Shinichi Sumita
Yokohama City University
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Featured researches published by Shinichi Sumita.
Pacing and Clinical Electrophysiology | 1999
Toshiyuki Ishikawa; Shinichi Sumita; Kazuo Kimura; Miyako Kikuchi; Masami Kosuge; Naomitsu Kuji; Tsutomu Endo; Teruyasu Sugano; Tomohiko Sigemasa; Izumi Kobayashi; Osamu Tochikubo; Takashi Usui
In patients with an implanted DDD pacemaker (PM), the atrial contribution may be interrupted by too short an atrioventricular (AV) delay, and filling time may be shortened by too long an AV delay. The AV delay at which the end of the A wave on transmitral flow coincides with complete closure of the mitral valve may be optimal. The subjects were 15 patients [70.3 ± 12.3 (SD) years old] with an implanted DDD PM. Cardiac output (CO) and pulmonary capillary wedge pressure (PCWP) were measured by Swan‐Ganz catheter. Transmitral flow was recorded by pulsed Doppler echocardiography. AV delay was prolonged stepwise by 25 msc. When the AV delay was set at 155 ± 26 ms, the end of the A wave coincided with complete closure of the mitral valve. When the AV delay was prolonged 25, 50, 75, and 100 ms from this AV delay, the interval between the end of the A wave and complete closure of mitral the valve was prolonged 16 ± 5, 39 ± 6, 65 ± 4 and 88 ± 5 ms, respectively (r = 0.97, P < 0.0001) and diastolic mitral regurgitation was observed during this period. Thus, the optimal AV delay may be predicted as follows: the slightly prolonged AV delay minus the interval between the end of the A wave and complete closure of the mitral valve. When the AV delay was set at 215 ms, there was a significant positive correlation between the predicted optimal AV delay (166 ± 23 ms) and the optimal AV delay (CO: 161 ± 26 msec, r = 0.93, P < 0.0001. PCWP: 161 ± 28 msec, r = 0.95, P < 0.0001). In conclusion, optimal AV delay can be predicted by this simple formula: slightly prolonged AV delay minus the interval between end of A wave and complete closure of mitral valve at the AV delay setting.
Circulation | 1997
Kazuhiro Ashino; Eiji Gotoh; Shinichi Sumita; Akihiko Moriya; Masao Ishii
BACKGROUND In patients with mitral stenosis, reduced cardiac output or altered pulmonary hemodynamics may increase sympathetic nerve activity. However, the magnitude of the increase in sympathetic activity in such patients and the effect of valvuloplasty on this activity are unknown. METHODS AND RESULTS We microneurographically measured muscle sympathetic nerve activity before and after mitral valvuloplasty in 10 patients (mean+/-SEM age, 48+/-2 years) with mitral stenosis and in 10 healthy volunteers (47+/-4 years); hemodynamic variables were also measured. Baroreflex sensitivity was assessed on the basis of the ratio of the change in heart rate or muscle sympathetic activity to the change in mean arterial pressure during intravenous infusion of sodium nitroprusside or phenylephrine. At baseline, muscle sympathetic activity was significantly higher in the patients with mitral stenosis than in the control subjects (42.1+/-3.2 versus 26.1+/-3.7 bursts/min, P<.05). However, there was no significant difference between the groups in sympathetic activity at 1 week after valvuloplasty. The reduction in sympathetic activity after valvuloplasty was maintained for > or = 6 months and correlated with the increase in cardiac index (r=.74, P<.05). Baroreflex sensitivity was significantly lower in the patients than in the control subjects, but after valvuloplasty there was no significant difference in baroreflex sensitivity between the groups. CONCLUSIONS Sympathetic activity is increased in patients with mitral stenosis. Mitral valvuloplasty in such patients results in early and long-lasting normalization of sympathetic nerve activity, possibly because of an improvement in arterial baroreflex sensitivity.
Pacing and Clinical Electrophysiology | 2006
Katsumi Matsumoto; Toshiyuki Ishikawa; Shinichi Sumita; Kohei Matsushita; Noriko Inoue; Tsukasa Kobayashi; Kazuaki Uchino; Kazuo Kimura; Satoshi Umemura
Introduction: Biatrial pacing is expected to have preventive effects on atrial fibrillation.
Pacing and Clinical Electrophysiology | 2001
Noritaka Toda; Toshiyuki Ishikawa; Naoki Nozawa; Izumi Kobayashi; Hisao Ochiai; Kazuyuki Miyamoto; Shinichi Sumita; Kazuo Kimura; Satoshi Umemura
TODA, N., et al.: Doppler Index and Plasma Level of Atrial Natriuretic Hormone Are Improved by Optimizing Atrioventricular Delay in Atrioventricular Block Patients with Implanted DDD Pacemakers. Doppler index is the sum of isovolumetric contraction time and isovolumetric relaxation time divided by ejection time and has clinical value as an index of combined systolic and diastolic myocardial performance. This crossover study compared the Doppler index and atrial natriuretic hormone (atrial natriuretic peptide) [ANP] between optimal (AV) delay and prolonged AV delay in patients with DDD pacemakers. The study included 14 patients (6 men, 8 women, age 78.4 ± 9.3 [SD] years) with AV block with an implanted DDD pacemaker. AV delay was prolonged in a 25‐ms, stepwise fashion starting from 125 ms to 250 ms. Pacing rate was set at 70 beats/min. Cardiac output (CO) was assessed by pulsed Doppler echocardiography, and optimal AV delay was defined as the AV delay at which CO was maximum, and an AV delay setting of 250 ms as prolonged AV delay. Plasma level of ANP and Doppler index determined by echocardiography were measured 1 week after programming. AV delay was switched to another AV delay and measurements were repeated after 1 week. Optimal AV delay was 159 ± 19 ms. Doppler index was significantly lower at optimal AV delay than at prolonged AV delay (0.68 ± 0.26 vs 0.92 ± 0.30, P < 0.05). The plasma ANP level was significantly lower at optimal AV delay than at prolonged AV delay (29.0 ± 30.7 vs 52.6 ± 44.9 pg/mL, P < 0.05). In conclusion, the Doppler index and the plasma ANP level were significantly lower at optimal AV delay than at prolonged AV delay. This study shows the importance of the optimal AV delay setting in patients with an implanted DDD pacemaker, the Doppler index and plasma ANP levels are good indicators for optimizing AV delay.
Pacing and Clinical Electrophysiology | 2002
Toshiyuki Ishikawa; Teruyasu Sugano; Shinichi Sumita; Noritaka Toda; Masami Kosuge; Izumi Kobayashi; Kohei Matsusita; Yasuo Ohkusu; Kazuo Kimura; Takashi Usui; Satoshi Umemura
ISHIKAWA, T., et al.: Optimal Atrioventricular Delay Setting Determined by QT Sensor of Implanted DDDR Pacemaker. QT interval (QTI) may change when cardiac function is improved by optimizing the AV delay. QTI is used as the sensor for rate responsive pacemakers. Evoked (e)QTI is measured as the time duration from the ventricular pace‐pulse to the T sense point, which is the steepest point of the intracardiac T wave. The relationship between AV delay and eQTI and cardiac function was studied in 13 patients (74.2 ± 9.3 [SD] years old) with an implanted QT‐driven DDDR pacemaker. A special pacemaker software module was downloaded into the pacemaker memory for eQTI data logging. AV delay was set at 100, 120, 150, 180, 210, and 240 ms. Cardiac output (CO) was measured by continuous Doppler echocardiography. eQTI was 343.3 ± 22.4, 345.1 ± 22.5, and 343.4 ± 23.2 ms (P < 0.01, repeated ANOVA) and CO was 4.2 ± 0.8, 4.6 ± 0.8, and 4.2 ± 0.8 L/min (P < 0.0001, repeated ANOVA) when AV delay was set at the AV delay shortened by one step (AV[−]) and prolonged by one step (AV[+]) from the AV delay at which QT interval was maximum (AV[max]) in seven patients, in whom the peak AV delay at which the eQTI was maximal could be identified. eQTI decreased from 341.1 ± 20.9 to 339.4 ± 21.1 ms (P < 0.0001) and CO decreased from 4.4 ± 1.4 to 4.1 ± 1.3 L/min (P < 0.005) when AV delay was prolonged from AV(max) to AV(+) in all patients. eQTI decreased from 345.1 ± 22.5 to 343.3 ± 22.4 ms (P < 0.0005) and CO decreased from 4.6 ± 0.8 to 4.2 ± 0.8 L/min (P < 0.05) when AV delay was shortened from AV(max) to AV(−) in seven patients. Thus, CO was maximal when AV delay was set at the AV delay at which eQTI was maximal. In conclusion, the optimal AV delay can be predicted from the eQTI sensed by an implanted pacemaker, and automatic setting of the optimal AV delay can be achieved by the QT sensor of an implanted pacemaker.
Annals of Nuclear Medicine | 2004
Yohei Yamakawa; Nobukazu Takahashi; Toshiyuki Ishikawa; Kazuaki Uchino; Yasuyuki Mochida; Toshiaki Ebina; Tsukasa Kobayashi; Kohei Matsushita; Katsumi Matsumoto; Noriko Kawasaki; Mie Shimura; Yasuo Ohkusu; Shinichi Sumita; Kazuo Kimura; Tomio Inoue; Satoshi Umemura
ObjectivesThis study sought to evaluate an imaging approach using gated99mTc-MIBI (MIBI) SPECT and gated18F-FDG (FDG) PET for assessment of myocardial viability and cardiac function.MethodsForty-eight patients (38 men, mean age 68.1 ± 9.6 years) underwent ECG-gated FDG PET and MIBI SPECT within a week. The baseline diagnoses were coronary artery disease (31), mitral regurgitation (1), paroxysmal arrhythmia (10), and dilated cardiomyopathy (6). The gated FDG PET data were analyzed using pFAST software, and the gated MIBI SPECT data were analyzed using QGS software. Fifteen patients were diagnosed with myocardial infarction, and follow-up study was performed to assess the functional outcome four months later. An improvement in LVEF of >5% was defined as significant. The LV myocardium was divided into 17 segments, and regional defect scores were visually assessed using a 4-point scale for each segment (0 = normal, 1 = mildly reduced, 2 = moderately reduced, 3 = absent). A segment with a greater defect score on MIBI SPECT than on FDG PET was defined as a mismatch. The patients were divided into two groups: those with at least two mismatched segments (MM-group), and those with none or one (M-group).ResultsLVEF, EDV and ESV measured by gated FDG PET were highly correlated with those obtained by gated MIBI SPECT (r = 0.848, 0.855 and 0.911, p < 0.0001, respectively). The mean values of LVEF did not differ significantly, but EDV and ESV obtained by gated FDG PET were significantly grater than those obtained by gated MIBI SPECT (p < 0.0001). In 15 patients diagnosed with myocardial infarction, a significant association (p < 0.05) was found between the relative uptake of FDG PET and MIBI SPECT and the functional outcome 4 months later. Global LV function improved in 6 of the 8 patients showing mismatch but in only 1 of the 7 patients with matched defects, resulting in a sensitivity of 86% and specificity of 75%. The overall accuracy to predict global functional outcome was high (80%).ConclusionThis imaging approach allows accurate evaluation of myocardial viability. Furthermore, the high correlations of gated FDG PET and gated MIBI SPECT measurements hold promise for the assessment of left ventricular function using gated FDG PET.
Pacing and Clinical Electrophysiology | 2006
Katsumi Matsumoto; Nobukazu Takahashi; Toshiyuki Ishikawa; Shinichi Sumita; Kohei Matsushita; Noriko Inoue; Tsukasa Kobayashi; Kazuaki Uchino; Kazuo Kimura; Tomio Inoue; Satoshi Umemura
Background: We assessed left ventricular (LV) function and myocardial glucose metabolism by fluoro‐18‐deoxyglucose (18F‐FDG) positron emission tomography (PET) in patients with tachycardia‐induced cardiomyopathy (TC).
Annals of Nuclear Medicine | 1996
Isao Mitani; Shinichi Sumita; Nobukazu Takahashi; Hisao Ochiai; Masao Ishii
Twenty-seven patients with essential hypertension were prospectively studied with123I-labeled metaiodobenzyl-guanidine (123I-MIBG) to assess the presence and location of impaired sympathetic innervation in hypertrophied myocardium. Thirteen patients had left ventricular hypertrophy on echocardiography, and 14 had normal echocardiograms. The wash-out ratio of123I-MIBG in these two groups did not differ significantly (35.3 ± 6.1 and 35.4 ± 5.1) but was higher than in control subjects (29.4 ± 6.7). The delayed heart-to-mediastinum count ratio was lower in the patients with hypertrophy than in the patients without hypertrophy (1.93 ± 0.28 and 2.22 ± 0.21; p < 0.05) and the control subjects (1.93 ± 0.28 and 2.33 ± 0.25; p < 0.05). On SPECT imaging, abnormalities in segmental uptake were frequent at the posterior and postero-lateral wall in both groups, although the hypertrophic group had more significant impairment. Our results lead to the hypothesis that hypertension in more advanced stages may be associated not only with hypertrophic changes but also with more advanced regional impairment of cardiac sympathetic innervation.
Pacing and Clinical Electrophysiology | 2009
Yuko Miki; Toshiyuki Ishikawa; Kohei Matsushita; Youhei Yamakawa; Katsumi Matsumoto; Shinichi Sumita; Kazuaki Uchino; Kazuo Kimura; Satoshi Umemura
Purpose: To predict the optimal atrioventricular (AV) delay using the phonocardiogram (PCG).
Pacing and Clinical Electrophysiology | 2003
Yasuo Ohkusu; Nobukazu Takahashi; Toshiyuki Ishikawa; Shinichi Sumita; Tsukasa Kobayashi; Kohei Matsushita; Youhei Yamakawa; Kazuaki Uchino; Kazuo Kimura; Tomio Inoue; Satoshi Umemura
OHKUSU, Y., et al.: Effect of Biventricular Pacing on Myocardial Glucose Metabolism in Patients with Heart Failure Using Fluoro‐18‐Deoxyglucose Positron Emission Tomography. Biventricular pacing has recently been found beneficial in the treatment of congestive heart failure (CHF). Meanwhile, positron emission tomography (PET) has emerged as a new method to analyze glucose metabolism in the heart. Five patients (mean age 68.8 ± 8.1 years , 4 men) who received biventricular pacing therapy for 5.8 ± 6.6 weeks for CHF were studied. Myocardial glucose metabolism was evaluated by PET with fluoro‐18‐deoxyglucose (18F‐FDG), and percent uptake (%uptake) of 18F‐FDG was calculated during biventricular pacing and compared with that during 1 hour of conventional RV pacing. Biventricular pacing was associated with a significant decrease in NYHA functional Class from 3.67 ± 0.52 to 2.50 ± 0.55. After 18F‐FDG PET, three of five patients remained clinically stable, and two died during follow‐up. Mean 18F‐FDG %uptake during biventricular pacing was not different than during short‐term RV pacing ( 62.1 ± 18.4 vs. 63.6 ± 17.0% ). However, patients who remained clinically stable had a lower value of 18F‐FDG %uptake in the septal region than patients who died ( 46.9 ± 5.6 vs 80.3 ± 1.3%, P < 0.01 ). One patient whose cardiac function improved significantly also had a small septal region of decreased 18F‐FDG uptake during RV pacing. In conclusion, biventricular pacing therapy was effective in this small group of patients with severe, drug‐resistant CHF. An evaluation of the effects of biventricular pacing on glucose metabolism in the subacute phase may help identify patients with a favorable long‐term response to this therapy. (PACE 2003; 26[Pt. II]:144–147)