Clinical Experience with Ivabradine in Acute Heart Failure

Cardiology ◽  
2016 ◽  
Vol 134 (3) ◽  
pp. 372-374 ◽  
Author(s):  
Marina Pascual Izco ◽  
Gonzalo Luis Alonso Salinas ◽  
Marcelo Sanmartín Fernández ◽  
Hugo Del Castillo Carnevalli ◽  
Manuel Jiménez Mena ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Blood Pressure ◽  
Randomized Trials ◽  
Beta Blockers ◽  
Treatment Results ◽  
Absolute Reduction ◽  
Attractive Option ◽  
And Oxidative Stress

Objective: Ivabradine has been shown to improve symptoms and to reduce rehospitalization and mortality in patients with severe chronic heart failure (HF). Its indication in acute HF is not clear. Acute HF patients could also benefit from HR reduction, as myocardial consumption and oxidative stress are related to tachycardia. Moreover, beta-blockers are contraindicated in cardiogenic shock and should not be initiated with congestive signs. Accordingly, we evaluated the role of ivabradine in acute HF patients. Methods: This was a retrospective analysis of 29 consecutive patients treated for acute HF in the Cardiac ICU, and for whom ivabradine was initiated during hospitalization between January 2011 and January 2014. All patients were in sinus rhythm and had a heart rate (HR) >70 bpm. Catecholamine use was necessary in 16 patients (57.1%) during the hospitalization, in 14 (87.5%) of these before ivabradine treatment. Results: Systolic blood pressure showed no variation during the first 24 h of ivabradine administration or at discharge. HR showed an absolute reduction of 10 bpm at 6 h (p < 0.001), 11 bpm at 24 h (p = 0.004) and 19 bpm (p < 0.001) at discharge. No episodes of significant bradycardia or hypotension were recorded after starting the drug. Conclusions: HR reduction with ivabradine in acute HF is well tolerated. It represents an attractive option, especially when there is excessive catecholamine-related tachycardia; this should be appropriately evaluated in randomized trials.

scholarly journals Rosiglitazone Decreases Blood Pressure in Female Dahl Rats: Role of Nitric Oxide and Oxidative Stress

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Julio C. Sartori‐Valinotti ◽  
Michael J. Ryan ◽  
Huimin Zhang ◽  
Jane F. Reckelhoff
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Blood Pressure ◽  
And Oxidative Stress

scholarly journals Supraphysiological Role of Melatonin Over Vascular Dysfunction of Pregnancy, a New Therapeutic Agent?

2021 ◽  
Vol 12 ◽  
Author(s):  
Francisco J. Valenzuela-Melgarejo ◽  
Constanza Lagunas ◽  
Fabiola Carmona-Pastén ◽  
Kevins Jara-Medina ◽  
Gustavo Delgado
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Vascular System ◽  
Systolic Pressure ◽  
Endothelial Damage ◽  
Scaffolding Protein ◽  
Placental Development ◽  
Melatonin Production ◽  
And Oxidative Stress

Hypertension can be induced by the disruption of factors in blood pressure regulation. This includes several systems such as Neurohumoral, Renin-angiotensin-aldosterone, the Circadian clock, and melatonin production, which can induce elevation and non-dipping blood pressure. Melatonin has a supraphysiological role as a chronobiotic agent and modulates vascular system processes via pro/antiangiogenic factors, inflammation, the immune system, and oxidative stress regulation. An elevation of melatonin production is observed during pregnancy, modulating the placenta and fetus’s physiological functions. Their impairment production can induce temporal desynchronization of cell proliferation, differentiation, or invasion from trophoblast cells results in vascular insufficiencies, elevating the risk of poor fetal/placental development. Several genes are associated with vascular disease and hypertension during pregnancy via impaired inflammatory response, hypoxia, and oxidative stress, such as cytokines/chemokines IL-1β, IL-6, IL-8, and impairment expression in endothelial cells/VSMCs of HIF1α and eNOS genes. Pathological placentas showed differentially expressed genes (DEG), including vascular genes as CITED2, VEGF, PL-II, PIGF, sFLT-1, and sENG, oncogene JUNB, scaffolding protein CUL7, GPER1, and the pathways of SIRT/AMPK and MAPK/ERK. Additionally, we observed modification of subunits of NADPH oxidase and extracellular matrix elements, i.e., Glypican and Heparanase and KCa channel. Mothers with a low level of melatonin showed low production of proangiogenic factor VEGF, increasing the risk of preeclampsia, premature birth, and abortion. In contrast, melatonin supplementation can reduce systolic pressure, prevent oxidative stress, induce the activation of the antioxidants system, and lessen proteinuria and serum level of sFlt-1. Moreover, melatonin can repair the endothelial damage from preeclampsia at the placenta level, increasing PIGF, Nrf-2, HO-1 production and reducing critical markers of vascular injury during the pregnancy. Melatonin also restores the umbilical and uterine blood flow after oxidative stress and inhibits vascular inflammation and VCAM-1, Activin-A, and sEng production. The beneficial effects of melatonin over pathological pregnancies can be partially observed in normal pregnancies, suggesting the dual role of/over placental physiology could contribute to protection and have therapeutic applications in vascular pathologies of pregnancies in the future.

scholarly journals Beta-Blockers and Oxidative Stress in Patients with Heart Failure

2011 ◽  
Vol 4 (8) ◽  
pp. 1088-1100 ◽  
Author(s):  
Kazufumi Nakamura ◽  
Masato Murakami ◽  
Daiji Miura ◽  
Kei Yunoki ◽  
Kenki Enko ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Beta Blockers ◽  
Patients With Heart Failure ◽  
And Oxidative Stress

Protective role of peroxiredoxin-4 in heart failure

2020 ◽  
Vol 134 (1) ◽  
pp. 71-72
Author(s):  
Naseer Ahmed ◽  
Masooma Naseem ◽  
Javeria Farooq
Keyword(s):  
Heart Failure ◽  
Cardiac Fibroblasts ◽  
Protective Role ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
Total Antioxidant ◽  
Galectin 3 ◽  
Consequent Increase ◽  
And Oxidative Stress

Abstract Recently, we have read with great interest the article published by Ibarrola et al. (Clin. Sci. (Lond.) (2018) 132, 1471–1485), which used proteomics and immunodetection methods to show that Galectin-3 (Gal-3) down-regulated the antioxidant peroxiredoxin-4 (Prx-4) in cardiac fibroblasts. Authors concluded that ‘antioxidant activity of Prx-4 had been identified as a protein down-regulated by Gal-3. Moreover, Gal-3 induced a decrease in total antioxidant capacity which resulted in a consequent increase in peroxide levels and oxidative stress markers in cardiac fibroblasts.’ We would like to point out some results stated in the article that need further investigation and more detailed discussion to clarify certain factors involved in the protective role of Prx-4 in heart failure.

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