scholarly journals 948-48 High-dose Lisinopril is More Effective than Low-dose in Suppressing Aldosterone in Patients with Chronic Heart Failure

1995 ◽  
Vol 25 (2) ◽  
pp. 177A
Author(s):  
Neil C. Davidson ◽  
Wendy J. Coutie ◽  
Allan D. Struthers
2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
K Labr ◽  
J Spinar ◽  
J Parenica ◽  
L Spinarova ◽  
F Malek ◽  
...  

Abstract Background Beta-blockers (BB) decrease morbidity and mortality in heart failure patients and are part of the first line treatment together with inhibitors of angiotensin converting enzyme. New metaanalysis from year 2014 of main BB studies in chronic heart failure showed no benefit of BB in patients with atrial fibrillation (AF). Methods 1088 at least one month stable chronic heart failure patients with ejection fraction <50% were included in FAR NHL (FARmacology and NeuroHumoraL activation) registry. Three centers with speciality in heart failure in the Czech Republic were participating from November 2014 to December 2015. Results 80% patients were male with median age 66 years. Aetiology of heart failure was in 49.4% ischemic heart disease, in 42.3% dilated cardiomyopathy, in 0.5% hypertrophy cardiomyopathy. From those receiving beta-blockers 20% received low dose similar to the starting dose, 57% medium dose and 17% high dose which was set as the target BB dose. Nearly 93.8% of patients received BB. But only 17.0% received the high dose of BB. 6.2% of patients were not treated by BB at all. One third of patients (34.5%) had atrial fibrillation in medical history or newly recorded on electrocardiogram. Patients with AF were much older (median 63 vs. 70 years, respectively; p<0.001), had higher heart rate (72 vs. 74 /min; p<0.006) and were also in higher class of NYHA (New York Heart Association; p=0.005). The primary endpoint was set as all cause death, mechanical circulatory support implantation, orthotopic heart transplantation or hospitalization for acute heart failure. Patients with AF survived without primary endpoint in 70.6%, patients without AF in 78.8% (p=0.005) even after age standardization. There was significantly different survival according to dose of beta-blocker, the higher was dose of BB, the higher was survival. Patients with no beta-blocker survived without primary endpoint in 63.9%, with low dose survived in 72.6%, medium dose in 77.0% and with high dose in 80.9%. We devided FAR NHL patients into two groups according to atrial fibrillation. Patients without AF had the better survival without primary endpoint. The higher dose of beta-blockers they got, the better survival they had (69.5%, 76.7%, 78.9%, 85.1%; p=0.007). Also patients with AF had better survival without primary endpoint, the higher dose of beta-blocker they got, the higher was their survival without endpoitnt (56.0%, 63.6%, 73.0%, 75.8%; p=0.007). Conclusion In FAR NHL registry of stable chronic heart failure patietnts was one third of patients with atrial fibrillation. Nearly 94% of patients received beta-blocker. But only 17% received the target dose. Pacients even with or without atrial fibrillation had the significantly better survival without primary endpoint the higher was the dose of beta-blocker.


Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Yoichi Sunagawa ◽  
Miho Suzuki ◽  
Masafumi Funamoto ◽  
Yasufumi Katanasaka ◽  
Hidetoshi Suzuki ◽  
...  

Introduction: Heart failure is associated with pathological growth and mitochondrial dysfunction of constituent cardiomyocytes. To achieve effective oral pharmacological therapy for heart failure, we screened compounds isolated from natural products and found that auraptene derived from the peel of Citrus Hassaku may be applicable to pharmacological therapy for heart failure. Hypothesis: We assessed the hypothesis that auraptene could improve the deterioration of mitochondrial function and the development of heart failure in rats with myocardial infarction (MI). Methods and Results: In cultured cardiomyocytes, auraptene (2.5-10 μM) dose-dependently repressed phenylephrine-induced hypertrophic responses such as increase in cell size and ANF and ET-1 promoter activations. Auraptene also activated mitochondrial- and lipid metabolism-related gene transcriptions, such as PGC1α, PPARα/γ, mCPT1, UCP3, and PDK4. One week after operation, 22 rats with a moderate size of MI (Fractional shortening (FS) < 40%) were then randomly assigned to vehicle (n=8), auraptene low-dose (5 mg/kg/day, n=7), or high-dose (50 mg/kg/day, n=7). Oral daily treatments with these agents were continued for 6 weeks. There were no differences in left ventricle (LV) geometric and functional data among the 3 MI groups before treatment. After treatment, LVFS was significantly higher in the auraptene low-dose (21%, p < 0.0001) and high-dose (26%, p < 0.0001) groups than the vehicle group (16%). LV wall thickness in the remote non-infarct area was significantly thinner in the auraptene low-dose (1.4 mm, p < 0.01) and high-dose (1.2 mm, p < 0.0001) groups than the vehicle group (2.5 mm). Histological analysis demonstrated that auraptene treatment significantly suppressed MI-induced increases in myocardial cell diameter and perivascular fibrosis compared with vehicle treatment. Moreover, auraptene also prevented the activations of ANF and MCP-1 mRNA levels and up-regulated mitochondrial- and lipid metabolism-related gene transcriptions in LV. Conclusions: Auraptene treatment prevents the worsening of LV systolic function and represses hypertrophy after MI in adult rats. A natural compound, auraptene is expected as a novel useful agent for heart failure therapy in humans.


1999 ◽  
Vol 5 (3) ◽  
pp. 70
Author(s):  
Tomohiro Harada ◽  
Eiji Ohtaki ◽  
Koichi Kitahara ◽  
Jun Umemura ◽  
Tetsuya Sumiyoshi ◽  
...  

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