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10. Predictive Value of the Cardio‐Ankle Vascular Index for Cardiovascular Events in Patients at Cardiovascular Risk

Author

Miyoshi, Toru, primary, Ito, Hiroshi, additional, Shirai, Kohji, additional, Horinaka, Shigeo, additional, Higaki, Jitsuo, additional, Yamamura, Shigeo, additional, Saiki, Atsuhito, additional, Takahashi, Mao, additional, Masaki, Mitsuru, additional, Okura, Takafumi, additional, Kotani, Kazuhiko, additional, Kubozono, Takuro, additional, Yoshioka, Ryo, additional, Kihara, Hajime, additional, Hasegawa, Koji, additional, Satoh‐Asahara, Noriko, additional, Orimo, Hajime, additional, Akasaki, Yuichi, additional, Asahara, Noriko, additional, Doi, Masayuki, additional, Fukuoka, Tomikazu, additional, Fukushima, Hiromichi, additional, Hara, Yuji, additional, Hirano, Keiichi, additional, Hitsumoto, Takashi, additional, Honda, Toshio, additional, Ichinari, Kotaro, additional, Ishimitsu, Toshihiko, additional, Ishimura, Kimihiko, additional, Iwataki, Mai, additional, Kaieda, Hiroshi, additional, Kajiya, Masahito, additional, Kamikawa, Shigeshi, additional, Kaneko, Hitoshi, additional, Kawakami, Hideo, additional, Kikuchi, Yuko, additional, Kiyokawa, Hajime, additional, Kobayashi, Takashi, additional, Koguchi, Wataru, additional, Koizumi, Mitsuteru, additional, Maguchi, Motofumi, additional, Minowa, Hitoshi, additional, Miyamoto, Michiaki, additional, Miyoshi, Akihito, additional, Miyoshi, Kenichi, additional, Miyoshi, Toru, additional, Murata, Maki, additional, Murata, Mitsunobu, additional, Nagao, Tomoaki, additional, Nakamura, Kazufumi, additional, Nakamura, Keigo, additional, Nakamura, Michitsugu, additional, Nakano, Nobuyuki, additional, Nanba, Seiji, additional, Nishimura, Kazuhisa, additional, Obata, Hachiro, additional, Ogurusu, Kazuro, additional, Oka, Takefumi, additional, Onimaru, Madoka, additional, Ono, Shiro, additional, Onoue, Go, additional, Sakuragi, Satoru, additional, Sarashina, Toshihiro, additional, Seta, Koichi, additional, Shibata, Yoshimasa, additional, Shimizu, Kazuhiro, additional, Sugiyama, Hiroyasu, additional, Sumimoto, Takumi, additional, Takahashi, Sho, additional, Takehana, Hitoshi, additional, Takeshima, Hiroshi, additional, Todoroki, Masakatsu, additional, Tominaga, Youkou, additional, Uraoka, Tadao, additional, Yagi, Hiroshi, additional, Yahata, Kensei, additional, Takata, Masanobu, additional, Otsuka, Kuniaki, additional, and Oikawa, Shinichi, additional

Published
2021
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11. Predictive Value of the Cardio-Ankle Vascular Index for Cardiovascular Events in Patients at Cardiovascular Risk

Author

Miyoshi, Toru, Ito, Hiroshi, Shirai, Kohji, Horinaka, Shigeo, Higaki, Jitsuo, Yamamura, Shigeo, Saiki, Atsuhito, Takahashi, Mao, Masaki, Mitsuru, Okura, Takafumi, Kotani, Kazuhiko, Kubozono, Takuro, Yoshioka, Ryo, Kihara, Hajime, Hasegawa, Koji, Satoh-Asahara, Noriko, Orimo, Hajime, Miyoshi, Toru, Ito, Hiroshi, Shirai, Kohji, Horinaka, Shigeo, Higaki, Jitsuo, Yamamura, Shigeo, Saiki, Atsuhito, Takahashi, Mao, Masaki, Mitsuru, Okura, Takafumi, Kotani, Kazuhiko, Kubozono, Takuro, Yoshioka, Ryo, Kihara, Hajime, Hasegawa, Koji, Satoh-Asahara, Noriko, and Orimo, Hajime

Abstract

BACKGROUND: Arterial stiffness is an important predictor of cardiovascular events; however, indexes for measuring arterial stiffness have not been widely incorporated into routine clinical practice. This study aimed to determine whether the cardio-ankle vascular index (CAVI), based on the blood pressure-independent stiffness parameter beta and reflecting arterial stiffness from the origin of the ascending aorta, is a good predictor of cardiovascular events in patients with cardiovascular disease risk factors in a large prospective cohort. METHODS AND RESULTS: This multicenter prospective cohort study, commencing in May 2013, with a 5-year follow-up period, included patients (aged 40-74 years) with cardiovascular disease risks. The primary outcome was the composite of cardiovascular death, nonfatal stroke, or nonfatal myocardial infarction. Among 2932 included patients, 2001 (68.3%) were men; the mean (SD) age at diagnosis was 63 (8) years. During the median follow-up of 4.9 years, 82 participants experienced primary outcomes. The CAVI predicted the primary outcome (hazard ratio, 1.38; 95% CI, 1.16-1.65; P<0.001). In terms of event subtypes, the CAVI was associated with cardiovascular death and stroke but not with myocardial infarction. When the CAVI was incorporated into a model with known cardiovascular disease risks for predicting cardiovascular events, the global chi(2) value increased from 33.8 to 45.2 (P<0.001), and the net reclassification index was 0.254 (P=0.024). CONCLUSIONS: This large cohort study demonstrated that the CAVI predicted cardiovascular events.

Published
2021

14. Solitary Right Ventricle Metastasis by Renal Cell Carcinoma

Author

Masaki, Mitsuru, Kuroda, Tadashi, Hosen, Naoki, Hirota, Hisao, Terai, Kazuo, Oshima, Yuichi, Nakaoka, Yoshikazu, Sugiyama, Shoko, Kimura, Ryusuke, Yoshihara, Satoshi, Kawakami, Manabu, Iizuka, Norishige, Tomita, Yasuhiko, Ogawa, Hiroyasu, Kawase, Ichiro, and Yamauchi-Takihara, Keiko

Published
2004

17. Acute effects of atrial fibrillation on atrial and ventricular function: a simultaneous invasive-echocardiographic hemodynamic study

Author

Yingxue Dong, Malini Madhavan, Brian D. Powell, Jae K. Oh, Rick A. Nishimura, Barry A. Borlaug, Douglas L. Packer, Jia Hui Wu, Yong Mei Cha, Masaki Mitsuru, Kan Dong, David O. Hodge, and Yan Zong Yang

Subjects
Acute effects, Male, medicine.medical_specialty, Ventricular function, business.industry, P wave, Hemodynamics, Atrial fibrillation, Middle Aged, medicine.disease, Ventricular Function, Left, Echocardiography, Internal medicine, Atrial Fibrillation, Cardiology, Medicine, Humans, Atrial Function, Left, Female, Prospective Studies, Cardiology and Cardiovascular Medicine, business, Prospective cohort study, Aged
Published
2013

18. Abstract 13770: DWS as an Index of Myocardial Stiffness and a Predictor of Heart Failure Outcome in Patients with Chronic Beta-blockade Therapy

Author

Soyama, Yuko, primary, Mano, Toshiaki, additional, Hirotani, Shinichi, additional, Masaki, Mitsuru, additional, Fukui, Miho, additional, Fujiwara, Shohei, additional, Sugahara, Masataka, additional, Komamura, Kazuo, additional, Kawabata, Masaaki L, additional, Tsujino, Takeshi, additional, and Masuyama, Tohru, additional

Published
2014
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19. Changes in collagen metabolism account for ventricular functional recovery following beta-blocker therapy in patients with chronic heart failure

Author

Fukui, Miho, primary, Goda, Akiko, additional, Komamura, Kazuo, additional, Nakabo, Ayumi, additional, Masaki, Mitsuru, additional, Yoshida, Chikako, additional, Hirotani, Shinichi, additional, Lee-Kawabata, Masaaki, additional, Tsujino, Takeshi, additional, Mano, Toshiaki, additional, and Masuyama, Tohru, additional

Published
2014
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20. The association between left ventricular twisting motion and mechanical dyssynchrony: a three-dimensional speckle tracking study

Author

Fujiwara, Shohei, primary, Komamura, Kazuo, additional, Nakabo, Ayumi, additional, Masaki, Mitsuru, additional, Fukui, Miho, additional, Sugahara, Masataka, additional, Itohara, Kanako, additional, Soyama, Yuko, additional, Goda, Akiko, additional, Hirotani, Shinichi, additional, Mano, Toshiaki, additional, and Masuyama, Tohru, additional

Published
2014
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25. Elevated Arterial Stiffness and Diastolic Dysfunction in Subclinical Hypothyroidism

Author

Masaki, Mitsuru, primary, Komamura, Kazuo, additional, Goda, Akiko, additional, Hirotani, Shinichi, additional, Otsuka, Misato, additional, Nakabo, Ayumi, additional, Fukui, Miho, additional, Fujiwara, Shohei, additional, Sugahara, Masataka, additional, Lee-Kawabata, Masaaki, additional, Tsujino, Takeshi, additional, Koshiba, Masahiro, additional, and Masuyama, Tohru, additional

Published
2014
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29. Electrophysiological and Hemodynamic Characteristics Associated With Obesity in Patients With Atrial Fibrillation

Author

Munger, Thomas M., primary, Dong, Ying-Xue, additional, Masaki, Mitsuru, additional, Oh, Jae K., additional, Mankad, Sunil V., additional, Borlaug, Barry A., additional, Asirvatham, Samuel J., additional, Shen, Win-Kuang, additional, Lee, Hon-Chi, additional, Bielinski, Suzette J., additional, Hodge, David O., additional, Herges, Regina M., additional, Buescher, Traci L., additional, Wu, Jia-Hui, additional, Ma, Changsheng, additional, Zhang, Yanhua, additional, Chen, Peng-Sheng, additional, Packer, Douglas L., additional, and Cha, Yong-Mei, additional

Published
2012
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42. Smad1 protects cardiomyocytes from ischemia-reperfusion injury

Author

Oshima Yuichi, Kimura Ryusuke, Izumi Masahiro, Kawase Ichiro, Masaki Mitsuru, Sugiyama Shoko, Yamauchi-Takihara Keiko, Hirota Hisao, Kuroda Tadashi, and Terai Kazuo

Subjects
Genetically modified mouse, Cardioprotection, Pathology, medicine.medical_specialty, animal structures, TUNEL assay, business.industry, Ischemia, Caspase 3, medicine.disease, biological factors, Endocrinology, Apoptosis, In vivo, Internal medicine, embryonic structures, Medicine, biological phenomena, cell phenomena, and immunity, Cardiology and Cardiovascular Medicine, business, Reperfusion injury
Abstract

Background: To investigate whether Smad1 signaling promotes cell survival in the adult heart, we subjected transgenic mice with cardiac-specific overexpression of smad1 gene (Smad1 TG) to ischemia-reperfusion injury. Methods and Results: The effect of BMP2 or adenovirus-mediated transfection of Smad1 on cardiomyocyte survival in hypoxia-reoxygenation were examined using rat neonatal cardiomyocytes. Either BMP2 or Smad1 significantly promoted cardioprotection against hypoxia-reoxygenation injury. To examine whether Smad1 activates and plays a role during ischemia-reperfusion of heart in vivo, we generated Smad1 TG mice by using the α-myosin heavy chain gene promoter. Phosphorylation of Smad1 increased in all smad1 transgene-positive mice heart. To examine whether Smad1 prevents injury of cardiomyocytes in vivo, we subjected Smad1 TG mice and wild-type mice to ischemia-reperfusion injury induced by 60 minutes of ligation of the left coronary artery and 60 minutes of reperfusion. Histological, TUNEL and DNA ladder analyses showed that Smad1 TG mice presented significantly smaller myocardial infarction and fewer apoptotic deaths of cardiomyocytes than the wild-type mice did. Interestingly, the increased expression of Bcl-xL was more remarkable, whereas caspase 3 was less activated, in the heart of Smad1 TG mice than that in the wild-type mice. Conclusion: These findings suggest that the Smad1 signaling pathway plays a role in cardioprotection against ischemia-reperfusion injury through the induction of Bcl-xL in vivo.

Published
2004
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43. The impairment of the parasympathetic modulation is involved in the age-related change in mitral E/ A ratio.

Author

Nakabo, Ayumi, Goda, Akiko, Masaki, Mitsuru, Otsuka, Misato, Yoshida, Chikako, Eguchi, Akiyo, Hirotani, Shinichi, Lee-Kawabata, Masaaki, Tsujino, Takeshi, and Masuyama, Tohru

Subjects
PARASYMPATHOLYTIC agents, MITRAL valve diseases, AGE factors in disease, MEASUREMENT of flow velocity, LEFT heart ventricle, CARDIAC contraction, ECHOCARDIOGRAPHY, ANATOMY
Abstract

The mitral early to late diastolic flow velocity ratio ( E/ A ratio) is age-dependent. It has been considered that its age dependency reflects the age-related lengthening of left ventricular (LV) relaxation; however, the change in E/ A ratio is far larger than that expected from those in LV relaxation. We hypothesized that an age-related reduction of the parasympathetic activity increases left atrial (LA) contractility, and that this accounts for the age-related change in E/ A ratio. (1) Exercise stress test was performed in 61 normal subjects (age range, 8-80 years, mean, 40 years) to assess heart rate (HR) recovery because slowed HR recovery indicates lowered parasympathetic activity. There were good interrelations among age, E/ A ratio, and HR recovery. Among those aged ≤30 years, the age no longer correlated with E/ A ratio or HR recovery, but there was a significant correlation between HR recovery and E/ A ratio ( r = 0.44, p < 0.05). (2) Pulsed Doppler and two-dimensional speckle tracking echocardiography (2DSTE) were performed before and after administration of parasympathetic blockade (atropine) in ten young healthy subjects. LA booster pump function was assessed with LA emptying index calculated by 2DSTE. LA emptying index was calculated from ([LA volume before the atrial contraction − minimal LA volume]/LA volume before the atrial contraction) × 100. Atropine increased mitral A velocity ( p < 0.001) and LA emptying index ( p < 0.05) along with a decrease in E/ A ratio ( p < 0.001). Parasympathetic withdrawal enhances LA contraction and increases mitral A velocity, which likely cause a reciprocal decrease in mitral E velocity and E/ A ratio. Thus, parasympathetic deactivation with aging should be closely involved in the age-related change in mitral E/ A ratio. [ABSTRACT FROM AUTHOR]

Published
2014
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46. [Comments on routine laboratory data that are of practical use for physicians].

Author

Honda T, Murakami J, Shimo M, Masaki M, Uehara Y, and Ogasawara R

Subjects
C-Reactive Protein analysis, Humans, Laboratories, Hospital, Physician's Role, Diagnostic Tests, Routine, Pathology, Clinical
Abstract

In the reversed clinicopathological conference (R-CPC), we analyzed a patient's pathosis using only the results of routine laboratory tests. R-CPC is one of the most effective training methods to acquire the abil- ity to interpret such data logically and reasonably. At the same time, we can know the limits of laboratory data, even though they can be analyzed in detail. In this R-CPC, three specialists in laboratory medicine discussed routine laboratory data of a patient with a ruptured abdominal aortic aneurysm. Then, they and moderators fielded a question-and-answer session with an audience in a hall. It was difficult for us to decide on the correct diagnosis, but we were able to analyze the data logically and reasonably in order to understand the patient's actual condition. It has been revealed that the Department of Laboratory Medicine can support physicians by adding comments to laboratory data that are of practical use to follow a patient.

Published
2014

47. [Verification of complete blood cell count (CBC) data from heparinized blood gas samples].

Author

Sakoguchi T, Fujii S, Inuzumi K, Kaminoh Y, Hirose M, Masaki M, and Koshiba M

Subjects
Gases, Heparin, Humans, Reproducibility of Results, Time Factors, Blood Cell Count methods, Blood Specimen Collection methods, Hematocrit methods, Platelet Count methods
Abstract

Complete blood cell count (CBC) data from heparinized blood gas (H-Gas) samples were verified with primary focus on the platelet count (PLT). When a part of H-Gas sample was taken to a separation tube from the blood collection syringe and CBC of the sample in the separation tube was repeatedly measured (Procedure 1), the PLT from 5 samples relative to that obtained immediately after the separation was gradually reduced to 72.6-94.2% during serial measurements (every 5 minutes, up to 30 minutes). The change in the scattergram pattern suggested that this PLT decrease was due to the formation of platelet clumps. The white blood cell count (WBC), red blood cell count (RBC), hemoglobin (Hb) and hematocrit (Ht) values did not significantly change during the repeated measurements. On the other hand, PLT was significantly improved to 96.8-99.8% when the H-Gas sample was kept in the blood collection syringe so as to minimizing the exposure to the air, and the sample for the measurement from H-Gas was taken every time to separation tube from the syringe, followed by CBC measurement without delay (Procedure 2). In addition, while there were significant variations (CV: 11.8-18.2%) in PLT reproducibility among H-Gas samples by Procedure 1, measurements utilizing the Procedure 2 resulted in much smaller variations (CV: 2.2-3.7%). Thus the CBC data obtained from H-Gas samples were equivalent to those from EDTA samples when the Procedure 2 was applied. These data suggest that H-Gas samples can be used for the accurate CBC measurement, including PLT, by applying the Procedure 2.

Published
2014

48. [Comments on routine laboratory data that are of practical use for physicians].

Author

Honda T, Matsuo S, Masaki M, Harada K, Takasaki T, and Nakamura F

Subjects
C-Reactive Protein analysis, Education, Medical trends, Humans, Laboratories, Hospital, Lymphocyte Count methods, Physicians, Pathology, Clinical education
Abstract

Routine laboratory data are not adequately used to follow a patient because medical students are not educated to comprehend them with time series analysis. The Department of Laboratory Medicine can support physicians by adding comments to laboratory data that are of practical use for following a patient. At Shinshu University School of Medicine, routine laboratory data are discussed by time series analysis in a reversed clinicopathological conference(R-CPC). The general status is checked and then the state of each organ is examined using routine laboratory data, and we can obtain much more information about the patient than from physical examinations. In this R-CPC, several specialists in laboratory medicine discussed routine laboratory data of a patient with severe inflammation. It was difficult to diagnose him with a bacterial infection. Elevation of white blood cell count and high C-reactive protein suggested bacterial infection, and decreased platelets showed the possibility of bacteremia. However, he was clinically diagnosed as having multiple trauma without bacterial infection after falling down a mountainside. If routine laboratory data are finely analyzed by specialists in laboratory medicine, physicians can obtain useful information for patient treatment from the Department of Laboratory Medicine.

Published
2013

49. [Update information for physicians on laboratory tests: recent progress in clinical laboratory testing. Topics: II. Particulars with special emphasis on novel laboratory tests; 8. Recent advances of laboratory medicine in rheumatic and allergic diseases].

Author

Koshiba M and Masaki M

Subjects
Autoantibodies analysis, Dermatomyositis diagnosis, Humans, Polymyositis diagnosis, RNA Polymerase III immunology, Scleroderma, Systemic diagnosis, Diagnostic Techniques and Procedures, Hypersensitivity diagnosis, Rheumatic Diseases diagnosis
Published
2011
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50. Smad1 protects cardiomyocytes from ischemia-reperfusion injury.

Author

Masaki M, Izumi M, Oshima Y, Nakaoka Y, Kuroda T, Kimura R, Sugiyama S, Terai K, Kitakaze M, Yamauchi-Takihara K, Kawase I, and Hirota H

Subjects
Animals, Animals, Newborn, Apoptosis, Cell Survival drug effects, Cells, Cultured, Disease Models, Animal, Humans, Mice, Mice, Transgenic, Myocardial Infarction pathology, Myocardial Infarction prevention & control, Phosphorylation, Rats, Rats, Wistar, Signal Transduction, Smad1 Protein genetics, Smad1 Protein metabolism, Transfection, Myocytes, Cardiac drug effects, Reperfusion Injury prevention & control, Smad1 Protein pharmacology
Abstract

Background: We previously reported that bone morphogenetic protein 2 (BMP2) protected against apoptosis of serum-deprived cardiomyocytes via induction of Bcl-xL through the Smad1 pathway. To investigate whether Smad1 signaling promotes cell survival in the adult heart, we subjected transgenic mice with cardiac-specific overexpression of smad1 gene (Smad1TG) to ischemia-reperfusion (I/R) injury., Methods and Results: The effects of BMP2 or adenovirus-mediated transfection of smad1 on cardiomyocyte survival in hypoxia-reoxygenation were examined using rat neonatal cardiomyocytes. BMP2 and Smad1 each significantly promoted survival and diminished apoptotic death of cardiomyocytes during hypoxia-reoxygenation. Interestingly, Smad1 was found to be activated during I/R in normal mouse heart. To examine physiological and pathological roles of Smad1 in I/R, we generated Smad1TG using the alpha-myosin heavy chain gene promoter. Phosphorylation of Smad1 was found in all smad1 transgene-positive mouse hearts. To examine whether Smad1 prevents injury of cardiomyocytes in vivo, we subjected Smad1TG and age-matched wild-type mice (WT) to I/R injury induced by 1 hour of ligation of the left coronary artery and 1 hour of reperfusion. TUNEL and DNA ladder analyses showed that Smad1TG had significantly smaller myocardial infarctions and fewer apoptotic deaths of cardiomyocytes than did WT. Interestingly, increased expression of Bcl-xL and beta-catenin was more remarkable whereas caspase3 was less activated in Smad1TG heart than in that of WT., Conclusions: These findings suggest that the Smad1 signaling pathway plays a role in cardioprotection against I/R injury.

Published
2005
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