Search results for "Cardioprotection"
showing 10 items of 35 documents
HERS study disturbs hormonal replacement therapy
2000
Cardiovascular protection of hormonal replacement therapy was considered a fact. The effects of estrogens on lipid levels and vascular health gave biological support to estrogen cardioprotection. The recently published HERS study showing no protective effects of estrogen and progesterone replacement therapy on the risk of myocardial infarction or coronary deaths is provoking perplexity. These surprising results may have several causes such as the use of progesterone, the associated use of cardioprotective agents or the short observation period. However, the study results scope is rectricted to secondary prevention. These cannot be extrapolated to frequent conditions of postmenopausal women …
Nitroglycerin-induced cardioprotection is endothelial nitric oxide synthase- dependent
2015
Purpose We sought to evaluate the contribution of the endogenous NO pathway to the cardioprotective action of nitroglycerin (NTG). Methods and Results Anesthetized rabbits were subjected to 30-min myocardial ischemia (isc) and 3-h reperfusion (rep) and randomized into: Control group (no further intervention); PostC group (application of 8 cycles 30-sec isc/rep) and NTG treated group (2 μg/kg-1/min-1 IV bolus) for 65 min starting 10 min prior to rep. In additional groups, pharmacological inhibitors of NOS, nNOS, iNOS, PI3K, adenosine receptors and PKG were administrated with or without NTG. The infarcted (I) to risk (R) ratio was estimated. In a second experimental series tissue samples were…
Inorganic Nitrate Therapy Improves Doxorubicin-Induced Cardiomyopathy
2011
The anthracycline doxorubicin (DOX) is a potent and effective antineoplastic antibiotic agent widely used in the treatment of a broad range of forms of cancer. The clinical use of DOX is limited by cardiotoxicity, which increases dose dependently and may lead to dilated cardiomyopathy and clinical
Heart Failure and Left Ventricular Dysfunction
2018
Heart failure (HF) and left ventricular (LV) dysfunction are the most concerning and serious cardiovascular complications of cancer therapies and cause an increase in morbidity and mortality. Some cancer treatments induce left ventricular dysfunction that appears early after exposure and therefore may adversely affect oncological therapy, while others generate cardiac injuries resulting in clinical problems only years later.
Cardioprotection by gene therapy
2015
Ischemic heart disease remains the leading cause of death worldwide. Ischemic pre-, post-, and remote conditionings trigger endogenous cardioprotection that renders the heart resistant to ischemic-reperfusion injury (IRI). Mimicking endogenous cardioprotection by modulating genes involved in cardioprotective signal transduction provides an opportunity to reproduce endogenous cardioprotection with better possibilities of translation into the clinical setting. Genes and signaling pathways by which conditioning maneuvers exert their effects on the heart are partially understood. This is due to the targeted approach that allowed identifying one or a few genes associated with IRI and cardioprote…
C1-esterase inhibitor in ischemia and reperfusion.
2002
Summary Myocardial injury from ischemia can be aggravated by reperfusion of the jeopardized area. The precise underlying mechanisms have not been clearly defined, but proinflammatory events including complement activation play important roles. Cardioprotection by complement inhibition inter alia C1-esterase-inhibitor (C1-INH) was examined in several experimental models and under clinical conditions with ischemia and reperfusion. C1-INH reduced local anaphylatoxin release revealing the importance of the classical complement pathway. Inhibition of local complement activation was accompanied by improvement of myocardial function and perfusion of the previously ischemic myocardium. Leukocyte en…
Cardioprotection by gene therapy: A review paper on behalf of the Working Group on Drug Cardiotoxicity and Cardioprotection of the Italian Society of…
2015
Ischemic heart disease remains the leading cause of death worldwide. Ischemic pre-, post-, and remote conditionings trigger endogenous cardioprotection that renders the heart resistant to ischemic-reperfusion injury (IRI). Mimicking endogenous cardioprotection by modulating genes involved in cardioprotective signal transduction provides an opportunity to reproduce endogenous cardioprotection with better possibilities of translation into the clinical setting. Genes and signaling pathways by which conditioning maneuvers exert their effects on the heart are partially understood. This is due to the targeted approach that allowed identifying one or a few genes associated with IRI and cardioprote…
Prevention and Clinical Management of Cardiovascular Damage Induced by Anticancer Drugs: Need gor Early Biomarkers snd Cardio- snd Vasculo-Protection…
2018
The use of chemotherapy has largely improved the prognosis of cancer patients in the past two decades. However, the advent of more effective anticancer therapies has led to a higher incidence of cardiovascular toxicity that shows an increased incidence and represents a significant determinant of quality of life and mortality during ongoing treatment and in long-term survivors of cancer. In this setting, the primary objective for cardiologists and oncologists is the early identification of patients at high risk for developing cardiovascular toxicity and the identification of the cardiovascular cardiotoxicity in the earliest stages to personalize cancer therapy, arrange preventive interventio…
From molecular mechanisms to clinical management of antineoplastic drug-induced cardiovascular toxicity: A translational overview
2019
Significance: Antineoplastic therapies have significantly improved the prognosis of oncology patients. However, these treatments can bring to a higher incidence of side-effects, including the worrying cardiovascular toxicity (CTX). Recent Advances: Substantial evidence indicates multiple mechanisms of CTX, with redox mechanisms playing a key role. Recent data singled out mitochondria as key targets for antineoplastic drug-induced CTX; understanding the underlying mechanisms is, therefore, crucial for effective cardioprotection, without compromising the efficacy of anti-cancer treatments. Critical Issues: CTX can occur within a few days or many years after treatment. Type I CTX is associated…
Investigating and re-evaluating the role of glycogen synthase kinase 3 beta kinase as a molecular target for cardioprotection by using novel pharmaco…
2019
Aims Glycogen synthase kinase 3 beta (GSK3β) link with the mitochondrial Permeability Transition Pore (mPTP) in cardioprotection is debated. We investigated the role of GSK3β in ischaemia (I)/reperfusion (R) injury using pharmacological tools. Methods and results Infarct size using the GSK3β inhibitor BIO (6-bromoindirubin-3'-oxime) and several novel analogues (MLS2776-MLS2779) was determined in anaesthetized rabbits and mice. In myocardial tissue GSK3β inhibition and the specificity of the compounds was tested. The mechanism of protection focused on autophagy-related proteins. GSK3β localization was determined in subsarcolemmal (SSM) and interfibrillar mitochondria (IFM) isolated from Lang…