Short-term and long-term hemodynamic and clinical effects of metoprolol alone and combined with amlodipine in patients with chronic heart failure

Kukin, Marrick; Freudenberger, Ronald S; Mannino, Michael M.; Kalman, Jill; Steinmetz, Marilyn; Buchholz-Varley, Cathleen; Ocampo, Ofelia

doi:10.1016/s0002-8703(99)70110-9

Cited by 15 publications

(7 citation statements)

References 23 publications

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“…This was, however, not consistent across all studies [21,22]. In our study we detected an association of the use of calcium channel blockers and mortality.…”

Section: Discussioncontrasting

confidence: 91%

Use of Calcium Channel Blockers is Associated with Mortality in Patients with Chronic Kidney Disease

Haider¹,

Sauter²,

Lindner³

et al. 2015

Kidney Blood Press Res

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Background/Aims: The use of antihypertensive medicines has been shown to reduce proteinuria, morbidity, and mortality in patients with chronic kidney disease (CKD). A specific recommendation for a class of antihypertensive drugs is not available in this population, despite the pharmacodynamic differences. We have therefore analysed the association between antihypertensive medicines and survival of patients with chronic kidney disease. Methods: Out of 2687 consecutive patients undergoing kidney biopsy a cohort of 606 subjects with retrievable medical therapy was included into the analysis. Kidney function was assessed by glomerular filtration rate (GFR) estimation at the time point of kidney biopsy. Main outcome variable was death. Results: Overall 114 (18.7%) patients died. In univariate regression analysis the use of alpha-blockers and calcium channel antagonists, progression of disease, diabetes mellitus (DM) type 1 and 2, arterial hypertension, coronary heart disease, peripheral vascular disease, male sex and age were associated with mortality (all p<0.05). In a multivariate Cox regression model the use of calcium channel blockers (HR 1.89), age (HR 1.04), DM type 1 (HR 8.43) and DM type 2 (HR 2.17) and chronic obstructive pulmonary disease (HR 1.66) were associated with mortality (all p < 0.05). Conclusion: The use of calcium channel blockers but not of other antihypertensive medicines is associated with mortality in primarily GN patients with CKD.

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“…This was, however, not consistent across all studies [21,22]. In our study we detected an association of the use of calcium channel blockers and mortality.…”

Section: Discussioncontrasting

confidence: 91%

Use of Calcium Channel Blockers is Associated with Mortality in Patients with Chronic Kidney Disease

Haider¹,

Sauter²,

Lindner³

et al. 2015

Kidney Blood Press Res

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“…In the early stage of β-blocker treatment, hypofunction in the left ventricle often occurs in patients due to the suppression in the β-adrenoceptors/cAMP/PKA pathway, which would lead to intolerance. Therefore, β-blockers cannot be used in the target dose for some patients ( Kukin et al, 1999 ). In that case, drugs to improve cardiac hypertrophy independent of the β-adrenoceptors/cAMP/PKA pathway such as wogonin, targeting the PI3K/Akt pathway, may be beneficially supplemented.…”

Section: Discussionmentioning

confidence: 99%

Wogonin Attenuates Isoprenaline-Induced Myocardial Hypertrophy in Mice by Suppressing the PI3K/Akt Pathway

Qian

Jia

et al. 2018

Front. Pharmacol.

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Many studies have focused on identifying therapeutic targets of myocardial hypertrophy for the treatment of correlative cardiac events. Wogonin is a natural flavonoid compound that displays a potent anti-hypertrophic effect. Knowledge of its pharmacological mechanisms might reveal an effective way to search for therapeutic targets. Myocardial hypertrophy was replicated by the subcutaneous implantation of an isoprenaline minipump in mice or isoprenaline treatment of H9C2 cells. Pathologic changes in cardiac structure were assessed by echocardiographic and histological examinations. The signaling transduction in hypertrophy-promoting pathways and the genes involved were detected by western blot and RT-qPCR. Wogonin significantly attenuated isoprenalineinduced myocardial hypertrophy in vivo and in vitro by suppressing phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) hypertrophy-promoting pathway. Wogonin promoted the ubiquitination and degradation of PI3K catalytic subunit alpha (Pik3ca), the catalytic subunit of PI3K, which was upregulated by isoprenaline treatment. Wogonin also increased the expression of neural precursor cells expressing developmentally down-regulated gene 4-like (Nedd4l), the ubiquitin E3 ligase of Pik3ca. Therefore, wogonin targets Nedd4l to induce the degradation of Pik3ca, which reverses the overactivation of the PI3K/Akt pathway and consequently relieves the isoprenaline-induced myocardial hypertrophy.

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“…Some, but not all βAAs improve symptoms and prolong survival of heart failure patients ( MERIT‐HF Study Group, 1999 ; CIBIS II Investigators and Committees, 1999 ; Packer et al ., 1996 ). Initiation of βAA therapy is often limited by worsening congestive heart failure, which may manifest as a decrease in haemodynamics ( Kukin et al ., 1999 ) or by β 2 ‐mediated bronchoconstriction. Therefore, low doses of the βAA are a necessity, especially in the beginning of a β‐adrenoceptor blocker treatment.…”

Section: Discussionmentioning

confidence: 99%

Nebivolol, bucindolol, metoprolol and carvedilol are devoid of intrinsic sympathomimetic activity in human myocardium

Brixius

Bundkirchen

Bölck

et al. 2001

British J Pharmacology

100

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The present study investigated whether or not there may be differences in the direct cardiac actions of the novel, highly β1‐selective adrenoceptor antagonist nebivolol (NEB) in comparison to metoprolol (MET), bisoprolol (BIS), carvedilol (CAR) and bucindolol (BUC) in human myocardium (n=9). The rank order of β1‐selectivity as judged by competition experiments to 3H‐CGP 12.1777 in the presence of CGP 207.12 A (300 nmol l−1, Kiβ2) or ICI 118.551 (50 nmol l−1, Kiβ1) were NEB(Kiβ2/Kiβ1: 40.7)>BIS(15.6)>MET(4.23)>CAR(0.73)>BUC(0.49). The rank order of the negative inotropic potency of the β‐adrenoceptor antagonists measured in left ventricular trabeculae (dilated cardiomyopathy, DCM) as judged by the concentration needed to induce a 50% decrease in isoprenaline (1 μmol l−1)‐stimulated force (IC50) was: MET (0.6 μmol l−1)>CAR (4.1 μmol l−1)>NEB (7.0 μmol l−1). NEB, BUC, MET and CAR did not not exert an intrinsic sympathomimetic activity (ISA) as determined by measurements of force development in forskolin (0.3 μmol l−1) pre‐treated left ventricular trabeculae, nor by measuring adenylate cyclase activity in forskolin (0.3 μmol l−1)‐stimulated assays (crude membranes). This also holds true for radioligand binding assays with or without guanine nucleotide guanyl‐5′‐yl imidodiphosphate (Gpp(NH)p). Although all studied β‐adrenoceptor antagonists lack intrinsic sympathomimetic activity (ISA), they differ in the β1‐selectivity as well as in their direct negative inotropic action. These differences as well as the mode of extracardiac action may have an impact on outcome of patients treated with β‐adrenoceptor antagonists. British Journal of Pharmacology (2001) 133, 1330–1338; doi:

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Short-term and long-term hemodynamic and clinical effects of metoprolol alone and combined with amlodipine in patients with chronic heart failure

Cited by 15 publications

References 23 publications

Use of Calcium Channel Blockers is Associated with Mortality in Patients with Chronic Kidney Disease

Use of Calcium Channel Blockers is Associated with Mortality in Patients with Chronic Kidney Disease

Wogonin Attenuates Isoprenaline-Induced Myocardial Hypertrophy in Mice by Suppressing the PI3K/Akt Pathway

Nebivolol, bucindolol, metoprolol and carvedilol are devoid of intrinsic sympathomimetic activity in human myocardium

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