial target for preventing HAFD.
  • Yoshihiro Sato, Sadako Motoyama, Keiichi Miyajima, Hideki Kawai, Masayoshi Sarai, Takashi Muramatsu, Hiroshi Takahashi, Hiroyuki Naruse, Amir Ahmadi, Yukio Ozaki, Hideo Izawa, Jagat Narula
    JACC. Cardiovascular imaging 2023年9月11日  
    BACKGROUND: Coronary computed tomography angiography (CTA) followed by computed tomography angiography-derived fractional flow reserve (FFRCT) is now commonly used for the management of chronic coronary syndrome (CCS). CTA-verified high-risk plaque (HRP) characteristics have also been reported to be associated with a greater likelihood of adverse cardiac events but have not been used for management decisions. OBJECTIVES: The aim of this study was to evaluate clinical outcomes based on a combination of point-of-care computed tomography angiography-derived fractional flow reserve (POC-FFRCT) and the presence of HRP in CCS patients initially treated medically or with revascularization based on invasive coronary angiography findings. METHODS: CTA was performed as the initial test in 5,483 patients presenting with CCS between September 2015 and December 2020 followed by invasive coronary angiography and revascularization as necessary. POC-FFRCT assessment and HRP characterization were obtained subsequently in 745 consecutive patients. We investigated how HRP and POC-FFRCT, which were not available during the original clinical decision making, correlated with the endpoint defined as a composite of cardiac death, acute coronary syndrome, and a need for unplanned revascularization. RESULTS: Cardiac events occurred in 20 patients (2.7%) during a median follow-up of 744 days. The event rate was significantly higher in patients with POC-FFRCT <0.80 compared with POC-FFRCT ≥0.8 (5.4 vs 0.5 per 100 vessel years; log-rank P < 0.0001) and in patients with HRP compared to those without HRP (3.6 vs 0.8 per 100 vessel years; log-rank P = 0.0001). POC-FFRCT <0.80 and the presence of HRP were the independent predictors of cardiac events (HR: 16.67; 95% CI: 2.63-105.39; P = 0.002) compared with POC-FFRCT ≥0.8 and absent HRP. For the vessels with POC-FFRCT <0.80 and HRP, a significantly higher rate of adverse events was observed in patients who did not undergo revascularization compared with those revascularized (16.4 vs 1.4 per 100 vessel years; log-rank P = 0.006). CONCLUSIONS: POC-FFRCT <0.80 and the presence of HRP were the independent predictors of cardiac events, and revascularization of HRP lesions with abnormal POC-FFRCT was associated with a lower event rate.

MISC

 306
  • 河村 大誠, 外畑 巌, 井澤 英夫, 曽村 富士, 石木 良治, 磯部 智, 吉田 幸彦, 因田 恭也, 赤星 誠, 永田 浩三, 平井 真理, 野田 明子, 岩瀬 三紀, 重村 一成, 西沢 孝夫, 寺澤 求, 横田 充弘
    Japanese circulation journal 64 774-774 2000年4月20日  
  • 石木 良治, 曽村 富士, 河村 大誠, 梅田 久視, 武市 康志, 稲垣 将文, 井澤 英夫, 永田 浩三, 祖父江 俊和, 平井 真理, 横田 充弘, 西澤 孝夫, 野田 明子, 岩瀬 三紀
    Japanese circulation journal 64 220-220 2000年3月1日  
  • 永田 浩三, 石木 良治, 曽村 富士, 井澤 英夫, 平井 真理, 岩瀬 三紀, 西澤 孝夫, 寺澤 求, 横田 充弘
    Japanese circulation journal 64 506-506 2000年3月1日  
  • 河村 大誠, 井澤 英夫, 曽村 富士, 石木 良治, 永田 浩三, 祖父江 俊和, 平井 真理, 横田 充弘, 野田 明子, 岩瀬 三紀
    Japanese circulation journal 64 638-638 2000年3月1日  
  • 岩瀬 三紀, 野田 明子, 北市 清幸, 西澤 孝夫, 横田 充弘, 長坂 徹郎, 井澤 英夫
    Japanese circulation journal 64 372-372 2000年3月1日  
  • 井澤 英夫, 横田 充弘
    現代医学 48(2) 247-252 2000年  
  • Ryoji Ishiki, Hitoshi Ishihara, Hideo Izawa, Kohzo Nagata, Makoto Hirai, Mitsuhiro Yokota
    Journal of Cardiovascular Pharmacology 35(6) 897-905 2000年  
    A recent long-term multicenter trial has shown that pimobendan is more effective when administered in low doses. However, no data are available concerning the effect of a low dose of pimobendan on the systolic and diastolic pressure-volume relations in patients with heart failure. Therefore we examined the effects of a single low dose of oral pimobendan, a calcium sensitizer, on systolic and diastolic hemodynamics in patients with cardiomyopathy and congestive heart failure. We measured the left ventricular (LV) pressure-volume relations using a conductance catheter with a micromanometer tip in 10 patients with chronic congestive heart failure resulting from idiopathic cardiomyopathy before and 45 and 90 min after administration of a single oral dose of 2.5 mg of pimobendan. End-systolic elastance was used as an index of LV contractility and was measured during transient occlusion of the inferior vena cava. End-systolic elastance increased significantly by 25% at 45 min (p &lt 0.05) and by 55% at 90 min (p &lt 0.01) without an increase in myocardial oxygen consumption: The inotropic effect was accompanied by improved ventriculoarterial coupling. This effect was attenuated in patients with severely impaired myocardial contractility. LV relaxation, assessed by the time constant of isovolumic pressure decay (T(1/2)), was significantly shortened at 90 min (from 47.7 ± 1.9 to 41.2 ± 1.7 ms p &lt 0.01), although it remained unchanged at 45 min. The diastolic pressure-volume relation showed a leftward and downward shift in all patients. These results indicate that low-dose oral pimobendan had favorable short-term inotropic and lusitropic effects in patients with congestive heart failure caused by idiopathic dilated cardiomyopathy, and may thus be a useful alternative to traditional agents. Further study in large-scale trial is merited.
  • Y Mitsuhiro, M Inagaki, H Izawa, R Ishiki, K Nagata, M Iwase, Y Yamada, M Koide
    CIRCULATION 100(18) 23-23 1999年11月  
  • 山内 正樹, 吉田 幸彦, 井澤 英夫, 飯野 重雄, 赤星 誠, 因田 恭也, 近藤 隆久, 平井 真理, 横田 充弘, 沢田 健
    63(2) 749 1999年8月20日  
  • 岩瀬 三紀, 野田 明子, 王 莉, 北市 清幸, 長谷川 高明, 古池 保雄, 井澤 英夫, 祖父江 俊和, 長坂 徹郎, 横田 充弘
    Journal of medical ultrasonics = 超音波医学 26(4) 576-576 1999年4月15日  
  • M Inagaki, M Yokota, H Izawa, R Ishiki, K Nagata, M Iwase, Y Yamada, M Koide, T Sobue
    CIRCULATION 99(14) 1822-1830 1999年4月  
    Background-The extent to which force-frequency and relaxation-frequency relations (FFR and RFR, respectively) and exercise-induced adrenergic stimulation affect myocardial inotropic and lusitropic reserves has not been established in patients with left ventricular (LV) hypertrophy (LVH). Methods and Results-We calculated the maximum first derivative of LV pressure (LV dP/dt(max)) and the LV pressure half-time (T-1/2) during pacing, exercise, and isoproterenol infusion in 17 patients with hypertensive WH and 9 control subjects to investigate the influence of increases in heart rate (HR) and adrenergic stimulation on inotropic and lusitropic reserves. Group A consisted of 10 LVH patients who showed a progressive increase in the HR-LV dP/dt(max) relation. Group B consisted of 7 LVH patients in whom the HR-dP/dt(max) relation at physiological pacing rates was biphasic. The LV mass index was larger and the LV ejection fraction was smaller in group B than in group A (244+/-72 g/m(2) versus 172+/-22 g/m(2) and 55 +/- 18% versus 72+/-6%, respectively; both P&lt;0.05). The increase in LV dP/dt(max) was seater during exercise than pacing alone for similar increases in HR in all groups (P&lt;0.05) (group A, 111+/-22% versus 25+/-14%; group B, 105+/-355 versus 14+/-10%; control, 111+/-24% versus 25+/-12%). T-1/2 was shorter (P&lt;0.05) during exercise than with pacing alone in all groups (group A, 41+/-6% versus 11+/-3%; group B, 38+/-9% versus 14+/-4%; control, 44+/-6% versus 12+/-5%). Isoproterenol infusion caused similar increases in LV dP/dt(max) and similar decreases in T-1/2 in all groups. Conclusions-The FFR was biphasic in patients with seven LVH irrespective of LV function but was preserved in patients with less severe LVH and control subjects. Importantly, the RFR and adrenergic control of both inotropic and lusitropic reserves were well preserved in all LVH patients. A biphasic FFR at physiological pacing rates may be one of the earliest markers of the transition from physiological adaptation to the pathological process in LVH patients.
  • M Inagaki, M Yokota, H Izawa, R Ishiki, K Nagata, M Iwase, Y Yamada, M Koide, T Sobue
    CIRCULATION 99(14) 1822-1830 1999年4月  
    Background-The extent to which force-frequency and relaxation-frequency relations (FFR and RFR, respectively) and exercise-induced adrenergic stimulation affect myocardial inotropic and lusitropic reserves has not been established in patients with left ventricular (LV) hypertrophy (LVH). Methods and Results-We calculated the maximum first derivative of LV pressure (LV dP/dt(max)) and the LV pressure half-time (T-1/2) during pacing, exercise, and isoproterenol infusion in 17 patients with hypertensive WH and 9 control subjects to investigate the influence of increases in heart rate (HR) and adrenergic stimulation on inotropic and lusitropic reserves. Group A consisted of 10 LVH patients who showed a progressive increase in the HR-LV dP/dt(max) relation. Group B consisted of 7 LVH patients in whom the HR-dP/dt(max) relation at physiological pacing rates was biphasic. The LV mass index was larger and the LV ejection fraction was smaller in group B than in group A (244+/-72 g/m(2) versus 172+/-22 g/m(2) and 55 +/- 18% versus 72+/-6%, respectively; both P&lt;0.05). The increase in LV dP/dt(max) was seater during exercise than pacing alone for similar increases in HR in all groups (P&lt;0.05) (group A, 111+/-22% versus 25+/-14%; group B, 105+/-355 versus 14+/-10%; control, 111+/-24% versus 25+/-12%). T-1/2 was shorter (P&lt;0.05) during exercise than with pacing alone in all groups (group A, 41+/-6% versus 11+/-3%; group B, 38+/-9% versus 14+/-4%; control, 44+/-6% versus 12+/-5%). Isoproterenol infusion caused similar increases in LV dP/dt(max) and similar decreases in T-1/2 in all groups. Conclusions-The FFR was biphasic in patients with seven LVH irrespective of LV function but was preserved in patients with less severe LVH and control subjects. Importantly, the RFR and adrenergic control of both inotropic and lusitropic reserves were well preserved in all LVH patients. A biphasic FFR at physiological pacing rates may be one of the earliest markers of the transition from physiological adaptation to the pathological process in LVH patients.
  • 稲垣 将文, 河村 大誠, 曽村 富士, 武市 康志, 石木 良治, 井澤 英夫, 永田 浩三, 祖父江 俊和, 平井 真理, 野田 明子, 岩瀬 三紀, 横田 充弘
    Japanese circulation journal 63(1) 643-643 1999年3月1日  
  • 井澤 英夫, 平井 真理, 石木 良治, 永田 浩三, 寺澤 求, 稲垣 将文, 武市 康志, 曽村 富士, 河村 大誠, 因田 恭也, 祖父江 俊和, 野田 明子, 横田 充弘
    Japanese circulation journal 63(1) 605-605 1999年3月1日  
  • 磯部 智, 安藤 晃禎, 井澤 英夫, 野々川 信, 平井 真理, 横田 充弘, 七里 守
    Japanese circulation journal 63(1) 601-601 1999年3月1日  
  • 石木 良治, 石原 均, 岩瀬 三紀, 祖父江 俊和, 井澤 英夫, 横田 充弘
    臨床薬理 30(1) 139-140 1999年  
  • 神田 裕文, 祖父江 俊和, 石原 均, 加藤 良三, 町井 剛, 井澤 英夫, 横田 充弘
    Japanese circulation journal 61 829-829 1998年3月20日  
  • 稲垣 将文, 岩瀬 三紀, 井澤 英夫, 武市 康志, 藤村 高陽, 市原 佐保子, 石木 良治, 曽村 富士, 祖父江 俊和, 横田 充弘
    Japanese circulation journal 62 181-181 1998年2月28日  
  • 市原 佐保子, 曽村 富士, 武市 康志, 石木 良治, 藤村 高陽, 稲垣 将文, 井澤 英夫, 祖父江 俊和, 岩瀬 三紀, 横田 充弘, 山田 芳司
    Japanese circulation journal 62 372-372 1998年2月28日  
  • 市原 佐保子, 曽村 富士, 武市 康志, 石木 良治, 藤村 高陽, 稲垣 将文, 井澤 英夫, 岩瀬 三紀, 祖父江 俊和, 横田 充弘, 山田 芳司
    Japanese circulation journal 62 593-593 1998年2月28日  
  • 石木 良治, 石原 均, 岩瀬 三紀, 井澤 英夫, 藤村 高陽, 市原 佐保子, 武市 康志, 曽村 富士, 祖父江 俊和, 横田 充弘
    Japanese circulation journal 62 446-446 1998年2月28日  
  • M Inagaki, H Izawa, M Iwase, T Sobue, M Yokota
    JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY 31(2) 322A-322A 1998年2月  
  • H Izawa, M Yokota, Y Takeichi, M Inagaki, K Nagata, M Iwase, T Sobue
    CIRCULATION 96(9) 2959-2968 1997年11月  
    Background Exercise-induced enhancement of the force frequency and relaxation-frequency relations has been studied in conscious animals but not in intact diseased human hearts. Methods and Results We evaluated left ventricular (LV) isovolumic contraction (dP/dt(max)) and relaxation (tau) during atrial pacing and dynamic exercise in 13 patients with nonobstructive hypertrophic cardiomyopathy (HCM) and 7 control subjects to investigate the influence of exercise on the force-frequency and relaxation-frequency relations. Group A consisted of 6 patients in whom the heart rate (HR)-dP/dt(max) relation was markedly enhanced during exercise (88+/-30%) compared with during pacing (34+/-15%). Group B consisted of 7 patients in whom the HR-dP/dt(max) relation showed similar enhancement during exercise (28+/-7%) and atrial pacing (28+/-11%). There was no difference in the HR-tau (derivative method [TD] and pressure half-time method [T-1/2]) relation between pacing and exercise in groups A and B. Both the mean maximal wall thickness and the hypertrophy score in group B were greater than in group A (27+/-5 versus 19+/-2 mm and 7+/-1 versus 5+/-1 points, respectively; both P&lt;.01). There was no difference in the LV peak systolic pressure, end-diastolic pressure, or the plasma level of catecholamines at baseline, at 50 W of exercise, and at peak pacing between groups A and B. The HR-dP/dt(max), relation in the control group was markedly enhanced during exercise (80+/-27%) compared with during pacing (32+/-14%). The HR-tau relation in the control group was enhanced during exercise (TD, 35+/-9%; T-1/2 34+/-8%) compared with during pacing (TD, 12+/-7%; T-1/2 14+/-7%). Conclusions Exercise-induced enhancement of the relaxation-frequency relation was inhibited in all HCM patients, regardless of the degree of LV hypertrophy. The patients without exercise-induced enhancement of the force-frequency relation had more severe LV hypertrophy than the patients with the enhancement, indicating that the adrenergic control of the force-frequency relation may, at least in part, depend on the severity of LV hypertrophy or the stage of HCM.
  • H Izawa, M Yokota, Y Takeichi, M Inagaki, K Nagata, M Iwase, T Sobue
    CIRCULATION 96(9) 2959-2968 1997年11月  
    Background Exercise-induced enhancement of the force frequency and relaxation-frequency relations has been studied in conscious animals but not in intact diseased human hearts. Methods and Results We evaluated left ventricular (LV) isovolumic contraction (dP/dt(max)) and relaxation (tau) during atrial pacing and dynamic exercise in 13 patients with nonobstructive hypertrophic cardiomyopathy (HCM) and 7 control subjects to investigate the influence of exercise on the force-frequency and relaxation-frequency relations. Group A consisted of 6 patients in whom the heart rate (HR)-dP/dt(max) relation was markedly enhanced during exercise (88+/-30%) compared with during pacing (34+/-15%). Group B consisted of 7 patients in whom the HR-dP/dt(max) relation showed similar enhancement during exercise (28+/-7%) and atrial pacing (28+/-11%). There was no difference in the HR-tau (derivative method [TD] and pressure half-time method [T-1/2]) relation between pacing and exercise in groups A and B. Both the mean maximal wall thickness and the hypertrophy score in group B were greater than in group A (27+/-5 versus 19+/-2 mm and 7+/-1 versus 5+/-1 points, respectively; both P&lt;.01). There was no difference in the LV peak systolic pressure, end-diastolic pressure, or the plasma level of catecholamines at baseline, at 50 W of exercise, and at peak pacing between groups A and B. The HR-dP/dt(max), relation in the control group was markedly enhanced during exercise (80+/-27%) compared with during pacing (32+/-14%). The HR-tau relation in the control group was enhanced during exercise (TD, 35+/-9%; T-1/2 34+/-8%) compared with during pacing (TD, 12+/-7%; T-1/2 14+/-7%). Conclusions Exercise-induced enhancement of the relaxation-frequency relation was inhibited in all HCM patients, regardless of the degree of LV hypertrophy. The patients without exercise-induced enhancement of the force-frequency relation had more severe LV hypertrophy than the patients with the enhancement, indicating that the adrenergic control of the force-frequency relation may, at least in part, depend on the severity of LV hypertrophy or the stage of HCM.
  • H Izawa, T Sobue, M Iwase, M Inagaki, R Ishiki, M Yokota
    CIRCULATION 96(8) 2199-2199 1997年10月  
  • 井澤 英夫, 武市 康志, 石木 良治, 市原 佐保子, 稲垣 将文, 藤村 高陽, 神田 裕文, 町井 剛, 加藤 良三, 岩瀬 三紀, 祖父江 俊和, 横田 充弘
    Japanese circulation journal 61 576-576 1997年3月5日  
  • 町井 剛, 井沢 英夫, 神田 裕文, 永田 浩三, 祖父江 俊和, 横田 充弘
    Japanese circulation journal 60 735-735 1997年1月20日  
  • Y Takeichi, K Nagata, H Izawa, M Iwase, T Sobue, M Sugawara, M Yokota
    HEART AND VESSELS 12 138-141 1997年  
    We investigated the effect of mild exercise on global and regional diastolic function in patients with hypertensive left ventricular hypertrophy (LVH), using simultaneous measurement of micromanometric left ventricular pressure and echocardiographic indexes. Although left ventricular end-diastolic pressure (LVEDP) at rest in the hypertensive LVH group was similar to that in the control normotensive group, who had no abnormality on echocardiography or cardiac catheterization, LVEDP showed a marked increase during exercise only in the hypertensive LVH group. The pressure-dimension relation was shifted upward during exercise in all patients with hypertensive LVH. We utilized a new index of regional diastolic myocardial stiffness, KDM, which is derived from the diastolic relation between the mean wall stress and the natural logarithm of the reciprocal of wall thickness. Although KDM at rest was similar in the two groups, KDM increased significantly during exercise, both in the septum and posterior wall in patients with hypertensive LVH. The present results imply that even low-grade exercise may have deleterious effects on regional myocardial performance in patients with hypertensive LVH.
  • H Ishihara, M Yokota, R Kato, H Kanda, S Ichihara, T Fujimura, Y Takeichi, R Ishiki, M Inagaki, H Izawa, T Machii, M Iwase, T Sobue
    HEART AND VESSELS 12 93-96 1997年  
    The aim of this study was to clarify that the depressed mechanoenergetics in patients with idiopathic dilated cardiomyopathy (DCM) resulted from compensation for the decreased contractility. The study population consisted of eight control subjects, with normal left ventricular size and ejection fraction and 31 patients with DCM. Left ventricular end-systolic elastance (Ees), effective arterial elastance (Ea), external work (EW), and the pressure-volume area (PVA) were measured, using a dual-field volume conductance catheter equipped with a micromanometer-tipped catheter. Ea/Ees was evaluated as ventriculoarterial coupling. Normal hearts worked at almost optimal condition (defined as Ea/Ees = 1/2), while ventriculoarterial coupling was far from the optimum (Ea &gt; Ees) in patients with DCM. Ees in patients with DCM was less than that in control subjects; however, Ea was similar in the two groups. The mismatch of Ea/Ees observed in DCM leads to depressed mechanoenergetics as a result of the compensatory response to maintain adequate blood pressure. Volume enlargement plays an important role in maintaining adequate blood pressure and cardiac output in the course of chronic deterioration of contractility.
  • Y Takeichi, K Nagata, H Izawa, M Iwase, T Sobue, M Sugawara, M Yokota
    HEART AND VESSELS 12 138-141 1997年  
    We investigated the effect of mild exercise on global and regional diastolic function in patients with hypertensive left ventricular hypertrophy (LVH), using simultaneous measurement of micromanometric left ventricular pressure and echocardiographic indexes. Although left ventricular end-diastolic pressure (LVEDP) at rest in the hypertensive LVH group was similar to that in the control normotensive group, who had no abnormality on echocardiography or cardiac catheterization, LVEDP showed a marked increase during exercise only in the hypertensive LVH group. The pressure-dimension relation was shifted upward during exercise in all patients with hypertensive LVH. We utilized a new index of regional diastolic myocardial stiffness, KDM, which is derived from the diastolic relation between the mean wall stress and the natural logarithm of the reciprocal of wall thickness. Although KDM at rest was similar in the two groups, KDM increased significantly during exercise, both in the septum and posterior wall in patients with hypertensive LVH. The present results imply that even low-grade exercise may have deleterious effects on regional myocardial performance in patients with hypertensive LVH.
  • H Ishihara, M Yokota, R Kato, H Kanda, S Ichihara, T Fujimura, Y Takeichi, R Ishiki, M Inagaki, H Izawa, T Machii, M Iwase, T Sobue
    HEART AND VESSELS 12 93-96 1997年  
    The aim of this study was to clarify that the depressed mechanoenergetics in patients with idiopathic dilated cardiomyopathy (DCM) resulted from compensation for the decreased contractility. The study population consisted of eight control subjects, with normal left ventricular size and ejection fraction and 31 patients with DCM. Left ventricular end-systolic elastance (Ees), effective arterial elastance (Ea), external work (EW), and the pressure-volume area (PVA) were measured, using a dual-field volume conductance catheter equipped with a micromanometer-tipped catheter. Ea/Ees was evaluated as ventriculoarterial coupling. Normal hearts worked at almost optimal condition (defined as Ea/Ees = 1/2), while ventriculoarterial coupling was far from the optimum (Ea &gt; Ees) in patients with DCM. Ees in patients with DCM was less than that in control subjects; however, Ea was similar in the two groups. The mismatch of Ea/Ees observed in DCM leads to depressed mechanoenergetics as a result of the compensatory response to maintain adequate blood pressure. Volume enlargement plays an important role in maintaining adequate blood pressure and cardiac output in the course of chronic deterioration of contractility.
  • H Izawa, M Yokota, K Nagata, M Iwase, T Sobue
    JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY 28(7) 1738-1745 1996年12月  
    Objectives. We investigated the effect of adrenergic stimulation on left ventricular relaxation in patients with hypertrophic cardiomyopathy. Background. Exercise-induced decreases in acceleration of left ventricular relaxation have been observed in patients with hypertrophic cardiomyopathy. However, data on sequential changes in left ventricular relaxation during exercise are limited, Methods. We measured right (fluid filled) and left (high fidelity micromanometer) ventricular pressures during moderate supine ergometer exercise and during rapid right atrial pacing in four groups of patients: 9 with severe hypertrophic cardiomyopathy, 9 with moderate hypertrophic cardiomyopathy. IO with hypertension and moderate hypertrophy and 5 control subjects, Results. There was a curvilinear relation between the time constant of relaxation (tau) and heart rate in all groups during exercise. There was no difference in the dope of this relation between the two hypertrophic cardiomyopathy subgroups, Although the slope of this relation between tau and heart rate was steeper in the hypertensive than the moderate hypertrophic cardiomyopathy group (p &lt; 0.001, analysis of covariance), the decrease in tau during right atrial paring was similar in both groups, There were no significant differences in plasma levels of catecholamines Pt rest or at peak exercise among groups or in maximal heart rate during pacing, Conclusions. Pacing-induced changes in tan in hypertrophic cardiomyopathy were similar to those in hypertensive hypertrophy, but remarkable decreases in exercise-induced acceleration of tau were observed only in hypertrophic cardiomyopathy. Our results may indicate a depressed left ventricular relaxation response to exercise-induced adrenergic stimulation in hypertrophic cardiomyopathy. (C) 1996 by the American College of Cardiology
  • H Izawa, M Yokota, K Nagata, M Iwase, T Sobue
    JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY 28(7) 1738-1745 1996年12月  
    Objectives. We investigated the effect of adrenergic stimulation on left ventricular relaxation in patients with hypertrophic cardiomyopathy. Background. Exercise-induced decreases in acceleration of left ventricular relaxation have been observed in patients with hypertrophic cardiomyopathy. However, data on sequential changes in left ventricular relaxation during exercise are limited, Methods. We measured right (fluid filled) and left (high fidelity micromanometer) ventricular pressures during moderate supine ergometer exercise and during rapid right atrial pacing in four groups of patients: 9 with severe hypertrophic cardiomyopathy, 9 with moderate hypertrophic cardiomyopathy. IO with hypertension and moderate hypertrophy and 5 control subjects, Results. There was a curvilinear relation between the time constant of relaxation (tau) and heart rate in all groups during exercise. There was no difference in the dope of this relation between the two hypertrophic cardiomyopathy subgroups, Although the slope of this relation between tau and heart rate was steeper in the hypertensive than the moderate hypertrophic cardiomyopathy group (p &lt; 0.001, analysis of covariance), the decrease in tau during right atrial paring was similar in both groups, There were no significant differences in plasma levels of catecholamines Pt rest or at peak exercise among groups or in maximal heart rate during pacing, Conclusions. Pacing-induced changes in tan in hypertrophic cardiomyopathy were similar to those in hypertensive hypertrophy, but remarkable decreases in exercise-induced acceleration of tau were observed only in hypertrophic cardiomyopathy. Our results may indicate a depressed left ventricular relaxation response to exercise-induced adrenergic stimulation in hypertrophic cardiomyopathy. (C) 1996 by the American College of Cardiology
  • H Izawa, M Yokota, T Sobue, M Iwase, M Inagaki, Y Takeichi
    CIRCULATION 94(8) 2944-2944 1996年10月  
  • 町井 剛, 祖父江 俊和, 永田 浩三, 井澤 英夫, 神田 裕文, 横田 充弘
    Japanese circulation journal 60 55-55 1996年2月20日  
  • 井澤 英夫, 横田 充弘, 祖父江 俊和, 稲垣 春夫, 小出 正文, 前田 雅彦, 斎藤 二三夫, 宮原 隆志
    臨床薬理 27(3) 583-588 1996年  
  • 神田 裕文, 横田 充弘, 祖父江 俊和, 石原 均, 永田 浩三, 井澤 英夫
    臨床薬理 27(4) 699-712 1996年  
  • 井澤 英夫, 祖父江 俊和, 鵜飼 雅彦, 石原 均, 横田 充弘, 宮原 隆志, 外畑 巌
    Japanese circulation journal 59 62-62 1995年3月1日  
  • K YAMAUCHI, Y TANAHASHI, M OKADA, J TSUZUKI, A SATO, K ABE, H INAGAKI, H AGETSUMA, R HATTORI, H IZAWA
    CLINICAL THERAPEUTICS 17(1) 52-59 1995年1月  
    The long-term effects of niceritrol on lipoprotein(a) (Lp[a]), lipids, apolipoproteins, and fibrinogen and fibrinolytic factors were evaluated in 20 out-patients who had serum Lp(a) levels higher than 20 mg/dL. The mean (+/-SE) levels of Lp(a) decreased from 33.6 +/- 2.3 mg/dL to 23.5 +/- 3.5 mg/dL after 12 months of niceritrol treatment (P &lt; 0.01). Serum levels of triglycerides and apolipoprotein E decreased significantly and high-density lipoprotein cholesterol (HDL-C) increased significantly after 12 months (P &lt; 0.05). There were no significant changes overall in fibrinogen and fibrinolytic factors, although fibrinogen concentrations showed a tendency to decrease with treatment. PAI-1 levels decreased significantly (P &lt; 0.05) after 6 months of niceritrol treatment. A significant correlation of percent reduction between Lp(a) and apolipoprotein B levels (P &lt; 0.01) was observed, suggesting that the Lp(a)-lowering effects of niceritrol may be due to niceritrol inhibition of apolipoprotein B synthesis, the major apolipoprotein of Lp(a). The ability of niceritrol to decrease Lp(a) levels and increase HDL-C levels, together with its tendency to lower fibrinogen levels, may help prevent coronary events in patients with high levels of Lp(a).
  • K YAMAUCHI, Y TANAHASHI, M OKADA, J TSUZUKI, A SATO, K ABE, H INAGAKI, H AGETSUMA, R HATTORI, H IZAWA
    CLINICAL THERAPEUTICS 17(1) 52-59 1995年1月  
    The long-term effects of niceritrol on lipoprotein(a) (Lp[a]), lipids, apolipoproteins, and fibrinogen and fibrinolytic factors were evaluated in 20 out-patients who had serum Lp(a) levels higher than 20 mg/dL. The mean (+/-SE) levels of Lp(a) decreased from 33.6 +/- 2.3 mg/dL to 23.5 +/- 3.5 mg/dL after 12 months of niceritrol treatment (P &lt; 0.01). Serum levels of triglycerides and apolipoprotein E decreased significantly and high-density lipoprotein cholesterol (HDL-C) increased significantly after 12 months (P &lt; 0.05). There were no significant changes overall in fibrinogen and fibrinolytic factors, although fibrinogen concentrations showed a tendency to decrease with treatment. PAI-1 levels decreased significantly (P &lt; 0.05) after 6 months of niceritrol treatment. A significant correlation of percent reduction between Lp(a) and apolipoprotein B levels (P &lt; 0.01) was observed, suggesting that the Lp(a)-lowering effects of niceritrol may be due to niceritrol inhibition of apolipoprotein B synthesis, the major apolipoprotein of Lp(a). The ability of niceritrol to decrease Lp(a) levels and increase HDL-C levels, together with its tendency to lower fibrinogen levels, may help prevent coronary events in patients with high levels of Lp(a).
  • H IZAWA, T SOBUE, H ISHIHARA, M UKAI, R KATO, K NAGATA, M YOKOTA
    CIRCULATION 90(4) 655-655 1994年10月  
  • M YOKOTA, F SAITO, H IZAWA, T MATSUNAMI, J YOSHIDA, H INAGAKI, SOTOBATA, I
    EUROPEAN HEART JOURNAL 15(7) 965-970 1994年7月  
  • M YOKOTA, F SAITO, H IZAWA, T MATSUNAMI, J YOSHIDA, H INAGAKI, SOTOBATA, I
    EUROPEAN HEART JOURNAL 15(7) 965-970 1994年7月  
  • 井澤 英夫, 祖父江 俊和, 鵜飼 雅彦, 岩瀬 三紀, 石原 均, 足立 昌由, 町井 剛, 西中 康人, 齋藤 英彦, 横田 充弘
    Japanese circulation journal 58 105-105 1994年3月1日  
  • Therapeutic Research 15 268-272 1994年  
  • M IWASE, K NAGATA, H IZAWA, M YOKOTA, S KAMIHARA, H INAGAKI, H SAITO
    AMERICAN HEART JOURNAL 126(2) 419-426 1993年8月  
    To confirm age-related changes in left and right ventricular filling velocity profiles and to compare left and right ventricular filling parameters in normal subjects, we performed pulsed Doppler echocardiographic studies in 108 normal subjects (72 men and 36 women) aged 15 to 78 years. An age-related decrease in peak early velocity (E velocity), an increase in peak atrial velocity (A velocity), and augmented ratio of A velocity to E velocity (A/E) were observed in left ventricle (r = -0.71, 0.63, and 0.83, respectively). Similar age-related changes were found in right ventricle (r = -0.71, 0.54, and 0.78). Aging had a greater effect on the filling of the left ventricle than the right one (i.e., a steeper slope). The difference between left and right ventricular filling increased with advancing age. Left ventricular filling indexes exceeded those of the right ventricle. Significant correlations were observed between the right and left ventricular filling parameters (r = 0.58 to 0.90). A strong relation was noted in A/E (r = 0.90). There was no significant relation between age and left ventricular mass. The left ventricular mass appeared to have little effect on left and right ventricular filling in normal individuals. Thus in clinical studies the age-related decrease in early diastolic filling and the increased atrial filling in both left and right ventricles should be considered. The atrial contribution to ventricular filling may be more pronounced in the left ventricle than the right ventricle in older subjects.