The Experts below are selected from a list of 240 Experts worldwide ranked by ideXlab platform
Frans H H Leenen - One of the best experts on this subject based on the ideXlab platform.
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Relevance of Angiotensin II for Cardiac Hypertrophy and Failure Induced by Cardiac Volume Overload
Heart Failure Reviews, 1999Co-Authors: Marcel Ruzicka, Frans H H LeenenAbstract:Angiotensin II can contribute to the development and maintenance of Cardiac hypertrophy indirectly via its hemodynamic effects and directly via its Cardiac trophic effects. Cardiac Volume overload by aortocaval shunt increases plasma angiotensin II as well as angiotensin II generated by Cardiac tissue. Plasma angiotensin II contributes to the Cardiac Volume overload via its hemodynamic effects, since blockers of the renin–angiotensin system attenuate the rise in left ventricular end-diastolic pressure (LVEDP). Increased Cardiac angiotensin II, generated by and dependent on Cardiac ACE, however, appears to drive the hypertrophic response. For a similar prevention of the rise in circulating angiotensin II and in LVEDP, only an angiotensin-converting enzyme (ACE) inhibitor with high affinity for Cardiac ACE (quinapril) also prevents the rise in Cardiac angiotensin II and—similar to an AT1 receptor blocker—the development of Cardiac hypertrophy. An ACE inhibitor with low affinity for Cardiac ACE (enalapril) does not prevent the rise in Cardiac angiotensin II by aortocaval shunt and the development of Cardiac hypertrophy. In the maintenance phase of Cardiac Volume overload, Cardiac angiotensin II returns to normal and hypertrophic growth and Cardiac remodeling cease. In this phase, enalapril causes regression of Cardiac hypertrophy in relation to its hemodynamic effects and in a manner similar to an AT1 receptor blocker. In other models of Cardiac Volume overload (e.g., aortic insufficiency or minoxidil treatment), data on plasma and Cardiac angiotensin II are missing, and the role of Cardiac angiotensin II in the development and maintenance of Cardiac hypertrophy is still to be assessed. Similarly, the role of Cardiac angiotensin II in the transition from maintenance phase into heart failure and the progression of heart failure has not yet been studied.
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Relevance of Angiotensin II for Cardiac Hypertrophy and Failure Induced by Cardiac Volume Overload
Heart Failure Reviews, 1999Co-Authors: Marcel Ruzicka, Frans H H LeenenAbstract:Angiotensin II can contribute to the development and maintenance of Cardiac hypertrophy indirectly via its hemodynamic effects and directly via its Cardiac trophic effects. Cardiac Volume overload by aortocaval shunt increases plasma angiotensin II as well as angiotensin II generated by Cardiac tissue. Plasma angiotensin II contributes to the Cardiac Volume overload via its hemodynamic effects, since blockers of the renin–angiotensin system attenuate the rise in left ventricular end-diastolic pressure (LVEDP). Increased Cardiac angiotensin II, generated by and dependent on Cardiac ACE, however, appears to drive the hypertrophic response. For a similar prevention of the rise in circulating angiotensin II and in LVEDP, only an angiotensin-converting enzyme (ACE) inhibitor with high affinity for Cardiac ACE (quinapril) also prevents the rise in Cardiac angiotensin II and—similar to an AT1 receptor blocker—the development of Cardiac hypertrophy. An ACE inhibitor with low affinity for Cardiac ACE (enalapril) does not prevent the rise in Cardiac angiotensin II by aortocaval shunt and the development of Cardiac hypertrophy. In the maintenance phase of Cardiac Volume overload, Cardiac angiotensin II returns to normal and hypertrophic growth and Cardiac remodeling cease. In this phase, enalapril causes regression of Cardiac hypertrophy in relation to its hemodynamic effects and in a manner similar to an AT1 receptor blocker.
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The renin-angiotensin system and Volume overload-induced changes in Cardiac collagen and elastin.
Circulation, 1994Co-Authors: Marcel Ruzicka, Fred W Keeley, Frans H H LeenenAbstract:BACKGROUNDBesides Cardiac load, the renin-angiotensin system (RAS) and aldosterone may regulate collagen accumulation during maturation or hypertrophic growth. The effect of Cardiac Volume overload on both left ventricular (LV) and right ventricular (RV) collagen and elastin and the possible role of the RAS in such changes have not yet been assessed.METHODS AND RESULTSIn the present study we assessed (1) the effects of 4 to 10 weeks of Volume overload by an aortocaval shunt or minoxidil on LV and RV collagen and elastin and (2) the potential of the angiotensin-converting enzyme inhibitor enalapril and the angiotensin II receptor blocker losartan to prevent and regress Volume overload-induced changes in Cardiac collagen and elastin. Cardiac Volume overload by aortocaval shunt or minoxidil treatment decreased LV collagen accumulation as compared with control rats. In contrast, RV collagen accumulation was potentiated during the initial weeks but not during chronic aortocaval shunt. Enalapril and losartan pr...
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The renin-angiotensin system and Volume overload-induced changes in Cardiac collagen and elastin.
Circulation, 1994Co-Authors: Marcel Ruzicka, Fred W Keeley, Frans H H LeenenAbstract:BACKGROUNDBesides Cardiac load, the renin-angiotensin system (RAS) and aldosterone may regulate collagen accumulation during maturation or hypertrophic growth. The effect of Cardiac Volume overload on both left ventricular (LV) and right ventricular (RV) collagen and elastin and the possible role of the RAS in such changes have not yet been assessed.METHODS AND RESULTSIn the present study we assessed (1) the effects of 4 to 10 weeks of Volume overload by an aortocaval shunt or minoxidil on LV and RV collagen and elastin and (2) the potential of the angiotensin-converting enzyme inhibitor enalapril and the angiotensin II receptor blocker losartan to prevent and regress Volume overload-induced changes in Cardiac collagen and elastin. Cardiac Volume overload by aortocaval shunt or minoxidil treatment decreased LV collagen accumulation as compared with control rats. In contrast, RV collagen accumulation was potentiated during the initial weeks but not during chronic aortocaval shunt. Enalapril and losartan pr...
Marcel Ruzicka - One of the best experts on this subject based on the ideXlab platform.
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Relevance of Angiotensin II for Cardiac Hypertrophy and Failure Induced by Cardiac Volume Overload
Heart Failure Reviews, 1999Co-Authors: Marcel Ruzicka, Frans H H LeenenAbstract:Angiotensin II can contribute to the development and maintenance of Cardiac hypertrophy indirectly via its hemodynamic effects and directly via its Cardiac trophic effects. Cardiac Volume overload by aortocaval shunt increases plasma angiotensin II as well as angiotensin II generated by Cardiac tissue. Plasma angiotensin II contributes to the Cardiac Volume overload via its hemodynamic effects, since blockers of the renin–angiotensin system attenuate the rise in left ventricular end-diastolic pressure (LVEDP). Increased Cardiac angiotensin II, generated by and dependent on Cardiac ACE, however, appears to drive the hypertrophic response. For a similar prevention of the rise in circulating angiotensin II and in LVEDP, only an angiotensin-converting enzyme (ACE) inhibitor with high affinity for Cardiac ACE (quinapril) also prevents the rise in Cardiac angiotensin II and—similar to an AT1 receptor blocker—the development of Cardiac hypertrophy. An ACE inhibitor with low affinity for Cardiac ACE (enalapril) does not prevent the rise in Cardiac angiotensin II by aortocaval shunt and the development of Cardiac hypertrophy. In the maintenance phase of Cardiac Volume overload, Cardiac angiotensin II returns to normal and hypertrophic growth and Cardiac remodeling cease. In this phase, enalapril causes regression of Cardiac hypertrophy in relation to its hemodynamic effects and in a manner similar to an AT1 receptor blocker. In other models of Cardiac Volume overload (e.g., aortic insufficiency or minoxidil treatment), data on plasma and Cardiac angiotensin II are missing, and the role of Cardiac angiotensin II in the development and maintenance of Cardiac hypertrophy is still to be assessed. Similarly, the role of Cardiac angiotensin II in the transition from maintenance phase into heart failure and the progression of heart failure has not yet been studied.
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Relevance of Angiotensin II for Cardiac Hypertrophy and Failure Induced by Cardiac Volume Overload
Heart Failure Reviews, 1999Co-Authors: Marcel Ruzicka, Frans H H LeenenAbstract:Angiotensin II can contribute to the development and maintenance of Cardiac hypertrophy indirectly via its hemodynamic effects and directly via its Cardiac trophic effects. Cardiac Volume overload by aortocaval shunt increases plasma angiotensin II as well as angiotensin II generated by Cardiac tissue. Plasma angiotensin II contributes to the Cardiac Volume overload via its hemodynamic effects, since blockers of the renin–angiotensin system attenuate the rise in left ventricular end-diastolic pressure (LVEDP). Increased Cardiac angiotensin II, generated by and dependent on Cardiac ACE, however, appears to drive the hypertrophic response. For a similar prevention of the rise in circulating angiotensin II and in LVEDP, only an angiotensin-converting enzyme (ACE) inhibitor with high affinity for Cardiac ACE (quinapril) also prevents the rise in Cardiac angiotensin II and—similar to an AT1 receptor blocker—the development of Cardiac hypertrophy. An ACE inhibitor with low affinity for Cardiac ACE (enalapril) does not prevent the rise in Cardiac angiotensin II by aortocaval shunt and the development of Cardiac hypertrophy. In the maintenance phase of Cardiac Volume overload, Cardiac angiotensin II returns to normal and hypertrophic growth and Cardiac remodeling cease. In this phase, enalapril causes regression of Cardiac hypertrophy in relation to its hemodynamic effects and in a manner similar to an AT1 receptor blocker.
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The renin-angiotensin system and Volume overload-induced changes in Cardiac collagen and elastin.
Circulation, 1994Co-Authors: Marcel Ruzicka, Fred W Keeley, Frans H H LeenenAbstract:BACKGROUNDBesides Cardiac load, the renin-angiotensin system (RAS) and aldosterone may regulate collagen accumulation during maturation or hypertrophic growth. The effect of Cardiac Volume overload on both left ventricular (LV) and right ventricular (RV) collagen and elastin and the possible role of the RAS in such changes have not yet been assessed.METHODS AND RESULTSIn the present study we assessed (1) the effects of 4 to 10 weeks of Volume overload by an aortocaval shunt or minoxidil on LV and RV collagen and elastin and (2) the potential of the angiotensin-converting enzyme inhibitor enalapril and the angiotensin II receptor blocker losartan to prevent and regress Volume overload-induced changes in Cardiac collagen and elastin. Cardiac Volume overload by aortocaval shunt or minoxidil treatment decreased LV collagen accumulation as compared with control rats. In contrast, RV collagen accumulation was potentiated during the initial weeks but not during chronic aortocaval shunt. Enalapril and losartan pr...
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The renin-angiotensin system and Volume overload-induced changes in Cardiac collagen and elastin.
Circulation, 1994Co-Authors: Marcel Ruzicka, Fred W Keeley, Frans H H LeenenAbstract:BACKGROUNDBesides Cardiac load, the renin-angiotensin system (RAS) and aldosterone may regulate collagen accumulation during maturation or hypertrophic growth. The effect of Cardiac Volume overload on both left ventricular (LV) and right ventricular (RV) collagen and elastin and the possible role of the RAS in such changes have not yet been assessed.METHODS AND RESULTSIn the present study we assessed (1) the effects of 4 to 10 weeks of Volume overload by an aortocaval shunt or minoxidil on LV and RV collagen and elastin and (2) the potential of the angiotensin-converting enzyme inhibitor enalapril and the angiotensin II receptor blocker losartan to prevent and regress Volume overload-induced changes in Cardiac collagen and elastin. Cardiac Volume overload by aortocaval shunt or minoxidil treatment decreased LV collagen accumulation as compared with control rats. In contrast, RV collagen accumulation was potentiated during the initial weeks but not during chronic aortocaval shunt. Enalapril and losartan pr...
H Sonntag - One of the best experts on this subject based on the ideXlab platform.
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changes in central venous pressure and pulmonary capillary wedge pressure do not indicate changes in right and left heart Volume in patients undergoing coronary artery bypass surgery
European Journal of Anaesthesiology, 1999Co-Authors: Wolfgang F Buhre, A Weyland, B Schorn, M Scholz, S Kazmaier, Andreas Hoeft, H SonntagAbstract:The value of pulmonary artery catheterization is a matter for discussion. Previous studies suggest that direct measurements of intravascular Volume distribution and Cardiac Volume indices may be of greater relevance than central venous and pulmonary capillary wedge pressure. We therefore used a thermo-dye dilution technique for the quantification of central blood Volume, right ventricular end-diastolic Volume and left heart Volume in patients undergoing coronary artery bypass surgery. Measurements were performed after the induction of anaesthesia as well as 1, 6 and 24 h after surgery. Central venous pressure was significantly increased at 1 and 6 h, whereas right ventricular end-diastolic Volume was increased only at 6 h post-operatively. Pulmonary capillary wedge pressure showed a tendency to increase whereas left heart and central blood Volume decreased significantly after surgery. The results of the present study suggest that changes in Cardiac filling pressure do not indicate changes in indices of Cardiac Volume in patients after coronary bypass surgery.
Wolfgang F Buhre - One of the best experts on this subject based on the ideXlab platform.
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changes in central venous pressure and pulmonary capillary wedge pressure do not indicate changes in right and left heart Volume in patients undergoing coronary artery bypass surgery
European Journal of Anaesthesiology, 1999Co-Authors: Wolfgang F Buhre, A Weyland, B Schorn, M Scholz, S Kazmaier, Andreas Hoeft, H SonntagAbstract:The value of pulmonary artery catheterization is a matter for discussion. Previous studies suggest that direct measurements of intravascular Volume distribution and Cardiac Volume indices may be of greater relevance than central venous and pulmonary capillary wedge pressure. We therefore used a thermo-dye dilution technique for the quantification of central blood Volume, right ventricular end-diastolic Volume and left heart Volume in patients undergoing coronary artery bypass surgery. Measurements were performed after the induction of anaesthesia as well as 1, 6 and 24 h after surgery. Central venous pressure was significantly increased at 1 and 6 h, whereas right ventricular end-diastolic Volume was increased only at 6 h post-operatively. Pulmonary capillary wedge pressure showed a tendency to increase whereas left heart and central blood Volume decreased significantly after surgery. The results of the present study suggest that changes in Cardiac filling pressure do not indicate changes in indices of Cardiac Volume in patients after coronary bypass surgery.
David J. Sahn - One of the best experts on this subject based on the ideXlab platform.
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Real-time 3-dimensional echocardiographic assessment of ventricular Volume, mass, and function in human fetuses.
PloS one, 2013Co-Authors: Minjuan Zheng, Micheal Schaal, Yan Chen, Weihui Shentu, Pengyuan Zhang, Muhammad Ashraf, David J. SahnAbstract:Objectives We sought to determine the feasibility and reproducibility of real-time 3-dimensional echocardiography (RT3DE) for evaluation of Cardiac Volume, mass, and function and to characterize maturational changes of these measurements in human fetuses.