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Hiroaki Matsuoka - One of the best experts on this subject based on the ideXlab platform.
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plasma brain natriuretic peptide is a biochemical marker for the prediction of progressive Ventricular Remodeling after acute myocardial infarction
American Heart Journal, 1998Co-Authors: Noritoshi Nagaya, Toshio Nishikimi, Yoichi Goto, Yuji Miyao, Yoshio Kobayashi, Isao Morii, Satoshi Daikoku, Takahiro Matsumoto, Shunichi Miyazaki, Hiroaki MatsuokaAbstract:To investigate the relation between plasma brain natriuretic peptide (BNP) and progressive Ventricular Remodeling, we measured plasma BNP and atrial natriuretic peptide (ANP) in 30 patients with acute myocardial infarction on days 2, 7, 14, and 30 after the onset. Left Ventricular end-diastolic volume index (EDVI), end-systolic volume index (ESVI), and ejection fraction (EF) on admission and 1 month after the onset were assessed by left ventriculography. Changes in EDVI (deltaEDVI), ESVI (deltaESVI), and EF (deltaEF) were obtained by subtracting respective acute-phase values from corresponding chronic-phase values. Plasma ANP on days 2 and 7 showed only weak correlations with deltaEDVI (r = 0.48 and 0.54; both p < 0.01), whereas plasma BNP on day 7 more closely correlated with deltaEDVI (r = 0.77; p < 0.001). When study patients were divided into two groups according to plasma BNP on day 7, the group with BNP higher than 100 pg/ml showed greater increases in left Ventricular volume and less improvement in EF compared with the other group with BNP lower than 100 pg/ml (deltaEDVI = 10.4 +/- 8 vs -3.4 +/- 9 ml/m2, deltaESVI = 6.2 +/- 7 vs -4.9 +/- 5 ml/m2, and deltaEF = 1.0% +/- 4% vs 4.9% +/- 5%; p < 0.05, respectively). Multiple regression analysis revealed that only plasma BNP on day 7, but not ANP, peak creatine phosphokinase level, left Ventricular end-diastolic pressure, or acute-phase EF, correlated independently with deltaEDVI (p < 0.01). These results suggest that plasma BNP may be a simple and useful biochemical marker for the prediction of progressive Ventricular Remodeling within the first 30 days of acute myocardial infarction.
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plasma brain natriuretic peptide is a biochemical marker for the prediction of progressive Ventricular Remodeling after acute myocardial infarction
American Heart Journal, 1998Co-Authors: Noritoshi Nagaya, Toshio Nishikimi, Yoichi Goto, Yuji Miyao, Yoshio Kobayashi, Isao Morii, Satoshi Daikoku, Takahiro Matsumoto, Shunichi Miyazaki, Hiroaki MatsuokaAbstract:Abstract To investigate the relation between plasma brain natriuretic peptide (BNP) and progressive Ventricular Remodeling, we measured plasma BNP and atrial natriuretic peptide (ANP) in 30 patients with acute myocardial infarction on days 2, 7, 14, and 30 after the onset. Left Ventricular end-diastolic volume index (EDVI), end-systolic volume index (ESVI), and ejection fraction (EF) on admission and 1 month after the onset were assessed by left ventriculography. Changes in EDVI (ΔEDVI), ESVI (ΔESVI), and EF (ΔEF) were obtained by subtracting respective acute-phase values from corresponding chronic-phase values. Plasma ANP on days 2 and 7 showed only weak correlations with ΔEDVI ( r = 0.48 and 0.54; both p r = 0.77; p 2 , DESVI = 6.2 ± 7 vs –4.9 ± 5 ml/m 2 , and DEF = 1.0% ± 4% vs 4.9% ± 5%; p p
Ravinay Bhindi - One of the best experts on this subject based on the ideXlab platform.
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the nrf2 activator dh404 attenuates adverse Ventricular Remodeling post myocardial infarction by modifying redox signalling
Free Radical Biology and Medicine, 2017Co-Authors: Kristen J Bubb, Owen Tang, Asa Birna Birgisdottir, Cindy Kok, Nathalie Rasko, Rebecca H Ritchie, Ravinay Bhindi, Thomas Steen HansenAbstract:Background The novel synthetic triterpenoid, bardoxolone methyl, has the ability to upregulate cytoprotective proteins via induction of the nuclear factor erythroid-2-related factor 2 (Nrf2) pathway. This makes it a promising therapeutic agent in disease states characterized by dysregulated oxidative signalling. We have examined the effect of a Nrf2 activator, dihydro-CDDO-trifluoroethyl amide (DH404), a derivative of bardoxolone methyl, on post-infarct cardiac Remodeling in rats. Methods/Results DH404, administered from day 2 post myocardial infarction (MI: 30 min transient ischemia followed by reperfusion) resulted in almost complete protection against adverse Ventricular Remodeling as assessed at day 28 (left Ventricular end-systolic area: sham 0.14±0.01 cm2, MI vehicle 0.29±0.04 cm2 vs. MI DH404 0.18±0.02 cm2, P<0.05); infarct size (21.3±3.4% MI vehicle vs. 10.9±2.3% MI DH404, P<0.05) with associated benefits on systolic function (fractional shortening: sham 71.9±2.6%, MI vehicle 36.2±1.9% vs. MI DH404 58.6±4.0%, P<0.05). These structural and functional benefits were associated with lower myocardial expression of atrial natriuretic peptide (ANP, P<0.01 vs. MI vehicle), and decreased fibronectin (P<0.01 vs. MI vehicle) in DH404-treated MI rats at 28 days. MI increased glutathionylation of endothelial nitric oxide synthase (eNOS) in vitro - a molecular switch that uncouples the enzyme, increasing superoxide production and decreasing nitric oxide (NO) bioavailability. MI-induced eNOS glutathionylation was substantially ameliorated by DH404. An associated increase in glutaredoxin 1 (Grx1) co-immunoprecipitation with eNOS without a change in expression was mechanistically intriguing. Indeed, in parallel in vitro experiments, silencing of Grx1 abolished the protective effect of DH404 against Angiotensin II-induced eNOS uncoupling. Conclusion The bardoxolone derivative DH404 significantly attenuated cardiac Remodeling post MI, at least in part, by re-coupling of eNOS and increasing the functional interaction of Grx1 with eNOS. This agent may have clinical benefits protecting against post MI cardiomyopathy.
Norman Sharpe - One of the best experts on this subject based on the ideXlab platform.
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effects of carvedilol on left Ventricular Remodeling after acute myocardial infarction the capricorn echo substudy
Circulation, 2004Co-Authors: Robert N Doughty, Gillian A Whalley, H Walsh, Greg D Gamble, Jose Lopezsendon, Norman SharpeAbstract:Background— The CAPRICORN trial has shown that carvedilol improved outcome in patients with left Ventricular dysfunction after acute myocardial infarction treated with ACE inhibitors. The aim of this substudy was to determine the effects of carvedilol on left Ventricular Remodeling in this patient group. Methods and Results— Patients entering the CAPRICORN trial from 13 centers in New Zealand, Australia, and Spain were recruited for this echocardiographic substudy. In 127 patients, quantitative 2D echocardiography was performed according to a standard protocol before randomization and repeated after 1, 3, and 6 months of treatment with carvedilol or placebo. Left Ventricular volumes, ejection fraction (Simpson’s method), and wall motion score index were determined in a blinded analysis at the Core Echo Laboratory. At 6 months, left Ventricular end systolic volume was 9.2 mL less in the carvedilol group than in the placebo group (P=0.023), and left Ventricular ejection fraction was 3.9% higher (P=0.015). L...
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left Ventricular Remodeling after myocardial infarction pathophysiology and therapy
Circulation, 2000Co-Authors: Martin St John Sutton, Norman SharpeAbstract:Left Ventricular Remodeling is the process by which Ventricular size, shape, and function are regulated by mechanical, neurohormonal, and genetic factors.1 2 Remodeling may be physiological and adaptive during normal growth or pathological due to myocardial infarction, cardiomyopathy, hypertension, or valvular heart disease (Figure 1⇓). This article will review postinfarction Remodeling, pathophysiological mechanisms, and therapeutic intervention. Figure 1. Diagrammatic representation of the many factors involved in the pathophysiology of Ventricular Remodeling. ECM indicates extracellular matrix; RAAS, renin-angiotensin-aldosterone system; CO, cardiac output; SVR, systemic vascular resistance; LV, left Ventricular; and AII, angiotensin II. ### Postinfarction Left Ventricular Remodeling The acute loss of myocardium results in an abrupt increase in loading conditions that induces a unique pattern of Remodeling involving the infarcted border zone and remote noninfarcted myocardium. Myocyte necrosis and the resultant increase in load trigger a cascade of biochemical intracellular signaling processes that initiates and subsequently modulates reparative changes, which include dilatation, hypertrophy, and the formation of a discrete collagen scar. Ventricular Remodeling may continue for weeks or months until the distending forces are counterbalanced by the tensile strength of the collagen scar. This balance is determined by the size, location, and transmurality of the infarct, the extent of myocardial stunning, the patency of the infarct-related artery, and local tropic factors.1 3 The myocardium consists of 3 integrated components: myocytes, extracellular matrix, and the capillary microcirculation that services the contractile unit assembly. Consideration of all 3 components provides important insights into the Remodeling process and a rationale for future therapeutic strategies. The cardiomyocyte is terminally differentiated and develops tension by shortening. The extracellular matrix provides a stress-tolerant, viscoelastic scaffold consisting of type I and type III collagen that couples myocytes and maintains the spatial relations between the myofilaments and their capillary microcirculation.4 5 The collagen framework couples adjacent myocytes by intercellular struts that …
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left Ventricular Remodeling with carvedilol in patients with congestive heart failure due to ischemic heart disease
Journal of the American College of Cardiology, 1997Co-Authors: Robert N Doughty, Gillian A Whalley, Greg D Gamble, Stephen Macmahon, Norman SharpeAbstract:Abstract Objectives. The aim of this study, a substudy of the Australia–New Zealand trial of carvedilol in patients with heart failure due to ischemic heart disease, was to determine the effects of this treatment on left Ventricular size and function with the use of quantitative two-dimensional (2D) echocardiography. Background. Beta-adrenergic blocking drugs have been shown to improve left Ventricular ejection fraction in patients with heart failure due to either ischemic heart disease or idiopathic dilated cardiomyopathy. However, the effects of such treatment on left Ventricular size remain uncertain. Methods. One hundred twenty-three patients from 10 centers in New Zealand and Australia participated in the 2D echocardiographic substudy. Echocardiography was performed before randomization and was repeated after 6 and 12 months of treatment. Left Ventricular end-diastolic and end-systolic volumes were measured from apical four- and two-chamber views with the use of a modified Simpson’s rule method. Results. After 12 months, heart rate was 8 beats/min lower in the carvedilol than in the placebo group, whereas left Ventricular end-diastolic and end-systolic volumes were increased in the placebo group but reduced in the carvedilol group. At 12 months, left Ventricular end-diastolic volume index was 14 ml/m2less in the carvedilol than in the placebo group (p = 0.0015); left Ventricular end-systolic volume index was 15.3 ml/m2less (p = 0.0001), and left Ventricular ejection fraction was 5.8% greater (p = 0.0015). Conclusions. In patients with heart failure due to ischemic heart disease, carvedilol therapy for 12 months reduced left Ventricular volumes, increased left Ventricular ejection fraction and prevented progressive left Ventricular dilation. These changes demonstrate a beneficial effect of carvedilol on left Ventricular Remodeling in heart failure. The observed changes may explain in part the improved clinical outcomes produced by treatment with carvedilol. (J Am Coll Cardiol 1997;29:1060–6) © 1997 by the American College of Cardiology
Noritoshi Nagaya - One of the best experts on this subject based on the ideXlab platform.
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plasma brain natriuretic peptide is a biochemical marker for the prediction of progressive Ventricular Remodeling after acute myocardial infarction
American Heart Journal, 1998Co-Authors: Noritoshi Nagaya, Toshio Nishikimi, Yoichi Goto, Yuji Miyao, Yoshio Kobayashi, Isao Morii, Satoshi Daikoku, Takahiro Matsumoto, Shunichi Miyazaki, Hiroaki MatsuokaAbstract:To investigate the relation between plasma brain natriuretic peptide (BNP) and progressive Ventricular Remodeling, we measured plasma BNP and atrial natriuretic peptide (ANP) in 30 patients with acute myocardial infarction on days 2, 7, 14, and 30 after the onset. Left Ventricular end-diastolic volume index (EDVI), end-systolic volume index (ESVI), and ejection fraction (EF) on admission and 1 month after the onset were assessed by left ventriculography. Changes in EDVI (deltaEDVI), ESVI (deltaESVI), and EF (deltaEF) were obtained by subtracting respective acute-phase values from corresponding chronic-phase values. Plasma ANP on days 2 and 7 showed only weak correlations with deltaEDVI (r = 0.48 and 0.54; both p < 0.01), whereas plasma BNP on day 7 more closely correlated with deltaEDVI (r = 0.77; p < 0.001). When study patients were divided into two groups according to plasma BNP on day 7, the group with BNP higher than 100 pg/ml showed greater increases in left Ventricular volume and less improvement in EF compared with the other group with BNP lower than 100 pg/ml (deltaEDVI = 10.4 +/- 8 vs -3.4 +/- 9 ml/m2, deltaESVI = 6.2 +/- 7 vs -4.9 +/- 5 ml/m2, and deltaEF = 1.0% +/- 4% vs 4.9% +/- 5%; p < 0.05, respectively). Multiple regression analysis revealed that only plasma BNP on day 7, but not ANP, peak creatine phosphokinase level, left Ventricular end-diastolic pressure, or acute-phase EF, correlated independently with deltaEDVI (p < 0.01). These results suggest that plasma BNP may be a simple and useful biochemical marker for the prediction of progressive Ventricular Remodeling within the first 30 days of acute myocardial infarction.
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plasma brain natriuretic peptide is a biochemical marker for the prediction of progressive Ventricular Remodeling after acute myocardial infarction
American Heart Journal, 1998Co-Authors: Noritoshi Nagaya, Toshio Nishikimi, Yoichi Goto, Yuji Miyao, Yoshio Kobayashi, Isao Morii, Satoshi Daikoku, Takahiro Matsumoto, Shunichi Miyazaki, Hiroaki MatsuokaAbstract:Abstract To investigate the relation between plasma brain natriuretic peptide (BNP) and progressive Ventricular Remodeling, we measured plasma BNP and atrial natriuretic peptide (ANP) in 30 patients with acute myocardial infarction on days 2, 7, 14, and 30 after the onset. Left Ventricular end-diastolic volume index (EDVI), end-systolic volume index (ESVI), and ejection fraction (EF) on admission and 1 month after the onset were assessed by left ventriculography. Changes in EDVI (ΔEDVI), ESVI (ΔESVI), and EF (ΔEF) were obtained by subtracting respective acute-phase values from corresponding chronic-phase values. Plasma ANP on days 2 and 7 showed only weak correlations with ΔEDVI ( r = 0.48 and 0.54; both p r = 0.77; p 2 , DESVI = 6.2 ± 7 vs –4.9 ± 5 ml/m 2 , and DEF = 1.0% ± 4% vs 4.9% ± 5%; p p
Yoshio Kobayashi - One of the best experts on this subject based on the ideXlab platform.
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deletion of cd28 co stimulatory signals exacerbates left Ventricular Remodeling and increases cardiac rupture after myocardial infarction
Circulation, 2016Co-Authors: Akihiko Kubota, Yoshio Kobayashi, Genzou Takemura, Hiroshi Hasegawa, Hiroyuki Tadokoro, Masanori Hirose, Yuka Kobara, Tomoko Yamadainagawa, Hiroyuki TakanoAbstract:Background Inflammatory responses, especially by CD4(+)T cells activated by dendritic cells, are known to be important in the pathophysiology of cardiac repair after myocardial infarction (MI). Although co-stimulatory signals through B7 (CD80/86) and CD28 are necessary for CD4(+)T cell activation and survival, the roles of these signals in cardiac repair after MI are still unclear. Methods and results C57BL/6 (Control) mice and CD28 knockout (CD28KO) mice were subjected to left coronary artery permanent ligation. The ratio of death by cardiac rupture within 5 days after MI was significantly higher in CD28KO mice compared with Control mice. Although there were no significant differences in the infarct size between the 2 groups, left Ventricular end-diastolic and end-systolic diameters were significantly increased, and fractional shortening was significantly decreased in CD28KO mice compared with Control mice. Electron microscopic observation revealed that the extent of extracellular collagen fiber was significantly decreased in CD28KO mice compared with Control mice. The number of α-smooth muscle actin-positive myofibroblasts was significantly decreased, and matrix metalloproteinase-9 activity and the mRNA expression of interleukin-1β were significantly increased in CD28KO mice compared with Control mice. Conclusions Deletion of CD28 co-stimulatory signals exacerbates left Ventricular Remodeling and increases cardiac rupture after MI through prolongation of the inflammatory period and reduction of collagen fiber in the infarct scars. (Circ J 2016; 80: 1971-1979).
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plasma brain natriuretic peptide is a biochemical marker for the prediction of progressive Ventricular Remodeling after acute myocardial infarction
American Heart Journal, 1998Co-Authors: Noritoshi Nagaya, Toshio Nishikimi, Yoichi Goto, Yuji Miyao, Yoshio Kobayashi, Isao Morii, Satoshi Daikoku, Takahiro Matsumoto, Shunichi Miyazaki, Hiroaki MatsuokaAbstract:To investigate the relation between plasma brain natriuretic peptide (BNP) and progressive Ventricular Remodeling, we measured plasma BNP and atrial natriuretic peptide (ANP) in 30 patients with acute myocardial infarction on days 2, 7, 14, and 30 after the onset. Left Ventricular end-diastolic volume index (EDVI), end-systolic volume index (ESVI), and ejection fraction (EF) on admission and 1 month after the onset were assessed by left ventriculography. Changes in EDVI (deltaEDVI), ESVI (deltaESVI), and EF (deltaEF) were obtained by subtracting respective acute-phase values from corresponding chronic-phase values. Plasma ANP on days 2 and 7 showed only weak correlations with deltaEDVI (r = 0.48 and 0.54; both p < 0.01), whereas plasma BNP on day 7 more closely correlated with deltaEDVI (r = 0.77; p < 0.001). When study patients were divided into two groups according to plasma BNP on day 7, the group with BNP higher than 100 pg/ml showed greater increases in left Ventricular volume and less improvement in EF compared with the other group with BNP lower than 100 pg/ml (deltaEDVI = 10.4 +/- 8 vs -3.4 +/- 9 ml/m2, deltaESVI = 6.2 +/- 7 vs -4.9 +/- 5 ml/m2, and deltaEF = 1.0% +/- 4% vs 4.9% +/- 5%; p < 0.05, respectively). Multiple regression analysis revealed that only plasma BNP on day 7, but not ANP, peak creatine phosphokinase level, left Ventricular end-diastolic pressure, or acute-phase EF, correlated independently with deltaEDVI (p < 0.01). These results suggest that plasma BNP may be a simple and useful biochemical marker for the prediction of progressive Ventricular Remodeling within the first 30 days of acute myocardial infarction.
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plasma brain natriuretic peptide is a biochemical marker for the prediction of progressive Ventricular Remodeling after acute myocardial infarction
American Heart Journal, 1998Co-Authors: Noritoshi Nagaya, Toshio Nishikimi, Yoichi Goto, Yuji Miyao, Yoshio Kobayashi, Isao Morii, Satoshi Daikoku, Takahiro Matsumoto, Shunichi Miyazaki, Hiroaki MatsuokaAbstract:Abstract To investigate the relation between plasma brain natriuretic peptide (BNP) and progressive Ventricular Remodeling, we measured plasma BNP and atrial natriuretic peptide (ANP) in 30 patients with acute myocardial infarction on days 2, 7, 14, and 30 after the onset. Left Ventricular end-diastolic volume index (EDVI), end-systolic volume index (ESVI), and ejection fraction (EF) on admission and 1 month after the onset were assessed by left ventriculography. Changes in EDVI (ΔEDVI), ESVI (ΔESVI), and EF (ΔEF) were obtained by subtracting respective acute-phase values from corresponding chronic-phase values. Plasma ANP on days 2 and 7 showed only weak correlations with ΔEDVI ( r = 0.48 and 0.54; both p r = 0.77; p 2 , DESVI = 6.2 ± 7 vs –4.9 ± 5 ml/m 2 , and DEF = 1.0% ± 4% vs 4.9% ± 5%; p p
