Objectives. To compare the effects of losartan, enalapril and their combination in the prevention ofleft ventricular remodeling (LVRM) after acute myocardial infarction (AMI) in the rat. Methods. AMI model was induced...Objectives. To compare the effects of losartan, enalapril and their combination in the prevention ofleft ventricular remodeling (LVRM) after acute myocardial infarction (AMI) in the rat. Methods. AMI model was induced in female SD rats by ligating left coronary artery. Forty-eight hours after the procedure, 83 surviving rats were randomized into one of the following 4 groups: 1 ) AMI control group (n =19), 2) losartan group (n= 22, 3 mg @ kg - 1 @ d - 1 ), 3 ) enalapril group (n = 20, 1 mg @ kg - 1 @ d - 1 ), 4) losartan - enalapril combinative group (n = 22, 3 and 1 mg @ kg- 1 @ d - 1 respectively). 5 ) sham-operated group ( n =10) and 6) normal rats group (n = 10) were selected randomly to serve as non-infarction controls. Losartan and enalapril were delivered by direct gastric gavage. After 4 weeks of medical therapy, hemodynamic studies were performed in each group, then the rat hearts were fixed with 10% formalin and pathologic analysis on them was performed. Complete experimental data was obtained in 56 rats, comprising 1 ) AMI controls (n = 11 ), 2) losartan group (n = 10), 3 ) enalapril group (n = 10), 4) the combination of losartan and enalapril group (n = 11 ),5) sham - operated group (n = 6) and 6) normal controls (n=8). Results. There were no significant differences among the 4 AMI groups in MI size (41.7% ～ 43.4%, all P＞ 0.05). Compared with sham group, the left ventricular (LV) end diastolic pressure (LVEDP), volume (LVV), long and short axis length (L and D), as well as LV absolute and relative weight (LVAW and LVRW)in AMI group were all significantly increased ( P ＜0.05 ～ 0. 001 ); whereas the maximum left ventricular pressure rising and droping rates ( + dp/dt) and their corrected values by LV systolic pressure ( + dp/dt/LVSP)were significantly reduced (all P ＜0.001 ), indicating LVRM occurred and LV systolic and diastolic function impaired after AMI. Compared with AMI group , LVEDP, LVV, LVAW and LVRW were all significantly decreased (P ＜0.05～0.001 ); while + dp/dt/LVSP were significantly enhanced in all 3 treatment groups (P ＜0.05～0.001 ) except -dp/dt/LVSP in losartan group (P＞ 0. 05 ). There were no significant differences in the above indices among the 3 treatment groups (all P＞ 0.05). Conclusion. Both losartan and enalapril can prevent from LVRM after AMI in the rat and improve LV function with equivalent effects. There seems no additive effect when the 2 drugs are used in combination.展开更多
We describe a rare case of a 60-year-old woman suffering from intramyocardial dissection and left ventricular aneurysm secondary to acute myocardial infarction. A rare form of ventricular septal rupture resulted from ...We describe a rare case of a 60-year-old woman suffering from intramyocardial dissection and left ventricular aneurysm secondary to acute myocardial infarction. A rare form of ventricular septal rupture resulted from intramyocardial dissection deterioration, which was iden- tified during echocardiographic follow-up. Surgical repair under beating-heart cardiopulmonary bypass was successful.展开更多
OBJECTIVE: To compare the effects of high, middle and low doses of enalapril in preventing left ventricular remodeling (LVRM) after acute myocardial infarction (AMI) in rats, especially evaluating the efficacy of low ...OBJECTIVE: To compare the effects of high, middle and low doses of enalapril in preventing left ventricular remodeling (LVRM) after acute myocardial infarction (AMI) in rats, especially evaluating the efficacy of low dose enalapril. METHODS: AMI was induced by ligating the left coronary artery in 149 female SD rats. 48 hours after the procedure, the 97 surviving rats were randomized to one of the following four groups: (1) AMI controls (n = 24), (2) high-dose (10 mg x kg(-1) x d(-1), n = 25), (3) middle-dose (1 mg x kg(-1) x d(-1), n = 23), and (4) low-dose (0.1 mg x kg(-1) x d(-1), n = 25) enalapril groups. In addition, sham-operated (n = 13) and normal rats (n = 10) were randomly selected to serve as non-infarction controls. Enalapril was delivered by direct gastric gavage. After 4 weeks of therapy, hemodynamic studies were performed, then the rat hearts were fixed with 10% formalin and pathology analysis was performed. Exclusive of the dead rats and those with MI size 55%, complete experimental data were obtained from 67 rats, which were comprised of (1) AMI controls (n = 13), (2) high-dose enalapril (n = 13), (3) middle-dose enalapril (n = 12), (4) low-dose enalapril (n = 12), (5) sham-operated (n = 8) and (6) normal (n = 9) groups. RESULTS: There were no significant differences among the four AMI groups in infarction size (all P > 0.05). Compared with the sham-operated group, the left ventricular (LV) end diastolic pressure (LVEDP), volume (LVV), absolute and relative weight (LVAW, LVRW) in AMI group were all significantly increased (all P展开更多
文摘Objectives. To compare the effects of losartan, enalapril and their combination in the prevention ofleft ventricular remodeling (LVRM) after acute myocardial infarction (AMI) in the rat. Methods. AMI model was induced in female SD rats by ligating left coronary artery. Forty-eight hours after the procedure, 83 surviving rats were randomized into one of the following 4 groups: 1 ) AMI control group (n =19), 2) losartan group (n= 22, 3 mg @ kg - 1 @ d - 1 ), 3 ) enalapril group (n = 20, 1 mg @ kg - 1 @ d - 1 ), 4) losartan - enalapril combinative group (n = 22, 3 and 1 mg @ kg- 1 @ d - 1 respectively). 5 ) sham-operated group ( n =10) and 6) normal rats group (n = 10) were selected randomly to serve as non-infarction controls. Losartan and enalapril were delivered by direct gastric gavage. After 4 weeks of medical therapy, hemodynamic studies were performed in each group, then the rat hearts were fixed with 10% formalin and pathologic analysis on them was performed. Complete experimental data was obtained in 56 rats, comprising 1 ) AMI controls (n = 11 ), 2) losartan group (n = 10), 3 ) enalapril group (n = 10), 4) the combination of losartan and enalapril group (n = 11 ),5) sham - operated group (n = 6) and 6) normal controls (n=8). Results. There were no significant differences among the 4 AMI groups in MI size (41.7% ～ 43.4%, all P＞ 0.05). Compared with sham group, the left ventricular (LV) end diastolic pressure (LVEDP), volume (LVV), long and short axis length (L and D), as well as LV absolute and relative weight (LVAW and LVRW)in AMI group were all significantly increased ( P ＜0.05 ～ 0. 001 ); whereas the maximum left ventricular pressure rising and droping rates ( + dp/dt) and their corrected values by LV systolic pressure ( + dp/dt/LVSP)were significantly reduced (all P ＜0.001 ), indicating LVRM occurred and LV systolic and diastolic function impaired after AMI. Compared with AMI group , LVEDP, LVV, LVAW and LVRW were all significantly decreased (P ＜0.05～0.001 ); while + dp/dt/LVSP were significantly enhanced in all 3 treatment groups (P ＜0.05～0.001 ) except -dp/dt/LVSP in losartan group (P＞ 0. 05 ). There were no significant differences in the above indices among the 3 treatment groups (all P＞ 0.05). Conclusion. Both losartan and enalapril can prevent from LVRM after AMI in the rat and improve LV function with equivalent effects. There seems no additive effect when the 2 drugs are used in combination.
文摘We describe a rare case of a 60-year-old woman suffering from intramyocardial dissection and left ventricular aneurysm secondary to acute myocardial infarction. A rare form of ventricular septal rupture resulted from intramyocardial dissection deterioration, which was iden- tified during echocardiographic follow-up. Surgical repair under beating-heart cardiopulmonary bypass was successful.
文摘OBJECTIVE: To compare the effects of high, middle and low doses of enalapril in preventing left ventricular remodeling (LVRM) after acute myocardial infarction (AMI) in rats, especially evaluating the efficacy of low dose enalapril. METHODS: AMI was induced by ligating the left coronary artery in 149 female SD rats. 48 hours after the procedure, the 97 surviving rats were randomized to one of the following four groups: (1) AMI controls (n = 24), (2) high-dose (10 mg x kg(-1) x d(-1), n = 25), (3) middle-dose (1 mg x kg(-1) x d(-1), n = 23), and (4) low-dose (0.1 mg x kg(-1) x d(-1), n = 25) enalapril groups. In addition, sham-operated (n = 13) and normal rats (n = 10) were randomly selected to serve as non-infarction controls. Enalapril was delivered by direct gastric gavage. After 4 weeks of therapy, hemodynamic studies were performed, then the rat hearts were fixed with 10% formalin and pathology analysis was performed. Exclusive of the dead rats and those with MI size 55%, complete experimental data were obtained from 67 rats, which were comprised of (1) AMI controls (n = 13), (2) high-dose enalapril (n = 13), (3) middle-dose enalapril (n = 12), (4) low-dose enalapril (n = 12), (5) sham-operated (n = 8) and (6) normal (n = 9) groups. RESULTS: There were no significant differences among the four AMI groups in infarction size (all P > 0.05). Compared with the sham-operated group, the left ventricular (LV) end diastolic pressure (LVEDP), volume (LVV), absolute and relative weight (LVAW, LVRW) in AMI group were all significantly increased (all P
