著者
Yamashita Takeshi Ogawa Satoshi Aizawa Yoshifusa Atarashi Hirotsugu Inoue Hiroshi Ohe Tohru Okumura Ken Kato Takao Kamakura Shiro Kumagai Koichiro Kurachi Yoshihisa Kodama Itsuo Koretsune Yukihiro Saikawa Tetsunori Sakurai Masayuki Sugi Kaoru Nakaya Haruaki Nakayama Toshio Hirai Makoto Fukatani Masahiko Mitamura Hideo Yamazaki Tsutomu
出版者
社団法人日本循環器学会
雑誌
Circulation journal : official journal of the Japanese Circulation Society (ISSN:13469843)
巻号頁・発行日
vol.67, no.9, pp.738-741, 2003-08-20
被引用文献数
22 50

The Japanese Rhythm Management Trial for Atrial Fibrillation (J-RHYTHM study) is a randomized comparative evaluation of rate control and rhythm control, both combined with antithrombotic therapy, as therapeutic strategies for the treatment of atrial fibrillation (AF). This study differs from the earlier AFFIRM and RACE studies in that it has a composite primary end-point representing mortality and also physical/psychological disablement (total mortality, symptomatic cerebral infarction, systemic embolism, major bleeding, hospitalization for heart failure requiring intravenous administration of diuretics, and patient disablement). Patients' will to change the therapeutic strategy to the other is also considered as an end-point representing disablement under the assigned strategy. The secondary end-point includes quality of life scores and the efficacy and safety of drugs used in treating AF. The J-RHYTHM study emphasizes patient-reported experience and perception of AF-specific disablement, and the safety of antiarrhythmics available in Japan; it will follow 2,600 patients treated at more than 150 sites in Japan for a 3-year period. (Circ J 2003; 67: 738-741)
著者
Koike Akira Hoshimoto Masayo Tajima Akihiko Nagayama Osamu Yamaguchi Kaori Goda Ayumi Yamashita Takeshi Sagara Koichi Itoh Haruki Aizawa Tadanori
出版者
社団法人日本循環器学会
雑誌
Circulation journal : official journal of the Japanese Circulation Society (ISSN:13469843)
巻号頁・発行日
vol.70, no.11, pp.1457-1461, 2006-10-20
被引用文献数
6 20

Background In a recent study the indexes of cerebral oxygenation decreased during maximal exercise in nearly half of all patients with left ventricular dysfunction. Whether these levels decrease severely enough to influence mental status or level of consciousness was evaluated in the present study. Methods and Results Forty-two patients with idiopathic dilated cardiomyopathy (IDC) and 29 healthy subjects underwent a symptom-limited maximal exercise test. The cerebral oxyhemoglobin (O_2Hb) and tissue oxygenation index (TOI) were continuously monitored using near-infrared spectroscopy. The changes in O_2Hb and TOI were also measured in 7 subjects: 2 who experienced episodes of reduced consciousness caused by sudden decreases in blood pressure during exercise recovery and 5 who exhibited sustained ventricular tachycardia during an electrophysiological study. The change in cerebral O_2Hb during exercise in patients with IDC averaged 0.38±3.39μmol/L, significantly lower than in the normal subjects (4.30±4.47μmol/L, p<0.0001). The cerebral O_2Hb decreased during exercise in 18 of 42 patients with IDC. The change in cerebral TOI in the IDC patients during exercise was significantly less than that in the normal subjects (-2.0±4.7 vs 2.1±5.8%, p=0.002). The mean decreases in cerebral O_2Hb and TOI were -5.34μmol/L and -9.7%, respectively, in the patients with reduced consciousness during exercise recovery, and -2.52μmol/L and -16.5%, respectively, in those with ventricular tachycardia. Conclusion The indexes of cerebral oxygenation may drop severely enough during maximal exercise in some patients with severe IDC that consciousness is affected.
著者
KOIKE Akira NAGAYAMA Osamu GODA Ayumi HOSHIMOTO Masayo YAMAGUCHI Kaori TAJIMA Akihiko UEJIMA Tokuhisa ITOH Haruki AIZAWA Tadanori
出版者
社団法人日本循環器学会
雑誌
Circulation journal : official journal of the Japanese Circulation Society (ISSN:13469843)
巻号頁・発行日
vol.71, no.9, pp.1418-1423, 2007-08-20
被引用文献数
1 5

<b>Background</b> It has been recently reported that cerebral oxyhemoglobin (O<sub>2</sub>Hb) decreases during exercise in nearly 50% of patients with dilated cardiomyopathy. The present study evaluated whether the inhalation of supplemental O<sub>2</sub> diminishes the decrease in cerebral O<sub>2</sub>Hb during exercise. <b>Methods and Results</b> Ten patients with a left ventricular ejection fraction <50% and a clearly observable decrease in cerebral O<sub>2</sub>Hb during preliminary exercise testing underwent 2 additional symptom-limited incremental exercise tests: 1 while breathing room air (control) and the other while breathing 50% O<sub>2</sub>. In the latter test, the switch from room air to 50% O<sub>2</sub> was performed, on average, at 43.0±14.2 W. Cerebral O<sub>2</sub>Hb was continuously monitored during exercise using near-infrared spectroscopy. In the control exercise test, cerebral O<sub>2</sub>Hb gradually decreased as the work rate increased in all the subjects. When the subjects breathed 50% O<sub>2</sub>, this decrease in cerebral O<sub>2</sub>Hb was diminished. The change in cerebral O<sub>2</sub>Hb from rest to peak exercise during the test under 50% O<sub>2</sub> was significantly higher than that during the control test (-0.23 ±1.89 vs -2.47±1.57 μmol/L, p=0.002). Similarly, the change in the cerebral tissue oxygenation index was significantly higher in the test under 50% O<sub>2</sub> (0.45 ±4.46 vs -3.33±3.06%, p=0.023). <b>Conclusions</b> Impaired cerebral oxygenation during moderate to heavy intensity exercise in patients with left ventricular dysfunction can be offset by breathing supplemental O<sub>2</sub>. (<i>Circ J</i> 2007; <b>71:</b> 1418 - 1423)<br>
著者
Nagasaka Shiro Katoh Hideki Niu Chim Feng Matsui Saori Urushida Tsuyoshi Satoh Hiroshi Watanabe Yasuhide Hayashi Hideharu
出版者
社団法人日本循環器学会
雑誌
Circulation journal : official journal of the Japanese Circulation Society (ISSN:13469843)
巻号頁・発行日
vol.71, no.3, pp.429-436, 2007-02-20
被引用文献数
2 23

Background The identification of protein kinase A(PKA) anchoring proteins on mitochondria implies a direct effect of PKA on mitochondrial function. However, little is known about the relationship between PKA and mitochondrial metabolism. Methods and Results The effects of PKA on the mitochondrial redox state(flavin adenine dinucleotide(FAD)), mitochondrial membrane potential(ΔΨ_m) and reactive oxygen species(ROS) production were investigated in saponin-permeabilized rat cardiomyocytes. The PKA catalytic subunit(PKA_<cat>; 50 unit/ml) increased FAD intensities by 56.6±7.9%(p<0.01), 2'7'-dichlorofluorescin diacetate(DCF) intensities by 10.5±3.3 fold(p<0.01) and depolarized ΔΨ_m to 48.1±9.5% of the control(p<0.01). Trolox(a ROS scavenger; 100μmol/L) inhibited PKA_<cat>-induced ΔΨ_m, FAD and DCF alteration. PKA_<cat>-induced ΔΨ_m depolarization was inhibited by an inhibitor of the inner membrane anion channel(IMAC), 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid(DIDS: 1μmol/L) but not by an inhibitor of mitochondrial permeability transition pore(mPTP), cyclosporine A(lOOnmol/L). Conclusions PKA_<cat> alters FAD and ΔΨ_m via mitochodrial ROS generation, and PKAcat-induced ΔΨ_m depolarization was not caused by mPTP but rather by DIDS-sensitive mechanisms, which could be caused by opening of the IMAC. The effects of PKA on mitochondrial function could be related to myocardial function under the condition of extensive β-adrenergic stimulation.