scholarly journals Na/K-ATPase Signaling and Cardiac Pre/Postconditioning with Cardiotonic Steroids

2018 ◽  
Vol 19 (8) ◽  
pp. 2336 ◽  
Author(s):  
Pauline Marck ◽  
Sandrine Pierre
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Clinical Research ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Ischemic Heart ◽  
Low Concentrations ◽  
Cardioprotective Action

The first reports of cardiac Na/K-ATPase signaling, published 20 years ago, have opened several major fields of investigations into the cardioprotective action of low/subinotropic concentrations of cardiotonic steroids (CTS). This review focuses on the protective cardiac Na/K-ATPase-mediated signaling triggered by low concentrations of ouabain and other CTS, in the context of the enduring debate over the use of CTS in the ischemic heart. Indeed, as basic and clinical research continues to support effectiveness and feasibility of conditioning interventions against ischemia/reperfusion injury in acute myocardial infarction (AMI), the mechanistic information available to date suggests that unique features of CTS-based conditioning could be highly suitable, alone /or as a combinatory approach.

scholarly journals Ischemia/Reperfusion Injury following Acute Myocardial Infarction: A Critical Issue for Clinicians and Forensic Pathologists

2017 ◽  
Vol 2017 ◽  
pp. 1-14 ◽  
Author(s):  
Margherita Neri ◽  
Irene Riezzo ◽  
Natascha Pascale ◽  
Cristoforo Pomara ◽  
Emanuela Turillazzi
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Sudden Death ◽  
Reperfusion Injury ◽  
Nitrosative Stress ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Critical Issue ◽  
Current Standard ◽  
Tissue Alterations

Acute myocardial infarction (AMI) is a leading cause of morbidity and mortality. Reperfusion strategies are the current standard therapy for AMI. However, they may result in paradoxical cardiomyocyte dysfunction, known as ischemic reperfusion injury (IRI). Different forms of IRI are recognized, of which only the first two are reversible: reperfusion-induced arrhythmias, myocardial stunning, microvascular obstruction, and lethal myocardial reperfusion injury. Sudden death is the most common pattern for ischemia-induced lethal ventricular arrhythmias during AMI. The exact mechanisms of IRI are not fully known. Molecular, cellular, and tissue alterations such as cell death, inflammation, neurohumoral activation, and oxidative stress are considered to be of paramount importance in IRI. However, comprehension of the exact pathophysiological mechanisms remains a challenge for clinicians. Furthermore, myocardial IRI is a critical issue also for forensic pathologists since sudden death may occur despite timely reperfusion following AMI, that is one of the most frequently litigated areas of cardiology practice. In this paper we explore the literature regarding the pathophysiology of myocardial IRI, focusing on the possible role of the calpain system, oxidative-nitrosative stress, and matrix metalloproteinases and aiming to foster knowledge of IRI pathophysiology also in terms of medicolegal understanding of sudden deaths following AMI.

Targeted pharmacotherapy for ischemia reperfusion injury in acute myocardial infarction

2020 ◽  
Vol 21 (15) ◽  
pp. 1851-1865
Author(s):  
Amit Rout ◽  
Udaya S Tantry ◽  
Marko Novakovic ◽  
Ajaypaul Sukhi ◽  
Paul A Gurbel
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion
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