Tsukasa Tajimi
Kyushu University
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Featured researches published by Tsukasa Tajimi.
American Heart Journal | 1982
Shunichi Kaseda; Yasushi Koiwaya; Tsukasa Tajimi; Arahito Mitsutake; Hideo Kanaide; Akira Takeshita; Yutaka Kikuchi; Motoomi Nakamura; Hisanori Mayumi; Masataka Komori; Kouichi Tokunaga
dine, procainamide, and disopyramide.6 Torsades de pointes was not observed in our patient, although it might be potentially manifested in the presence of significant flecainide-induced QT, prolongation. In our current controlled study of 14 patients with ventricular ectopy taking flecainide versus quinidine, four patients randomized to quinidine had clinical side efl’ects such as diarrhea, causing them to discontinue treatment. It appears that flecainide results in less frequency of similar side effects and possesses potent suppression (> 85 % ) of VPCs. While the single patient presented herein manifeste,d the unusual response of VT with flecainide, a number of studies including our own L* have shown no other or similar adverse effects. F’lecainide remains a promising new antiarrhythmic agent that warrants further clinical investigation.
American Heart Journal | 1992
Hideo Yamamoto; Hitoshi Yoshimura; Mitsuru Noma; Hisashi Kai; Satoshi Suzuki; Tsukasa Tajimi; Masayoshi Sugihara; Yutaka Kikuchi
The objective of this study was to determine if endothelium-dependent vasodilation is preserved in the spastic segment of the epicardial coronary artery. Segmental responses of the coronary artery to substance P were examined by the use of a quantitative angiographic technique in 21 patients with variant angina. Coronary diameter at the basal state did not differ between the spastic and the nonspastic segments (2.3 +/- 0.2 mm, 2.3 +/- 0.4 mm, p greater than 0.05). Changes in coronary diameter in response to substance P did not differ between segments with ergonovine-induced spasm and nonspastic segments. Maximal dilation averaged 27.1 +/- 9.5% in the spastic segment and 24.4 +/- 9.6% in the nonspastic segment (expressed as a percent increase over the value before drug administration). It appears that both the potential of the endothelium to release endothelium-dependent relaxing factor and the dilating response of the smooth muscle to endothelium-dependent relaxing factor are preserved, even in the spastic segment.
American Heart Journal | 1994
Hisashi Kai; Hideo Yamamoto; Mitsuru Noma; Satoshi Suzuki; Hitoshi Yoshimura; Tsukasa Tajimi; Masayoshi Sugihara; Yutaka Kikuchi
This study was performed to determine the effects of long-term intravenous infusion on the coronary vasodilating actions of continuous intravenous and bolus intracoronary administration of isosorbide dinitrate (ISDN). With quantitative coronary angiography, the coronary diameter and the vasodilating response to intracoronary ISDN (1 mg) at angiographically normal segments were studied before and after intravenous administration of ISDN, 10 to 60 micrograms/min for 1 hour, 2 days, or 5 days. The vasodilating effects of intravenous ISDN were 72% +/- 13%, 65% +/- 21%, and 6% +/- 11% of the response to intracoronary ISDN in the baseline study in each group. Irrespective of the duration of intravenous infusion, subsequent intracoronary ISDN dilated coronary arteries to extent similar to that observed in each baseline study. In conclusion, significant coronary vasodilating effects of intravenous ISDN were observed after a 2-day infusion, whereas tolerance to the vasodilating effects apparently developed within 5 days of infusion. The vasodilating response to bolus intracoronary ISDN was preserved even when the vasodilating effects of intravenous ISDN were no longer present.
Journal of Cardiovascular Pharmacology | 2004
Keiji Oi; Hiroaki Shimokawa; Yoji Hirakawa; Hideki Tashiro; Ryuichi Nakaike; Toshiyuki Kozai; Keizaburo Ohzono; Kunihiko Yamamoto; Samon Koyanagi; Shuichi Okamatsu; Tsukasa Tajimi; Yutaka Kikuchi; Akira Takeshita
Postprandial increase in remnant lipoprotein concentrations has been suggested as an important atherogenic factor. However, the influence of these remnants on the development of restenosis after percutaneous coronary intervention (PCI) remains to be examined. The present study was designed to address this point. In 60 consecutive patients with successful PCI, the influences of possible risk factors on the development of restenosis, including remnant-like particles (RLP) cholesterol (RLP-C) and triglyceride (RLP-TG), were examined. While mean concentrations of RLP-C and RLP-TG were normal in fasting state, postprandial change in RLP-C concentrations was a significant and independent risk factor for restenosis after PCI. The calculated cut-off index (COI) for the change was +64%. When the patients were divided into 2 groups according to this COI, minimal lumen diameter (MLD) and reference coronary diameter were comparable before and immediately after PCI between the high- (COI < 64%) and the low- (COI < 64%) responders. However, follow-up coronary angiography 3 to 6 months after PCI demonstrated that MLD, late loss, and loss index were all worse in the high responders compared with the low responders. These results indicate that post-prandial increase in RLP-C concentrations is an independent risk factor for restenosis after successful PCI, even in patients with normal fasting RLP-C levels.
Recent Progress in Mitral Valve Disease | 1984
Kirk L. Peterson; Tsukasa Tajimi
: Determination of the optimal time for surgical intervention in chronic mitral regurgitation has remained controversial. There are similarly important factors in favor of temporizing with medical treatment alone as there are in support of relatively early surgery (Table 1). Since rheumatic valvulitis may play a subordinate role, in contrast to etiologies such as myxomatous degeneration of the mitral valve, rupture of chordae tendineae, papillary muscle dysfunction due to coronary artery disease and other causes, left ventricular function is generally determined by the adaptations of the myocardium to the volume overload, or to ischemia or infarction from coronary artery disease rather than to a concomitant myocarditis. Based on actuarial survival curves in symptomatic patients with combined mitral regurgitation and stenosis or mitral regurgitation alone, it can be assumed that surgery can result in improved survival, in particular if a reconstructive mitral valve procedure rather than prosthetic valve replacement is performed. Medical treatment is carried out with digitalis to enhance myocardial contractility, diuretics and vasodilators to reduce pre- and afterload with resultant diminished effective mitral orifice area and regurgitant volume, lowering of pulmonary artery and pulmonary venous pressures and an increase in systemic cardiac output. Presently, however, there is no convincing evidence that symptom-status is improved or the natural history favorably affected over a number of years. For assessment of left ventricular myocardial function the end-systolic pressure/volume or the end-systolic stress/volume index appear preferable. Values of the latter less than or equal to 2.2 are associated with increased postoperative mortality and improbable improvement in functional status. Additionally, patients with an ejection fraction less than 40% or end-diastolic volume greater than 140 ml/m2 as well as those with end-diastolic dimension greater than 8 cm or end-systolic dimension greater than 5.5 cm have less favorable postoperative survival or further deterioration in ventricular function. Impaired right ventricular function secondary to the increased afterload imposed by pulmonary hypertension generally can be normalized postoperatively. Depression of right ventricular myocardial contractility is not, however, a common pathophysiologic feature in chronic mitral regurgitation.(ABSTRACT TRUNCATED AT 250 WORDS)
Japanese Circulation Journal-english Edition | 1995
Hideo Yamamoto; Hitoshi Yoshimura; Mitsuru Noma; Satoshi Suzuki; Hisashi Kai; Tsukasa Tajimi; Masayoshi Sugihara; Yutaka Kikuchi
European Heart Journal | 1983
Tsukasa Tajimi; Kenji Sunagawa; Akira Yamada; Yoshiaki Nose; A. Takershita; Yutaka Kikuchi; Motoomi Nakamura
Chest | 1988
Satoshi Suzuki; Tsukasa Tajimi; Akira Takeshita; Motoomi Nakamura; Kazuhiko Kinoshita; Kouichi Tokunaga
Journal of Cardiology | 2007
Koji Ito; Mitsuru Noma; Masahiro Mohri; Kohtaro Abe; Umpei Yamamoto; Kenji Miyata; Hideki Origuchi; Hideo Yamamoto; Tsukasa Tajimi; Yutaka Kikuchi
American Heart Journal | 1993
Mitsuru Noma; Yutaka Kikuchi; Hitoshi Yoshimura; Hideo Yamamoto; Tsukasa Tajimi