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Bonpei Takase - One of the best experts on this subject based on the ideXlab platform.
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Effect of Nipradilol on Silent Myocardial Ischemia and Heart Rate Variability in Chronic Stable Angina
Cardiovascular Drugs and Therapy, 2002Co-Authors: Bonpei Takase, Hiroyuki Hikita, Kimio Satomura, Takemi Mastui, Fumitaka Ohsuzu, Akira KuritaAbstract:Purpose : Silent myocardial ischemic episodes as well as decreased heart rate variability (HRV) indices are associated with an unfavorable outcome in patients with coronary artery disease. Nipradilol, which is a non-selective beta-adrenergic and nitrate-like vasodilator anti-anginal agent developed in Japan, may ameliorate silent myocardial ischemia, while it also improves exercise tolerance and HRV indices in patients with chronic stable angina. Methods : To investigate the effect of Nipradilol (6 mg daily) on silent myocardial ischemic episodes and HRV indices, and to study its effect on the relationship between them, 24 patients with chronic stable angina underwent exercise treadmill testing and a 24-hour ambulatory electrocardiogram (ECG). The study protocol utilized a single blind, 4-week placebo-controlled design. The HRV indices from ambulatory ECG included mean RR (ms), SDNN (ms), SDANN (ms), SD (ms), rMSSD (ms), pNN50 (%); frequency analysis of HRV consisted of total (ms, 0.01–1.00 Hz), low (ms, 0.04–0.15 Hz) and high (ms, 0.15–0.40 Hz) components. Results : Nipradilol significantly decreased the mean heart rate at submaximal and maximal exercise and the mean pressure rate product at submaximal and maximal exercise. It significantly improved exercise-induced maximal ST segment depression from −1.7 ± 0.6 mm to −1.1 ± 0.7 mm ( p > 0.05). Silent myocardial ischemic episodes recorded during the 24-hour ambulatory ECG significantly decreased after Nipradilol administration. Nipradilol also significantly influenced several HRV indices as well as the relationship between silent myocardial ischemic episodes and the HRV indices. Nipradilol significantly increased SD, rMSSD, pNN50, total spectra, low frequency spectra and high frequency spectra. In addition, Nipradilol significantly decreased the LF/HF ratio from 1.7 (1.5–2.0) to 1.5 (1.3–1.8). These effects of Nipradilol on HRV indices concomitantly occurred with the reduction in silent myocardial ischemic episodes. Conclusion : Nipradilol was found to effectively improve the episodes of silent myocardial ischemia as well as exercise-induced ischemia probably due to its beta-blocking properties and not nitrate-like actions. In addition, Nipradilol also had a favorable effect on the HRV indices.
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effect of Nipradilol on silent myocardial ischemia plasma beta endorphin and bradykinin in chronic stable angina
Clinical Cardiology, 1996Co-Authors: Bonpei Takase, Hiroyuki Hikita, Kimio Satomura, Akira Kurita, Akimi Uehata, Toshihiko Nishioka, Hideki Mitani, Kyoichi Mizuno, Haruo NakamuraAbstract:HYPOTHESIS This study was undertaken to investigate the effect of Nipradilol on the total ischemic burden and on plasma levels of beta-endorphin and bradykinin. METHODS Sixteen patients with chronic stable angina were subjected to exercise treadmill testing and 24-h ambulatory electrocardiogram (ECG). RESULTS Nipradilol significantly decreased both mean heart rate and mean pressure rate product at submaximal and maximal exercise. It significantly improved exercise-induced maximal ST-segment depression from -2.7 +/- 0.5 mm to -1.3 +/- 0.6 mm (p < 0.05) and reduced the number of leads with significant ST-segment depression (4.0 +/- 1.2 vs. 2.0 +/- 1.8, p < 0.05). Silent ischemic episodes recorded in 24-h ambulatory ECG were significantly decreased by Nipradilol administration, concomitantly with a decrement of mean heart rate and observed maximal heart rate. Patients with exercise-induced silent myocardial ischemia showed significantly increased plasma levels of beta-endorphin during both the placebo and Nipradilol phases of the study. However, during the Nipradilol phase, bradykinin did not change significantly at rest and at peak exercise. CONCLUSION Nipradilol effectively controls exercise-induced myocardial ischemia and silent myocardial ischemic episodes, and does not influence the response of plasma levels of beta-endorphin to exercise stress testing in patients with exercise-induced silent myocardial ischemia.
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Effect of Nipradilol on silent myocardial ischemia, plasma beta‐endorphin, and bradykinin in chronic stable angina
Clinical cardiology, 1996Co-Authors: Bonpei Takase, Hiroyuki Hikita, Kimio Satomura, Akira Kurita, Akimi Uehata, Toshihiko Nishioka, Hideki Mitani, Kyoichi Mizuno, Haruo NakamuraAbstract:HYPOTHESIS This study was undertaken to investigate the effect of Nipradilol on the total ischemic burden and on plasma levels of beta-endorphin and bradykinin. METHODS Sixteen patients with chronic stable angina were subjected to exercise treadmill testing and 24-h ambulatory electrocardiogram (ECG). RESULTS Nipradilol significantly decreased both mean heart rate and mean pressure rate product at submaximal and maximal exercise. It significantly improved exercise-induced maximal ST-segment depression from -2.7 +/- 0.5 mm to -1.3 +/- 0.6 mm (p < 0.05) and reduced the number of leads with significant ST-segment depression (4.0 +/- 1.2 vs. 2.0 +/- 1.8, p < 0.05). Silent ischemic episodes recorded in 24-h ambulatory ECG were significantly decreased by Nipradilol administration, concomitantly with a decrement of mean heart rate and observed maximal heart rate. Patients with exercise-induced silent myocardial ischemia showed significantly increased plasma levels of beta-endorphin during both the placebo and Nipradilol phases of the study. However, during the Nipradilol phase, bradykinin did not change significantly at rest and at peak exercise. CONCLUSION Nipradilol effectively controls exercise-induced myocardial ischemia and silent myocardial ischemic episodes, and does not influence the response of plasma levels of beta-endorphin to exercise stress testing in patients with exercise-induced silent myocardial ischemia.
Makoto Araie - One of the best experts on this subject based on the ideXlab platform.
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Neuroprotective effect and intraocular penetration of Nipradilol, a beta-blocker with nitric oxide donative action. Invest Ophthalmol Vis Sci. 2001;42:688–694. Clinical Ophthalmology Publish your work in this journal Clinical Ophthalmology is an inte
2013Co-Authors: Ken Mizuno, Takashi Koide, Mitsuo Yoshimura, Makoto AraieAbstract:PURPOSE. To investigate the effect of Nipradilol, an �1,�-blocker with a nitric oxide donative action, on N-methyl-D-aspartate (NMDA)–induced retinal damage in rats and to determine whether topically instilled Nipradilol penetrates the ipsilateral posterior retina–choroid at pharmacologically active concentrations in rabbits. METHODS. To determine effects on NMDA-induced damage, drugs were injected alone or with NMDA into the vitreous of one eye, and cell loss in the ganglion cell layer (GCL) and thinning of the retinal neural cell layers were histologically evaluated. To evaluate posterior penetration, first, [ 14 C]-Nipradilol was instilled, and its tissue concentration was measured. Second, Nipradilol or timolol was instilled, and their effects on intravitreal injection of endothelin-1–induced retinal artery contraction were compared, to evaluate whether a pharmacologically active level of Nipradilol penetrates the inner limiting layer by topical application. RESULTS. Intravitreous injection of NMDA reduced cell numbers in the GCL and the thickness of the inner plexiform layer (IPL) to 50.4 % � 2.6 % and 47.8 % � 4.9 % (n � 8) of control, respectively. Nipradilol alone had no effect. Coadministration of Nipradilol with NMDA reduced cell numbers in the GCL and IPL thickness to 67.8 % � 2.2 % and 74.4 % � 5.2 % of control, respectively (P � 0.05–0.01). Sodium nitroprusside, but not timolol or bunazosin, also significantly prevented the NMDAinduced reduction of cell numbers in the GCL and IPL thickness. Radioactivity of Nipradilol was found in the ipsilateral posterior retina–choroid at 318.6 � 42.9 ng/g (n � 4), which was significantly higher than in the contralateral control (107.4 � 21.8 ng/g). Topical application of Nipradilol, but not timolol, significantly suppressed the endothelin-1–induced contraction of the retinal artery (83.95 % � 8.15 % and 35.24% � 5.62 % of baseline vessel diameter for Nipradilol and timolol, respectively). CONCLUSIONS. Nipradilol suppressed the NMDA-induced retinal damage in rats for which nitric oxide released from Nipradilol may be responsible. Posterior penetration studies suggested that an effective concentration of Nipradilol reached the posterior retina after topical application. (Invest Ophthalmol Vi
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Phase III long-term study and comparative clinical study of Nipradilol ophthalmic solution in patients with primary open-angle glaucoma and ocular hypertension.
Arzneimittel-Forschung, 2011Co-Authors: Mikiko Kanno, Yoshiaki Kitazawa, Ikuo Azuma, Kanjiro Masuda, Makoto Araie, Masahiro Takase, Yoshihiko Shiose, Nobuya Ogawa, Shigehiro OhdoAbstract:Nipradilol (CAS 81486-22-8) is a non-selective beta-blocker with alpha-1 blocking and nitroglycerin-like vasodilating activities. In the present communication, the long-term efficacy and safety of Nipradilol were investigated and the efficacy, safety and utility of topical Nipradilol and timolol (CAS 91524-16-2) were compared in patients with primary open-angle glaucoma or ocular hypertension. In the long-term study, Nipradilol for 1 year (52 weeks) was performed by registration method. 67 out of 68 patients were subjected to analysis and 57 patients (83.8 %) completed 52-week instillation. 0.25 % Nipradilol was applied twice daily to patients. As a result, intraocular pressure (IOP) decreased significantly by 4.0 mmHg to 4.8 mmHg compared with the baseline without tachyphylaxis. The incidence of adverse events was 12.5 % at 52 weeks by analysis with Kaplan-Meier life-table method. It showed no significant trend of increase after 3 months. In the multi-centered double-masked comparative randomized study, 0.25 % Nipradilol was assigned to 96 patients and 0.5 % timolol to 100 patients. Each patient was instilled Nipradilol or timolol twice daily for 8 weeks. IOP significantly decreased by 4.2 mmHg and by 4.7 mmHg at 8 weeks and the incidence of adverse events was 10.5 % and 12.1 % in the Nipradilol and timolol group, respectively. No significant between-group difference in IOP reduction or incidence of adverse events was seen. Topical Nipradilol showed long-term ocular hypotensive effects and clinical safety in a 52-week study, and its efficacy and safety equivalent to timolol was confirmed in a 8-week comparative study.
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Phase III long-term study and comparative clinical study of Nipradilol ophthalmic solution in patients with primary open-angle glaucoma and ocular hypertension.
Drug Research, 2011Co-Authors: Mikiko Kanno, Yoshiaki Kitazawa, Ikuo Azuma, Kanjiro Masuda, Makoto Araie, Masahiro Takase, Yoshihiko Shiose, Nobuya Ogawa, Shigehiro OhdoAbstract:Nipradilol (CAS 81486-22-8) is a non-selective β-blocker with α-1 blocking and nitroglycerin-like vasodilating activities. In the present communication, the longterm efficacy and safety of Nipradilol were investigated and the efficacy, safety and utility of topical Nipradilol and timolol (CAS 91524-16-2) were compared in patients with primary open-angle glaucoma or ocular hypertension. In the long-term study, Nipradilol for 1 year (52 weeks) was performed by registration method. 67 out of 68 patients were subjected to analysis and 57 patients (83.8 %) completed 52-week instillation. 0.25 % Nipradilol was applied twice daily to patients. As a result, intraocular pressure (IOP) decreased significantly by 4.0 mmHg to 4.8 mmHg compared with the baseline without tachyphylaxis. The incidence of adverse events was 12.5 % at 52 weeks by analysis with Kaplan-Meier life-table method. It showed no significant trend of increase after 3 months. In the multi-centered double-masked comparative randomized study, 0.25 % Nipradilol was assigned to 96 patients and 0.5 % timolol to 100 patients. Each patient was instilled Nipradilol or timolol twice daily for 8 weeks. IOP significantly decreased by 4.2 mmHg and by 4.7 mmHg at 8 weeks and the incidence of adverse events was 10.5 % and 12.1 % in the Nipradilol and timolol group, respectively. No significant between-group difference in IOP reduction or incidence of adverse events was seen. Topical Nipradilol showed long-term ocular hypotensive effects and clinical safety in a 52-week study, and its efficacy and safety equivalent to timolol was confirmed in a 8-week comparative study.
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Visual field loss in patients with normal-tension glaucoma under topical Nipradilol or timolol: Subgroup and subfield analyses of the Nipradilol-timolol study
Japanese Journal of Ophthalmology, 2010Co-Authors: Makoto Araie, Shiroaki Shirato, Yoshiaki Kitazawa, Yoshio Yamazaki, Yasuo OhashiAbstract:Purpose To estimate the deterioration rates of visual field loss in Japanese normal-tension glaucoma (NTG) patients under either topical Nipradilol or timolol, and to explore intergroup differences in the treatment results. Methods A total of 146 NTG patients with mild to moderate damage were randomized to either Nipradilol or timolol and followed for 3 years with a periodic comprehensive ophthalmological visual field examination (30-2 Humphrey perimeter program) every 6 months (the Nipradilol-Timolol Study). The time course of mean deviation (MD), the average total deviation (TD_mean) in four subfields, and the corrected pattern standard deviation (CPSD) were compared between the two groups using regression analysis with a linear mixed effect model. Results The estimated slope for MD (dB/year) was −0.03 in the Nipradilol and −0.05 in the timolol group ( P > 0.4). In both groups, TD_mean in the superior-central subfield and CPSD showed significant changes (−0.3 and 0.2–0.3, P ≤ 0.001). In the patients with early visual field loss or those younger than 40 years, deterioration of some visual field parameters tended to be slower in the Nipradilol group than in the timolol group. Conclusion During 3 years of monotherapy with either Nipradilol or timolol in NTG patients, only TD_mean in the superior-central subfield and the CPSD changed significantly without any intergroup differences.
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Route of penetration of topically instilled Nipradilol into the ipsilateral posterior retina.
Investigative ophthalmology & visual science, 2009Co-Authors: Ken Mizuno, Takashi Koide, Kimio Sawanobori, Shunsuke Shimada, Junko Mori, Makoto AraieAbstract:PURPOSE To investigate how topically instilled Nipradilol penetrates the ipsilateral posterior retina-choroid in normal rabbit eyes. METHODS Albino rabbits were used. Topical instillation (1%, 100 microL) or intracameral (0.1%, 100 microL) or sub-Tenon injection (0.1%, 10 microL) of [(14)C]Nipradilol was performed in one eye. Ocular and periocular distribution and the concentrations of [(14)C]Nipradilol were determined by whole-head autoradiography, the results of which were validated by measurements in isolated tissues. In addition, the unchanged form of nonradiolabeled Nipradilol in the posterior retina after topical instillation (1%, 100 microL) was quantified by liquid chromatography-tandem mass spectrometry (LC/MS/MS). RESULTS Autoradiography revealed that the Nipradilol concentration after topical instillation was higher in the ipsilateral posterior retina-choroid than on the contralateral side (142.9 ng/g vs. 108.3 ng/g, P = 0.026), and in the periocular tissue around the optic nerve insertion on the ipsilateral side than on the contralateral side (207.1 ng/g vs. 141.1 ng/g, P < 0.001). After intracameral injection, radioactivity was observed only in anterior, but not posterior parts of the eye. Radioactivity was observed only in the ipsilateral posterior retina-choroid and periocular tissues around the optic nerve insertion after sub-Tenon injection. The results in the isolated tissues validated autoradiographic evaluations. CONCLUSIONS These results suggest that diffusion from posterior periocular tissues across the posterior sclera may be the main route for local penetration of the instilled drug to reach the posterior retina-choroid in albino rabbits.
Akira Kurita - One of the best experts on this subject based on the ideXlab platform.
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Effect of Nipradilol on Silent Myocardial Ischemia and Heart Rate Variability in Chronic Stable Angina
Cardiovascular Drugs and Therapy, 2002Co-Authors: Bonpei Takase, Hiroyuki Hikita, Kimio Satomura, Takemi Mastui, Fumitaka Ohsuzu, Akira KuritaAbstract:Purpose : Silent myocardial ischemic episodes as well as decreased heart rate variability (HRV) indices are associated with an unfavorable outcome in patients with coronary artery disease. Nipradilol, which is a non-selective beta-adrenergic and nitrate-like vasodilator anti-anginal agent developed in Japan, may ameliorate silent myocardial ischemia, while it also improves exercise tolerance and HRV indices in patients with chronic stable angina. Methods : To investigate the effect of Nipradilol (6 mg daily) on silent myocardial ischemic episodes and HRV indices, and to study its effect on the relationship between them, 24 patients with chronic stable angina underwent exercise treadmill testing and a 24-hour ambulatory electrocardiogram (ECG). The study protocol utilized a single blind, 4-week placebo-controlled design. The HRV indices from ambulatory ECG included mean RR (ms), SDNN (ms), SDANN (ms), SD (ms), rMSSD (ms), pNN50 (%); frequency analysis of HRV consisted of total (ms, 0.01–1.00 Hz), low (ms, 0.04–0.15 Hz) and high (ms, 0.15–0.40 Hz) components. Results : Nipradilol significantly decreased the mean heart rate at submaximal and maximal exercise and the mean pressure rate product at submaximal and maximal exercise. It significantly improved exercise-induced maximal ST segment depression from −1.7 ± 0.6 mm to −1.1 ± 0.7 mm ( p > 0.05). Silent myocardial ischemic episodes recorded during the 24-hour ambulatory ECG significantly decreased after Nipradilol administration. Nipradilol also significantly influenced several HRV indices as well as the relationship between silent myocardial ischemic episodes and the HRV indices. Nipradilol significantly increased SD, rMSSD, pNN50, total spectra, low frequency spectra and high frequency spectra. In addition, Nipradilol significantly decreased the LF/HF ratio from 1.7 (1.5–2.0) to 1.5 (1.3–1.8). These effects of Nipradilol on HRV indices concomitantly occurred with the reduction in silent myocardial ischemic episodes. Conclusion : Nipradilol was found to effectively improve the episodes of silent myocardial ischemia as well as exercise-induced ischemia probably due to its beta-blocking properties and not nitrate-like actions. In addition, Nipradilol also had a favorable effect on the HRV indices.
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effect of Nipradilol on silent myocardial ischemia plasma beta endorphin and bradykinin in chronic stable angina
Clinical Cardiology, 1996Co-Authors: Bonpei Takase, Hiroyuki Hikita, Kimio Satomura, Akira Kurita, Akimi Uehata, Toshihiko Nishioka, Hideki Mitani, Kyoichi Mizuno, Haruo NakamuraAbstract:HYPOTHESIS This study was undertaken to investigate the effect of Nipradilol on the total ischemic burden and on plasma levels of beta-endorphin and bradykinin. METHODS Sixteen patients with chronic stable angina were subjected to exercise treadmill testing and 24-h ambulatory electrocardiogram (ECG). RESULTS Nipradilol significantly decreased both mean heart rate and mean pressure rate product at submaximal and maximal exercise. It significantly improved exercise-induced maximal ST-segment depression from -2.7 +/- 0.5 mm to -1.3 +/- 0.6 mm (p < 0.05) and reduced the number of leads with significant ST-segment depression (4.0 +/- 1.2 vs. 2.0 +/- 1.8, p < 0.05). Silent ischemic episodes recorded in 24-h ambulatory ECG were significantly decreased by Nipradilol administration, concomitantly with a decrement of mean heart rate and observed maximal heart rate. Patients with exercise-induced silent myocardial ischemia showed significantly increased plasma levels of beta-endorphin during both the placebo and Nipradilol phases of the study. However, during the Nipradilol phase, bradykinin did not change significantly at rest and at peak exercise. CONCLUSION Nipradilol effectively controls exercise-induced myocardial ischemia and silent myocardial ischemic episodes, and does not influence the response of plasma levels of beta-endorphin to exercise stress testing in patients with exercise-induced silent myocardial ischemia.
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Effect of Nipradilol on silent myocardial ischemia, plasma beta‐endorphin, and bradykinin in chronic stable angina
Clinical cardiology, 1996Co-Authors: Bonpei Takase, Hiroyuki Hikita, Kimio Satomura, Akira Kurita, Akimi Uehata, Toshihiko Nishioka, Hideki Mitani, Kyoichi Mizuno, Haruo NakamuraAbstract:HYPOTHESIS This study was undertaken to investigate the effect of Nipradilol on the total ischemic burden and on plasma levels of beta-endorphin and bradykinin. METHODS Sixteen patients with chronic stable angina were subjected to exercise treadmill testing and 24-h ambulatory electrocardiogram (ECG). RESULTS Nipradilol significantly decreased both mean heart rate and mean pressure rate product at submaximal and maximal exercise. It significantly improved exercise-induced maximal ST-segment depression from -2.7 +/- 0.5 mm to -1.3 +/- 0.6 mm (p < 0.05) and reduced the number of leads with significant ST-segment depression (4.0 +/- 1.2 vs. 2.0 +/- 1.8, p < 0.05). Silent ischemic episodes recorded in 24-h ambulatory ECG were significantly decreased by Nipradilol administration, concomitantly with a decrement of mean heart rate and observed maximal heart rate. Patients with exercise-induced silent myocardial ischemia showed significantly increased plasma levels of beta-endorphin during both the placebo and Nipradilol phases of the study. However, during the Nipradilol phase, bradykinin did not change significantly at rest and at peak exercise. CONCLUSION Nipradilol effectively controls exercise-induced myocardial ischemia and silent myocardial ischemic episodes, and does not influence the response of plasma levels of beta-endorphin to exercise stress testing in patients with exercise-induced silent myocardial ischemia.
Haruo Nakamura - One of the best experts on this subject based on the ideXlab platform.
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effect of Nipradilol on silent myocardial ischemia plasma beta endorphin and bradykinin in chronic stable angina
Clinical Cardiology, 1996Co-Authors: Bonpei Takase, Hiroyuki Hikita, Kimio Satomura, Akira Kurita, Akimi Uehata, Toshihiko Nishioka, Hideki Mitani, Kyoichi Mizuno, Haruo NakamuraAbstract:HYPOTHESIS This study was undertaken to investigate the effect of Nipradilol on the total ischemic burden and on plasma levels of beta-endorphin and bradykinin. METHODS Sixteen patients with chronic stable angina were subjected to exercise treadmill testing and 24-h ambulatory electrocardiogram (ECG). RESULTS Nipradilol significantly decreased both mean heart rate and mean pressure rate product at submaximal and maximal exercise. It significantly improved exercise-induced maximal ST-segment depression from -2.7 +/- 0.5 mm to -1.3 +/- 0.6 mm (p < 0.05) and reduced the number of leads with significant ST-segment depression (4.0 +/- 1.2 vs. 2.0 +/- 1.8, p < 0.05). Silent ischemic episodes recorded in 24-h ambulatory ECG were significantly decreased by Nipradilol administration, concomitantly with a decrement of mean heart rate and observed maximal heart rate. Patients with exercise-induced silent myocardial ischemia showed significantly increased plasma levels of beta-endorphin during both the placebo and Nipradilol phases of the study. However, during the Nipradilol phase, bradykinin did not change significantly at rest and at peak exercise. CONCLUSION Nipradilol effectively controls exercise-induced myocardial ischemia and silent myocardial ischemic episodes, and does not influence the response of plasma levels of beta-endorphin to exercise stress testing in patients with exercise-induced silent myocardial ischemia.
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Effect of Nipradilol on silent myocardial ischemia, plasma beta‐endorphin, and bradykinin in chronic stable angina
Clinical cardiology, 1996Co-Authors: Bonpei Takase, Hiroyuki Hikita, Kimio Satomura, Akira Kurita, Akimi Uehata, Toshihiko Nishioka, Hideki Mitani, Kyoichi Mizuno, Haruo NakamuraAbstract:HYPOTHESIS This study was undertaken to investigate the effect of Nipradilol on the total ischemic burden and on plasma levels of beta-endorphin and bradykinin. METHODS Sixteen patients with chronic stable angina were subjected to exercise treadmill testing and 24-h ambulatory electrocardiogram (ECG). RESULTS Nipradilol significantly decreased both mean heart rate and mean pressure rate product at submaximal and maximal exercise. It significantly improved exercise-induced maximal ST-segment depression from -2.7 +/- 0.5 mm to -1.3 +/- 0.6 mm (p < 0.05) and reduced the number of leads with significant ST-segment depression (4.0 +/- 1.2 vs. 2.0 +/- 1.8, p < 0.05). Silent ischemic episodes recorded in 24-h ambulatory ECG were significantly decreased by Nipradilol administration, concomitantly with a decrement of mean heart rate and observed maximal heart rate. Patients with exercise-induced silent myocardial ischemia showed significantly increased plasma levels of beta-endorphin during both the placebo and Nipradilol phases of the study. However, during the Nipradilol phase, bradykinin did not change significantly at rest and at peak exercise. CONCLUSION Nipradilol effectively controls exercise-induced myocardial ischemia and silent myocardial ischemic episodes, and does not influence the response of plasma levels of beta-endorphin to exercise stress testing in patients with exercise-induced silent myocardial ischemia.
Hiroyuki Hikita - One of the best experts on this subject based on the ideXlab platform.
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Effect of Nipradilol on Silent Myocardial Ischemia and Heart Rate Variability in Chronic Stable Angina
Cardiovascular Drugs and Therapy, 2002Co-Authors: Bonpei Takase, Hiroyuki Hikita, Kimio Satomura, Takemi Mastui, Fumitaka Ohsuzu, Akira KuritaAbstract:Purpose : Silent myocardial ischemic episodes as well as decreased heart rate variability (HRV) indices are associated with an unfavorable outcome in patients with coronary artery disease. Nipradilol, which is a non-selective beta-adrenergic and nitrate-like vasodilator anti-anginal agent developed in Japan, may ameliorate silent myocardial ischemia, while it also improves exercise tolerance and HRV indices in patients with chronic stable angina. Methods : To investigate the effect of Nipradilol (6 mg daily) on silent myocardial ischemic episodes and HRV indices, and to study its effect on the relationship between them, 24 patients with chronic stable angina underwent exercise treadmill testing and a 24-hour ambulatory electrocardiogram (ECG). The study protocol utilized a single blind, 4-week placebo-controlled design. The HRV indices from ambulatory ECG included mean RR (ms), SDNN (ms), SDANN (ms), SD (ms), rMSSD (ms), pNN50 (%); frequency analysis of HRV consisted of total (ms, 0.01–1.00 Hz), low (ms, 0.04–0.15 Hz) and high (ms, 0.15–0.40 Hz) components. Results : Nipradilol significantly decreased the mean heart rate at submaximal and maximal exercise and the mean pressure rate product at submaximal and maximal exercise. It significantly improved exercise-induced maximal ST segment depression from −1.7 ± 0.6 mm to −1.1 ± 0.7 mm ( p > 0.05). Silent myocardial ischemic episodes recorded during the 24-hour ambulatory ECG significantly decreased after Nipradilol administration. Nipradilol also significantly influenced several HRV indices as well as the relationship between silent myocardial ischemic episodes and the HRV indices. Nipradilol significantly increased SD, rMSSD, pNN50, total spectra, low frequency spectra and high frequency spectra. In addition, Nipradilol significantly decreased the LF/HF ratio from 1.7 (1.5–2.0) to 1.5 (1.3–1.8). These effects of Nipradilol on HRV indices concomitantly occurred with the reduction in silent myocardial ischemic episodes. Conclusion : Nipradilol was found to effectively improve the episodes of silent myocardial ischemia as well as exercise-induced ischemia probably due to its beta-blocking properties and not nitrate-like actions. In addition, Nipradilol also had a favorable effect on the HRV indices.
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effect of Nipradilol on silent myocardial ischemia plasma beta endorphin and bradykinin in chronic stable angina
Clinical Cardiology, 1996Co-Authors: Bonpei Takase, Hiroyuki Hikita, Kimio Satomura, Akira Kurita, Akimi Uehata, Toshihiko Nishioka, Hideki Mitani, Kyoichi Mizuno, Haruo NakamuraAbstract:HYPOTHESIS This study was undertaken to investigate the effect of Nipradilol on the total ischemic burden and on plasma levels of beta-endorphin and bradykinin. METHODS Sixteen patients with chronic stable angina were subjected to exercise treadmill testing and 24-h ambulatory electrocardiogram (ECG). RESULTS Nipradilol significantly decreased both mean heart rate and mean pressure rate product at submaximal and maximal exercise. It significantly improved exercise-induced maximal ST-segment depression from -2.7 +/- 0.5 mm to -1.3 +/- 0.6 mm (p < 0.05) and reduced the number of leads with significant ST-segment depression (4.0 +/- 1.2 vs. 2.0 +/- 1.8, p < 0.05). Silent ischemic episodes recorded in 24-h ambulatory ECG were significantly decreased by Nipradilol administration, concomitantly with a decrement of mean heart rate and observed maximal heart rate. Patients with exercise-induced silent myocardial ischemia showed significantly increased plasma levels of beta-endorphin during both the placebo and Nipradilol phases of the study. However, during the Nipradilol phase, bradykinin did not change significantly at rest and at peak exercise. CONCLUSION Nipradilol effectively controls exercise-induced myocardial ischemia and silent myocardial ischemic episodes, and does not influence the response of plasma levels of beta-endorphin to exercise stress testing in patients with exercise-induced silent myocardial ischemia.
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Effect of Nipradilol on silent myocardial ischemia, plasma beta‐endorphin, and bradykinin in chronic stable angina
Clinical cardiology, 1996Co-Authors: Bonpei Takase, Hiroyuki Hikita, Kimio Satomura, Akira Kurita, Akimi Uehata, Toshihiko Nishioka, Hideki Mitani, Kyoichi Mizuno, Haruo NakamuraAbstract:HYPOTHESIS This study was undertaken to investigate the effect of Nipradilol on the total ischemic burden and on plasma levels of beta-endorphin and bradykinin. METHODS Sixteen patients with chronic stable angina were subjected to exercise treadmill testing and 24-h ambulatory electrocardiogram (ECG). RESULTS Nipradilol significantly decreased both mean heart rate and mean pressure rate product at submaximal and maximal exercise. It significantly improved exercise-induced maximal ST-segment depression from -2.7 +/- 0.5 mm to -1.3 +/- 0.6 mm (p < 0.05) and reduced the number of leads with significant ST-segment depression (4.0 +/- 1.2 vs. 2.0 +/- 1.8, p < 0.05). Silent ischemic episodes recorded in 24-h ambulatory ECG were significantly decreased by Nipradilol administration, concomitantly with a decrement of mean heart rate and observed maximal heart rate. Patients with exercise-induced silent myocardial ischemia showed significantly increased plasma levels of beta-endorphin during both the placebo and Nipradilol phases of the study. However, during the Nipradilol phase, bradykinin did not change significantly at rest and at peak exercise. CONCLUSION Nipradilol effectively controls exercise-induced myocardial ischemia and silent myocardial ischemic episodes, and does not influence the response of plasma levels of beta-endorphin to exercise stress testing in patients with exercise-induced silent myocardial ischemia.