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Katsuomi Iwakura - One of the best experts on this subject based on the ideXlab platform.
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intravenous nicorandil in conjunction with Coronary Reperfusion therapy is associated with better clinical and functional outcomes in patients with acute myocardial infarction
Circulation, 2003Co-Authors: Ken Sugimoto, Hiroshi Ito, Katsuomi Iwakura, Akinobu Kato, Masashi Ikushima, Koji Tanaka, Ryusuke Kimura, Tohru Masuyama, Toshio Ogihara, Shigeo KawanoAbstract:The aim of this retrospective study was to assess whether intravenous nicorandil, a hybrid of NO and a KATP channel opener, in conjunction with percutaneous Coronary intervention (PCI) improves the long-term prognosis in patients with acute myocardial infarction (AMI). Intravenous nicorandil has already been shown to improve the in-hospital prognosis of patients with anterior AMI. The study population consisted of 272 patients with a reperfused AMI who were admitted during a similar time interval, before (control; n=114) and after nicorandil treatment (n=158). In the nicorandil group, a 4 mg bolus injection was given, followed by 6 mg/h infusion for 24 h and then oral nicorandil at 15 mg/day for at least 1 month. In the patients with an anterior AMI, left ventricular (LV) function was better and the frequency of LV remodeling was lower after 3 months in the nicorandil group; however, in those with a non-anterior AMI, there were no differences in functional outcome and the frequency of LV remodeling between the 2 groups. The frequency of cardiac events was significantly lower in the nicorandil group, and the use of nicorandil was derived as a potential factor related to freedom from cardiac events (p<0.01, odds ratio = 0.27). Nicorandil treatment was associated with better myocardial perfusion and a better functional and clinical outcome than PCI alone, and this beneficial effect was maintained for a long time, particularly in patients with anterior AMI.
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Predictive factors for development of the no-reflow phenomenon in patients with reperfused anterior wall acute myocardial infarction
Journal of the American College of Cardiology, 2001Co-Authors: Katsuomi Iwakura, Hiroshi Ito, Shigeo Kawano, Yasunori Shintani, Koichi Yamamoto, Akinobu Kato, Masashi Ikushima, Koji Tanaka, M Kitakaze, Masatsugu HoriAbstract:OBJECTIVES We sought to elucidate the clinical factors related to the development of no-reflow phenomenon after successful Coronary Reperfusion in patients with an acute myocardial infarction (AMI). BACKGROUND Myocardial contrast echocardiography revealed that the no-reflow phenomenon is observed in some patients with a reperfused AMI, and those patients usually have poor functional and clinical outcomes. It is still unknown what clinical factors are related to the development of the no-reflow phenomenon. METHODS Myocardial contrast echocardiography was performed 15 min after successful Coronary Reperfusion therapy in 199 patients with an anterior wall AMI who underwent successful Coronary Reperfusion with primary Coronary angioplasty within 24 h after the onset of AMI. Multiple logistic regression analysis was used to identify independent predictors of the no-reflow phenomenon. RESULTS Seventy-nine patients showed the no-reflow phenomenon. Univariate analysis indicated that pre-infarction angina within 48 h before symptom onset, Killip class, Thrombolysis in Myocardial Infarction flow grade 0 on the initial Coronary angiogram, the number of abnormal Q-waves and the wall motion score (WMS) on the echocardiogram obtained at hospital admission are related to the no-reflow phenomenon. Multivariate logistic regression analysis revealed that all of these factors, except for Killip class, are independent predictive factors of the no-reflow phenomenon. CONCLUSIONS Development of the no-reflow phenomenon is related to the severity of myocardial damage (number of Q-waves), the size of the risk area (WMS) and the occlusion status of infarct-related artery. In addition, ischemic preconditioning (pre-infarction angina) seems to be the factor that attenuates the no-reflow phenomenon.
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early temporal changes in Coronary flow velocity patterns in patients with acute myocardial infarction demonstrating the no reflow phenomenon
American Journal of Cardiology, 1999Co-Authors: Katsuomi Iwakura, Hiroshi Ito, Masatsugu Hori, Ken Sugimoto, Tohru Masuyama, Nagahiro Nishikawa, Kazuya Hiraoka, Yorihiko Higashino, Kenshi Fujii, Takazo MinaminoAbstract:Coronary flow velocity pattern in patients with acute myocardial infarction demonstrating no-reflow phenomenon is characterized with early systolic retrograde flow and rapid deceleration of diastolic flow velocity. In this study, we investigated the early temporal changes in microvascular function in patients with the no-reflow phenomenon. Among 144 patients with a first acute myocardial infarction, 33 exhibited sizable no-reflow phenomenon after Coronary Reperfusion with myocardial contrast echocardiography. We assessed temporal changes in Coronary flow velocity patterns with the Doppler guidewire. The early systolic retrograde flow was observed ≤10 seconds after Reperfusion in 16 patients (group A) or later in 17 patients (331 ± 327 seconds, group B). Diastolic deceleration rate was higher in group A than in group B at 1 minute after Reperfusion. It gradually increased in group B and showed comparable value to group A 10 minutes later. Group A had longer elapsed time from symptom onset to Reperfusion and a greater number of infarct Q waves before Reperfusion than group B (14 ± 13 vs 5 ± 2 hours, p <0.01; and 3 ± 2 vs 2± 1, p <0.02). In contrast, the incidence of transient ST reelevation shortly after Reperfusion was higher in group B (76% vs 25%, p <0.01). Thus, the characteristic Coronary flow velocity pattern is either established at the moment of Coronary Reperfusion or progresses thereafter in patients with no-reflow phenomenon. This suggests different mechanisms of developing ischemic microvascular injury.
Borja Ibanez - One of the best experts on this subject based on the ideXlab platform.
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study design for the effect of metoprolol in cardioprotection during an acute myocardial infarction metocard cnic a randomized controlled parallel group observer blinded clinical trial of early pre Reperfusion metoprolol administration in st segment elevation myocardial infarction
American Heart Journal, 2012Co-Authors: Borja Ibanez, Valentin Fuster, Carlos Macaya, Vicente Sanchezbrunete, Gonzalo Pizarro, Pedro Lopezromero, Alonso Mateos, Jesus JimenezborregueroAbstract:Background Infarct size predicts post-infarction mortality. Oral β-blockade within 24 hours of a ST-segment elevation acute myocardial infarction (STEMI) is a class-IA indication, however early intravenous (IV) β-blockers initiation is not encouraged. In recent magnetic resonance imaging (MRI)–based experimental studies, the β 1 -blocker metoprolol has been shown to reduce infarct size only when administered before Coronary Reperfusion. To date, there is not a single trial comparing the pre- vs. post-Reperfusion β-blocker initiation in STEMI. Objective The METOCARD-CNIC trial is testing whether the early initiation of IV metoprolol before primary percutaneous Coronary intervention (pPCI) could reduce infarct size and improve outcomes when compared to oral post-pPCI metoprolol initiation. Design The METOCARD-CNIC trial is a randomized parallel-group single-blind (to outcome evaluators) clinical effectiveness trial conducted in 5 Counties across Spain that will enroll 220 participants. Eligible are 18- to 80-year-old patients with anterior STEMI revascularized by pPCI ≤6 hours from symptom onset. Exclusion criteria are Killip-class ≥III, atrioventricular block or active treatment with β-blockers/bronchodilators. Primary end point is infarct size evaluated by MRI 5 to 7 days post-STEMI. Prespecified major secondary end points are salvage-index, left ventricular ejection fraction recovery (day 5-7 to 6 months), the composite of (death/malignant ventricular arrhythmias/reinfarction/admission due to heart failure), and myocardial perfusion. Conclusions The METOCARD-CNIC trial is testing the hypothesis that the early initiation of IV metoprolol pre-Reperfusion reduces infarct size in comparison to initiation of oral metoprolol post-Reperfusion. Given the implications of infarct size reduction in STEMI, if positive, this trial might evidence that a refined use of an approved inexpensive drug can improve outcomes of patients with STEMI.
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the cardioprotection granted by metoprolol is restricted to its administration prior to Coronary Reperfusion
International Journal of Cardiology, 2011Co-Authors: Borja Ibanez, Giovanni Cimmino, Susanna Pratgonzalez, Gemma Vilahur, Randolph Hutter, Mario J Garcia, Valentin Fuster, Javier Sanz, Lina BadimonAbstract:Background Myocardial infarct size is a strong predictor of cardiovascular events. Intravenous metoprolol before Coronary Reperfusion has been shown to reduce infarct size; however, it is unknown whether oral metoprolol initiated early after Reperfusion, as clinical guidelines recommend, is similarly cardioprotective. We compared the extent of myocardial salvage associated with intravenous pre-Reperfusion-metoprolol administration in comparison with oral post-Reperfusion-metoprolol or placebo. We also studied the effect on suspected markers of Reperfusion injury.
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early metoprolol administration before Coronary Reperfusion results in increased myocardial salvage analysis of ischemic myocardium at risk using cardiac magnetic resonance
Circulation, 2007Co-Authors: Borja Ibanez, Giovanni Cimmino, Susanna Pratgonzalez, Gemma Vilahur, Mario J Garcia, Valentin Fuster, Javier Sanz, Walter S Speidl, Antonio Pinero, Juan J BadimonAbstract:Background— β-Blockers improve clinical outcome when administered early after acute myocardial infarction. However, whether β-blockers actually reduce the myocardial infarction size is still in dis...
Hiroshi Ito - One of the best experts on this subject based on the ideXlab platform.
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intravenous nicorandil in conjunction with Coronary Reperfusion therapy is associated with better clinical and functional outcomes in patients with acute myocardial infarction
Circulation, 2003Co-Authors: Ken Sugimoto, Hiroshi Ito, Katsuomi Iwakura, Akinobu Kato, Masashi Ikushima, Koji Tanaka, Ryusuke Kimura, Tohru Masuyama, Toshio Ogihara, Shigeo KawanoAbstract:The aim of this retrospective study was to assess whether intravenous nicorandil, a hybrid of NO and a KATP channel opener, in conjunction with percutaneous Coronary intervention (PCI) improves the long-term prognosis in patients with acute myocardial infarction (AMI). Intravenous nicorandil has already been shown to improve the in-hospital prognosis of patients with anterior AMI. The study population consisted of 272 patients with a reperfused AMI who were admitted during a similar time interval, before (control; n=114) and after nicorandil treatment (n=158). In the nicorandil group, a 4 mg bolus injection was given, followed by 6 mg/h infusion for 24 h and then oral nicorandil at 15 mg/day for at least 1 month. In the patients with an anterior AMI, left ventricular (LV) function was better and the frequency of LV remodeling was lower after 3 months in the nicorandil group; however, in those with a non-anterior AMI, there were no differences in functional outcome and the frequency of LV remodeling between the 2 groups. The frequency of cardiac events was significantly lower in the nicorandil group, and the use of nicorandil was derived as a potential factor related to freedom from cardiac events (p<0.01, odds ratio = 0.27). Nicorandil treatment was associated with better myocardial perfusion and a better functional and clinical outcome than PCI alone, and this beneficial effect was maintained for a long time, particularly in patients with anterior AMI.
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Predictive factors for development of the no-reflow phenomenon in patients with reperfused anterior wall acute myocardial infarction
Journal of the American College of Cardiology, 2001Co-Authors: Katsuomi Iwakura, Hiroshi Ito, Shigeo Kawano, Yasunori Shintani, Koichi Yamamoto, Akinobu Kato, Masashi Ikushima, Koji Tanaka, M Kitakaze, Masatsugu HoriAbstract:OBJECTIVES We sought to elucidate the clinical factors related to the development of no-reflow phenomenon after successful Coronary Reperfusion in patients with an acute myocardial infarction (AMI). BACKGROUND Myocardial contrast echocardiography revealed that the no-reflow phenomenon is observed in some patients with a reperfused AMI, and those patients usually have poor functional and clinical outcomes. It is still unknown what clinical factors are related to the development of the no-reflow phenomenon. METHODS Myocardial contrast echocardiography was performed 15 min after successful Coronary Reperfusion therapy in 199 patients with an anterior wall AMI who underwent successful Coronary Reperfusion with primary Coronary angioplasty within 24 h after the onset of AMI. Multiple logistic regression analysis was used to identify independent predictors of the no-reflow phenomenon. RESULTS Seventy-nine patients showed the no-reflow phenomenon. Univariate analysis indicated that pre-infarction angina within 48 h before symptom onset, Killip class, Thrombolysis in Myocardial Infarction flow grade 0 on the initial Coronary angiogram, the number of abnormal Q-waves and the wall motion score (WMS) on the echocardiogram obtained at hospital admission are related to the no-reflow phenomenon. Multivariate logistic regression analysis revealed that all of these factors, except for Killip class, are independent predictive factors of the no-reflow phenomenon. CONCLUSIONS Development of the no-reflow phenomenon is related to the severity of myocardial damage (number of Q-waves), the size of the risk area (WMS) and the occlusion status of infarct-related artery. In addition, ischemic preconditioning (pre-infarction angina) seems to be the factor that attenuates the no-reflow phenomenon.
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early temporal changes in Coronary flow velocity patterns in patients with acute myocardial infarction demonstrating the no reflow phenomenon
American Journal of Cardiology, 1999Co-Authors: Katsuomi Iwakura, Hiroshi Ito, Masatsugu Hori, Ken Sugimoto, Tohru Masuyama, Nagahiro Nishikawa, Kazuya Hiraoka, Yorihiko Higashino, Kenshi Fujii, Takazo MinaminoAbstract:Coronary flow velocity pattern in patients with acute myocardial infarction demonstrating no-reflow phenomenon is characterized with early systolic retrograde flow and rapid deceleration of diastolic flow velocity. In this study, we investigated the early temporal changes in microvascular function in patients with the no-reflow phenomenon. Among 144 patients with a first acute myocardial infarction, 33 exhibited sizable no-reflow phenomenon after Coronary Reperfusion with myocardial contrast echocardiography. We assessed temporal changes in Coronary flow velocity patterns with the Doppler guidewire. The early systolic retrograde flow was observed ≤10 seconds after Reperfusion in 16 patients (group A) or later in 17 patients (331 ± 327 seconds, group B). Diastolic deceleration rate was higher in group A than in group B at 1 minute after Reperfusion. It gradually increased in group B and showed comparable value to group A 10 minutes later. Group A had longer elapsed time from symptom onset to Reperfusion and a greater number of infarct Q waves before Reperfusion than group B (14 ± 13 vs 5 ± 2 hours, p <0.01; and 3 ± 2 vs 2± 1, p <0.02). In contrast, the incidence of transient ST reelevation shortly after Reperfusion was higher in group B (76% vs 25%, p <0.01). Thus, the characteristic Coronary flow velocity pattern is either established at the moment of Coronary Reperfusion or progresses thereafter in patients with no-reflow phenomenon. This suggests different mechanisms of developing ischemic microvascular injury.
Michael Loos - One of the best experts on this subject based on the ideXlab platform.
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application of c1 esterase inhibitor during Reperfusion of ischemic myocardium dose related beneficial versus detrimental effects
Circulation, 2001Co-Authors: Georg Horstick, Axel Heimann, Gerd Hafner, Oliver Berg, Michael Loos, Otto Gotze, Benjamin Bierbach, Steffen E Petersen, Sucharit Bhakdi, Harald DariusAbstract:Background— Complement activation during Reperfusion of ischemic myocardium augments myocardial injury, and complement inhibition with C1-esterase inhibitor (C1-INH) at the time of Reperfusion exerts marked cardioprotective effects in experimental studies. Application of C1-INH in newborns, however, was recently reported to have dangerous and even lethal side effects. This study addresses the essential role of dosage in studies using C1-INH. Methods and Results— Cardioprotection by C1-INH was examined in a pig model with 60 minutes of Coronary occlusion followed by 120 minutes of Reperfusion. C1-INH was administered intravenously 5 to 10 minutes before Coronary Reperfusion without heparin at a dose of 40, 100, and 200 IU/kg body wt. Compared with the NaCl controls, C1-INH 40 IU/kg reduced myocardial injury (44.1±13.8% versus 76.7±4.6% necrosis of area at risk, P≤0.05) and significantly suppressed local C3a and C5a generation. Myocardial protection was accompanied by reduced plasma concentrations of creati...
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intraCoronary application of c1 esterase inhibitor improves cardiac function and reduces myocardial necrosis in an experimental model of ischemia and Reperfusion
Circulation, 1997Co-Authors: Georg Horstick, Axel Heimann, Otto Go Tze, Gerd Hafner, Oliver Berg, Peter Bo Ehmer, Phillip Becker, Harald Darius, Hansju Rgen Rupprecht, Michael LoosAbstract:Background Myocardial injury from ischemia can be aggravated by Reperfusion of the jeopardized area. The precise underlying mechanisms have not been clearly defined, but proinflammatory events, including complement activation, leukocyte adhesion, and infiltration and release of diverse mediators, probably play important roles. The present study addresses the possibility of reducing Reperfusion damage by the application of C1 esterase inhibitor (C1-INH). Methods and Results Cardioprotection by C1-INH 20 IU/kg IC was examined in a pig model with 60 minutes of Coronary occlusion, followed by 120 minutes of Reperfusion. C1-INH was administered during the first 5 minutes of Coronary Reperfusion. Compared with the NaCl controls, C1-INH reduced myocardial injury (48.8±7.8% versus 73.4±4.0% necrosis of area at risk, P≤.018). C1-INH treatment significantly reduced circulating C3a and slightly attenuated C5a plasma concentrations. Myocardial protection was accompanied by reduced plasma concentration of creatine kin...
Harald Darius - One of the best experts on this subject based on the ideXlab platform.
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application of c1 esterase inhibitor during Reperfusion of ischemic myocardium dose related beneficial versus detrimental effects
Circulation, 2001Co-Authors: Georg Horstick, Axel Heimann, Gerd Hafner, Oliver Berg, Michael Loos, Otto Gotze, Benjamin Bierbach, Steffen E Petersen, Sucharit Bhakdi, Harald DariusAbstract:Background— Complement activation during Reperfusion of ischemic myocardium augments myocardial injury, and complement inhibition with C1-esterase inhibitor (C1-INH) at the time of Reperfusion exerts marked cardioprotective effects in experimental studies. Application of C1-INH in newborns, however, was recently reported to have dangerous and even lethal side effects. This study addresses the essential role of dosage in studies using C1-INH. Methods and Results— Cardioprotection by C1-INH was examined in a pig model with 60 minutes of Coronary occlusion followed by 120 minutes of Reperfusion. C1-INH was administered intravenously 5 to 10 minutes before Coronary Reperfusion without heparin at a dose of 40, 100, and 200 IU/kg body wt. Compared with the NaCl controls, C1-INH 40 IU/kg reduced myocardial injury (44.1±13.8% versus 76.7±4.6% necrosis of area at risk, P≤0.05) and significantly suppressed local C3a and C5a generation. Myocardial protection was accompanied by reduced plasma concentrations of creati...
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intraCoronary application of c1 esterase inhibitor improves cardiac function and reduces myocardial necrosis in an experimental model of ischemia and Reperfusion
Circulation, 1997Co-Authors: Georg Horstick, Axel Heimann, Otto Go Tze, Gerd Hafner, Oliver Berg, Peter Bo Ehmer, Phillip Becker, Harald Darius, Hansju Rgen Rupprecht, Michael LoosAbstract:Background Myocardial injury from ischemia can be aggravated by Reperfusion of the jeopardized area. The precise underlying mechanisms have not been clearly defined, but proinflammatory events, including complement activation, leukocyte adhesion, and infiltration and release of diverse mediators, probably play important roles. The present study addresses the possibility of reducing Reperfusion damage by the application of C1 esterase inhibitor (C1-INH). Methods and Results Cardioprotection by C1-INH 20 IU/kg IC was examined in a pig model with 60 minutes of Coronary occlusion, followed by 120 minutes of Reperfusion. C1-INH was administered during the first 5 minutes of Coronary Reperfusion. Compared with the NaCl controls, C1-INH reduced myocardial injury (48.8±7.8% versus 73.4±4.0% necrosis of area at risk, P≤.018). C1-INH treatment significantly reduced circulating C3a and slightly attenuated C5a plasma concentrations. Myocardial protection was accompanied by reduced plasma concentration of creatine kin...