Protective effect of melatonin in atherosclerotic cardiovascular disease: A comprehensive review

2021 ◽  
Vol 4 (3) ◽  
pp. 408-430
Author(s):  
Madhuri Datta ◽  
Romit Majumder ◽  
Aindrila Chattopadhyay ◽  
Debasish Bandyopadhyay
Keyword(s):  
Heart Failure ◽  
Conventional Therapy ◽  
Death Rate ◽  
Synergistic Effects ◽  
Atherosclerotic Cardiovascular Disease ◽  
Comprehensive Review ◽  
Cardiovascular Tissue ◽  
Pathological Conditions ◽  
Heart Disorders

Heart failure is characterized by the heart losing its capacity to pump sufficient blood to match the body’s demand. It is caused by  a variety of cardiovascular impairments. Among them,  atherosclerosis is the most common one. Although, a variety of medicines selectively target this pathology, the death rate due to atherosclerosis associated heart disorders remain high. To address this issue,  the use of antioxidants combined with conventional therapy to achieve synergistic effects has gained popularity. Melatonin is one of such antioxidants. In addition to its potent antioxidant activity, this molecule acts in harmony to protect the cardiovascular tissue. This review explores the various mechanisms by which melatonin protects the cardiovascular tissue. This information will contribute further insights into the role of melatonin in maintaining cardiovascular homeostasis in normal as well as in pathological conditions. It will also help us to better understand the potential synergistic effects of melatonin with conventional therapy to successfully target the heart failure associated with atherosclerosis.  

scholarly journals Role of interleukin-18 and plasma B-type natriuretic peptide in predicting requirement of kidney replacement therapy and/or mortality in individuals with acute heart disorders

2019 ◽  
Vol 8 (4) ◽  
pp. 292-300
Author(s):  
Aida Hamzić-Mehmedbašić ◽  
Damir Rebić ◽  
Amina Valjevac ◽  
Hajrunisa Čubro ◽  
Azra Durak Nalbantić ◽  
...  
Keyword(s):  
Heart Failure ◽  
Replacement Therapy ◽  
Natriuretic Peptide ◽  
Left Ventricular ◽  
Apache Ii Score ◽  
Interleukin 18 ◽  
Cutoff Value ◽  
Coronary Syndrome ◽  
Heart Disorders

Introduction: Although many predictive tools have already been developed, efforts are still proceeding to identify a reliable biomarker to predict the prognosis of the patients with acute heart disorders. Objectives: The aim was to evaluate the role of renal injury biomarkers (serum cystatin C, serum and urine interleukin-18, IL-18) and heart failure biomarkers (plasma B-type natriuretic peptide, BNP) in the prediction of the postdischarge requirement of renal replacement therapy (RRT) and/or 6-month mortality in patients with acute heart disorders. Patients and Methods: In patients diagnosed with acute heart disorders (acute heart failure [AHF] and/or acute coronary syndrome [ACS]) and admitted to the intensive care units, baseline clinical parameters, renal and cardiac biomarkers were determined. Patients were followed up for 6 months. The composite outcome was the postdischarge requirement of RRT and/or 6-month mortality. Results: Of 120 patients, 5.8% continued RRT after discharge. The 6-month mortality was 20%. Cox logistic regression analysis showed that urine IL-18 (P=0.021), plasma BNP (P=0.046), Acute Physiology and Chronic Health Evaluation (APACHE) II score (P=0.002), and left ventricular diastolic dysfunction (P=0.045) were independent predictors of the postdischarge requirement of RRT and/or 6-month mortality. For predicting RRT and/or 6-month mortality, using urine IL-18 cutoff value of 29.1 pg/mL showed 66.7% sensitivity and 67.7% specificity (area under the curve, AUC 0.70, P=0.003), while using plasma BNP cutoff value of 881.6 pg/mL showed 66.7% sensitivity and 70.8% specificity (AUC 0.76, P<0.001). Conclusion: Urine IL-18 and plasma BNP are independently predictive for the postdischarge requirement of RRT and/or 6-month mortality in patients with acute heart disorders.

scholarly journals Vitamin C and Cardiovascular Disease: An Update

Antioxidants ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 1227
Author(s):  
Marco B. Morelli ◽  
Jessica Gambardella ◽  
Vanessa Castellanos ◽  
Valentina Trimarco ◽  
Gaetano Santulli
Keyword(s):  
Heart Failure ◽  
Cardiovascular Disease ◽  
Vitamin C ◽  
Antioxidant Properties ◽  
Cerebrovascular Diseases ◽  
Preclinical Studies ◽  
Cardiovascular Disorders ◽  
Beneficial Effects ◽  
Pathological Conditions

The potential beneficial effects of the antioxidant properties of vitamin C have been investigated in a number of pathological conditions. In this review, we assess both clinical and preclinical studies evaluating the role of vitamin C in cardiac and vascular disorders, including coronary heart disease, heart failure, hypertension, and cerebrovascular diseases. Pitfalls and controversies in investigations on vitamin C and cardiovascular disorders are also discussed.

The Significance of the Late Na+ Current for Arrhythmia Induction and the Therapeutic Antiarrhythmic Potential of Ranolazine

2016 ◽  
Vol 22 (1) ◽  
pp. 40-50 ◽  
Author(s):  
Fleur E. Mason ◽  
Samuel Sossalla
Keyword(s):  
Heart Failure ◽  
Clinical Studies ◽  
Na Current ◽  
Clinical Role ◽  
Cellular Electrophysiology ◽  
Pathological Conditions ◽  
Myocardial Pathology ◽  
Antiarrhythmic Effects

The purpose of this article is to review the basis of arrhythmogenesis, the functional and clinical role of the late Na current, and its therapeutic inhibition. Under pathological conditions such as ischemia and heart failure this current is abnormally enhanced and influences cellular electrophysiology as a proarrhythmic substrate in myocardial pathology. Ranolazine the only approved late Na current blocker has been demonstrated to produce antiarrhythmic effects in the atria and the ventricle. We summarize recent experimental and clinical studies of ranolazine and other experimental late Na current blockers and discuss the significance of the available data.

scholarly journals Synergistic effects of ivabradine and metformin in the treatment of concomitant chronic heart failure and diabetes mellitus by regulating the activity of the H19/miR-423-5p/HCN4 axis

2021 ◽  
Author(s):  
Fang Zhang ◽  
Weijun Jiang ◽  
Yating Liu ◽  
Liu Li ◽  
Rui Wang ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Heart Failure ◽  
Chronic Heart Failure ◽  
Real Time ◽  
Therapeutic Effect ◽  
Real Time Pcr ◽  
Molecular Mechanisms ◽  
Target Genes ◽  
Synergistic Effects

IntroductionIn this study, the molecular mechanisms underlying the therapeutic effect of metformin (MET) and ivabradine (IBD) in the treatment of concomitant chronic heart failure (CHF) and diabetes mellitus (DM) were investigated.Material and methodsBasic and cardiac indexes were measured to study the therapeutic effect of MET and IBD. Real-time PCR, IHC assays, in-silicon analysis, luciferase assays, real-time PCR and Western blot assays were conducted to clarify the molecular mechanisms underlying the interaction between MET and IBD.ResultsMET administration restored the normal values of general/cardiac indexes in CHF rats. The abnormal values of echocardiographic indexes in CHF rats with STZ-induced DM were all corrected by a certain degree after the MET administration. Moreover, the injection of STZ up-regulated the expression of plasma NE/BNP-45, while the IBD administration reduced the levels of NE/BNP-45 in CHF rats. Furthermore, the administration of MET also reduced the NE level in CHF rats, indicating that both MET and IBD can exert a therapeutic effect on CHF rats. Additionally, in-silicon analysis and luciferase assays verified the role of H19 and HCN4 as target genes of miR-423-5p. In fact, the transfection of MET or H19 siRNA1/2 into HL-1 and H9C2 cells down-regulated the levels of H19 and HCN4 while increasing the level of miR-423-5p.ConclusionsMET reduces H19 expression via inducing methylation of its promoter, and the inhibited H19 expression suppresses HCN4 expression by up-regulating miR-423-5p expression. As a result, the suppressed expression of HCN4 reduces heart rate and exhibits a therapeutic effect in the treatment of concomitant CHF and DM.

scholarly journals Sex Differences and Regulatory Actions of Estrogen in Cardiovascular System

2021 ◽  
Vol 12 ◽  
Author(s):  
Kazutaka Ueda ◽  
Nobuaki Fukuma ◽  
Yusuke Adachi ◽  
Genri Numata ◽  
Hiroyuki Tokiwa ◽  
...  
Keyword(s):  
Heart Failure ◽  
Sex Differences ◽  
Hormone Replacement ◽  
Tissue Homeostasis ◽  
Cardiovascular Tissue ◽  
Full Extent ◽  
Great Progress ◽  
Regulatory Actions ◽  
Made In

Great progress has been made in the understanding of the pathophysiology of cardiovascular diseases (CVDs), and this has improved the prevention and prognosis of CVDs. However, while sex differences in CVDs have been well documented and studied for decades, their full extent remains unclear. Results of the latest clinical studies provide strong evidence of sex differences in the efficacy of drug treatment for heart failure, thereby possibly providing new mechanistic insights into sex differences in CVDs. In this review, we discuss the significance of sex differences, as rediscovered by recent studies, in the pathogenesis of CVDs. First, we provide an overview of the results of clinical trials to date regarding sex differences and hormone replacement therapy. Then, we discuss the role of sex differences in the maintenance and disruption of cardiovascular tissue homeostasis.

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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